Treatment of Beard Hair Loss in Male Frontal Fibrosing Alopecia (FFA)

Beard Hair Loss in Males with FFA

I’ve selected this question below for this week’s question of the week. It allows us to review treatments for beard hair loss in males with FFA.

Question

I was diagnosed with LPP three months ago. My beard and hair are falling. Also persistent redness is in the beard area. My dermatologist started a steroid (1 month course) and 200 mg hydroxychloroquine treatment. We’re almost in the third month, but I continue see how my beard hairs are falling. Do you think is better to go with Methotrexate instead of keep trying with Hydroxychloroquine? I do not want to lose all my beard hair.

I am male, 34 yo, with itching and redness, hair shedding. I’m on hydroxychloroquine with oral Minoxidil and isotretinoin, healthy man, I’m in the third month of treatment, the hair starts to falling in March and begins in my beard, I lost some of the beard and hair.

Answer

Thanks for this really important question. In case you have not had a chance to review it yet, be sure to review the article on male frontal fibrosing alopecia that I wrote a few weeks ago. It summarizes all the studies on FFA in males published so far. As you’ll see in that article, there is alot of information summarizing the features of male FFA, but few that actually review treatment for FFA in males and fewer yet that specifically focus on the treatment of beard FFA.

It sounds like you are on a really good starting plan. My feeling is generally that I would not abandon a ‘potentially’ good treatment too soon. There is some evidence from medical studies that hydroxychloroquine can help males with FFA. I think that you and your dermatologist may want to make sure you are on an appropriate dose of hydroxychloroquine. Depending on your weight, it might be possible to go up on the dose. The following table is a guide:

It may be possible at this stage to add some very safe treatments to ‘help out’ the hydroxychloroquine and the isotretinoin. I can’t say what is right for you specifically as I don’t know all your information but this might include a mild topical steroid once or twice weekly and the use of a non-steroid like topical pimecroliumus, topical tacrolimus or having a compounding pharmacist make up topical tofacitinib (if possible to do so in your country). I do support using the non steroid quite often because the non steroid does not cause atrophy and generally won’t cause steroid telangiectasias (redness from dilated blood vessels). The beard area in FFA can often be red so we don’t want to over do the steroid effect.

I also advise many of my own patients to start oral cetirizine as this has a pretty good safety profile overall and may provide benefit. 10-20 mg is often used.

Oral minoxidil, isotretinoin and hydroxychloroquine are part of a really solid plan. These other options (cetirizine, topical steroid and topical non steroids) may help. As far as the scalp goes, I am a big fan of getting my own patients on topical or oral finasteride or dutasteride because of how well it helps the scalp. As far as the beard goes, we don’t have any evidence finasteride or dutasteride actually helps the beard in FFA but we also don’t have any evidence that it does not. It could be that finasteride and dutasteride are not only antiandrogenic - but antifibrotic or antinflammatory in some other way.

I would encourage you to take photos of the scalp and beard and eyebrows every 4 weeks. If you have not already, I would encourage you to take a set of photographs today. This will be really helpful as this is what is going to guide you and your doctors about what to do next.

There are two choices if the plan discussed above still does not seem to be working. The first would be to stop the isotretinoin and add oral doxycycline. Doxycycline can be used with hydroxychloroquine but doxycycline can not be used with isotretinoin due to an interaction between the two drugs. This step might be considered before methotrexate but there is nothing really wrong with going to methotrexate immediately next. One of the reasons I often recommend doxycycline over methotrexate to my own patients is because it is safer overall. I often combine hydroxychloroquine with doxycycline (100 mg once to twice daily) and cetrizine (10 mg to 20 mg daily) and add on low dose naltrexone (3 mg nightly) if needed. Topical fluocinonide “gel” is used on the beard once to twice weekly and topical tofacitinib or topical tacrolimus is used 3-5 times weekly on the beard.

In refractory cases, I start methotrexate or cyclosporine or apremilast.

Thanks again for the great question. I do think you are on a really solid plan and you’ve got a good plan for second steps if this does not work. We still don’t have great research studies to guide us as to exactly what to do next but I hope these suggestions are helpful for you.

Here is a list of first, second line and third line treatment (in my opinion) for FFA. As I mentioned above, how best to treat beard FFA is not clear. But this is a general approach.

What treatments for Androgenetic Alopecia Regrow Hair and Which just Stop it from Getting Worse?

Treatments for Androgenetic Hair Loss in Women

I’ve selected this question below for this week’s question of the week. It allows us to review treatments for androgenetic alopecia.

Question

I know there are many treatments for female androgenetic hair loss. I would like to know which treatments come with the chance that it will regrow hair and which just stop it from getting worse? How are these divided

Thank you

Answer

Thanks for the great question.

Every single recognized treatment for androgenetic hair loss comes with the potential to 'regrow hair.' That does not mean that it actually will regrow hair for any given person, but all come with some chance.

Again, it might not do that for every single user, but every treatment has this chance. If it does not, it doesn't work at all! There is no treatment in the world that "just maintains" hair. We do not categorize treatments in terms of “this group is a group that grows hair” and “this group is a group that just maintains it.”

Every single treatment has a certain percent of patients that will regrow some hair, a certain percent that will regrow a lot of hair, a certain percentage that will not regrow all that much but will maintain, and a certain percentage that the product won't help at all and hair loss will occur.

Example with topical minoxidil

For example, consider topical minoxidil:

30%-40% of women using topical minoxidil will regrow some hair with a 15-20% of women will regrow a lot of hair

30% of women using topical minoxidil will not regrow all that much but will still benefit from using the product because it will help maintain density.

30-40 % of women using topical minoxidil won't get much help at all from using the product.

Thanks and I hope this helps.

Dry & Brittle Hair after Using Isotretinoin

Dry hair after Isotretinoin

I’ve selected this question below for this week’s question of the week. It allows us to review some of the reasons for post isotretinoin scalp dryness.

Answer

My  hair is  so  brittle  after stopping  isotretinoin. It’s also quite dry.  What  might  be  the  cause?  Was it the drug?

Answer

Thanks for the question.

It's possible, but there  are many  causes actually.  One  needs  to  ideally have a  proper scalp  examination  and have the story reviewed from start to  finish.  (By ‘start’  I  mean not just  the start of last month  up  until  today but a full history from birth). One  needs  to  consider  many things.  

Isotretinoin can cause dryness that takes a while to settle after stopping. In many patients it does but one might need to be a bit gentler on t he hair for 3-6 months than they might have otherwise. I like my patients to reduce chemical and fragrance and potential irritants that can worsen they way the scalp feels. sometimes we switch away from a sulphate containing shampoo for a few months to allow the scalp to return back to normal.

Other causes of scalp dryness and brittleness need to be ruled out. If they are ruled out, I often consider a corticosteroid oil for my own patients along with the sulphate free shampoo. For my patients, the steroid oil is used once or twice weekly for 2-3 weeks before going down to once every two weeks for 2-3 months. Periodic use of an oil like coconut oil can also help provided there is not a lot of seborrheic dermatitis that is also on the scalp. I don’t know if that’s appropriate for you because I don’t know your story but that is something you can speak to your dermatologist about if everything else is completely ruled out.

The main issue is to be incredibly gentle on the hair and scalp for 3-6 months.

But what other conditions need to be considered ?

1) Seborrheic Dermatitis

One needs  to consider  seborrheic dermatitis that has  now  flared after stopping Accutane.   For  some people,  Accutane  treats some coexisting seborrheic dermatitis without  the  patient even knowing  and  then the  condition  flares when stopping.  

2) Hair styling Issues

One  needs  to consider  the  possibility that  overprocessing, coloring and/or heating of hair  is leading to  the  increased dryness. In  other  words, how  has  one’s  hair styling  practices  changed recently?  

3) Shampoo and Conditioner Issues

 One  also needs to consider  irritation from shampoos and conditioners and other topical products.   Has  a shampoo  or  conditioner or styling product changed?  

4) Autoimmune and inflammatory Issues

Of  course, with dryness one  needs  to  consider  inflammatory  scalp  issues  including autoimmune  issues,  psoriasis  and scarring alopecias  that have activated  or even  flared  post  stopping  Accutane. Fortunately,  they are rare  in  a situation like this.  But a dermatologist  can properly evaluate.  

5) Hormonal and Metabolic Issues

Finally, once needs to  consider  a variety  of metabolic and/or hormonal  issues  including those related to thyroid hormones,  estrogen  hormones or  androgen  hormones.  These  can  affect dryness  in  a  dramatic way.   Other  inflammatory scalp conditions  are  possible and  can be ruled  out  following proper examination.   

Spironolactone and Low Blood Pressure: How much will it drop?

Spironolactone and the Risk of Hypotension

I’ve selected this question below for this week’s question of the week. It allows us to the review some key data regarding blood pressure changes with spironolactone.

Question

I have been given a prescription for spironolactone for female pattern hair loss. I am concerned it might lower my blood pressure as my blood pressure often runs on the lower side of normal. Do you have any data on the chances of patients getting low blood pressure among users of this drug. How much does blood pressure usually drop?

Answer

Thanks for the great question. We’ve talked about the side effects of spironolactone in prior posts.

As far as changes in blood pressure among healthy women, the data has not been all that clear - until recently.

Garg and colleagues recently published a retrospective case series of 403 adult women treated for acne with spironolactone between 2008 and 2019. If we look into that data a bit closer, we can gain some valuable information on how it might affect blood pressure in those with androgenetic hair loss.

Does spironolactone affect blood pressure in health individuals? A new study suggests yes, but not by very much.

The median age of women in this study was 26. For 85 % of patients, the initial dose was 100 mg. Thereafter the dose increased for 50 % of women, stayed the same for 37.5 % and decreased in the remaining women.

Data was available regarding before and after blood pressure readings in 267 patients. The mean decrease in systolic blood pressure was 3.5 mm Hg (95% CI, 2.0 to 4.9) and the mean decrease in diastolic blood pressure was 0.9 mm Hg (95% CI, -0.2 to 2.1). The data was “statistically significant” meaning that spironolactone truly does affect blood pressure - it’s just the changes are quire small. No patient in the study needed to stop spironolactone because of blood pressure problems.

Summary and Comment

This was a nice study because good data and numbers on exactly how spironolactone affects blood pressure in healthy women have been hard to come by. We know that spironolactone can lower blood pressure in those with “ high blood pressure” by as much as 16 mm Hg systolic and 6 mm Hg diastolic. This data comes from a recently meta-analysis by Liu et al. This would lead many to believe that there must be a pretty big risk of low blood pressure in all our patients who use the drug for androgenetic hair loss. However, the real data says otherwise: healthy women who use spironolactone don’t get all that big of a change in their blood pressure and if they do - it does not typically affect them all that much

This study gives us some really good numbers to go on. For most healthy individuals spironolactone doesn’t affect blood pressure enough to really make a difference. If one is concerned, then baseline blood pressure testing and periodic follow up blood pressure testing is appropriate along with a slow increases in the dose. I have prescribed spironolactone to many patients who report low blood pressure and most patients tolerate 50-100 mg doses without any issues. So, is there ever an issue? Of course there is. Fortunately, it’s not common and patients who report lower blood pressure don’t necessarily need to lose out on a potentially effective treatment for them. We need to be cautious about going up too fast or to too high of a dose. Far too many people with androgenetic hair loss have completely shut off any sort of discussion about using spironolactone out of fears about low blood pressure. This study suggests we need to be cautious but not fearful. Low blood pressure is usually not a significant problem.

Reference

Garg et al. Long-term use of spironolactone for acne in women: A case series of 403 patients. J Am Acad Dermatol. . 2021 May;84(5):1348-1355.

Lui et al. Addition of spironolactone in patients with resistant hypertension: A meta-analysis of randomized controlled trials. Clin Exp Hypertens. 2017;39(3):257-263.

How does my treatment plan for LPP sound to you?

Treatment of LPP

I’ve selected this question below for this week’s question of the week. It allows us to the review some key concepts in the treatment of lichen planopilaris and the importance of photos in the long term evaluation of LPP disease activity.

Question

I have been diagnosed by biopsy 18 months ago with lichen planopilaris. I am a 74 year old woman and I noticed about three years before that I was thinning at the front of my head. My dermatologist has tried to help me with an antibiotic which I took for 6 months, to help the inflammation, or lower it. It wasn't effective and I don't think one should remain on this antibiotic for a longer time. The hair loss is also behind my ears and a little on my crown.

Since the beginning of April, I have been taking Hydroxychloroquine 200 mg every day in an attempt to stem the hair loss. I have not had any of the possible side effects thankfully. In fact, in the two months since I started this medication, I notice that I really don't have an itchy scalp any longer and much less frequently, an itchy back, My scalp isn't tender and not red close to the hairline as it was before this medication. Thankfully, I do not have any health problems and the only medication I take is for an under active thyroid.

Can you please advise if this would be a plan of action that you would advise?

Answer

Thanks for the great question. I’m so glad things seem moving in the right direction for you.

I can’t tell you if you are using the perfect plan because not enough time has elapsed. What I can say is there are good things in your story above that indicate you are indeed on track.

However, if you take a photo of your scalp in 2 years from now and it looks 100 % the same (or better) than the that photo that I’m going to enoucrage you to please take tonight ….. I can tell you that you are indeed on the right track!

Let’s look at some important points.

When we successfully treat scarring alopecia, we want several things to happen:

a) We want the rate of hair shedding to return back to ”normal”

b) We want scalp symptoms to disappear such that there is no itching, burning or tenderness

c) We want any scalp redness to disappear

d) We want hair loss to stop such that it’s not getting worse and worse over time.

e) Finally, if we catch LPP “early enough” in its disease evolution, we even want a bit of improvement in hair density to occur.

So are you successfully treating your scarring alopecia ?

It certainly sounds like you are treating your LPP quite well so far in your treatment journey. However, I can’t know for sure if the disease activity has “stopped”. Sometimes there will be clues when your dermatologist examines your scalp up close with trichoscopy that the disease activity has been reduced. For example, if you once had perifollicular scale (scale around the hairs) or had perifolliicular redness (redness around the hairs) when the scalp was examined by trichsocpy and now you do not have these findings, it means that your LPP disease activity has been reduced. If it was once possible to easy pull a great number of hairs from the scalp (i.e. a positive pull test) and now it is not so easy to extract hairs, then it may mean your disease activity has reduced.

The mistake that many patients and physicians make is assuming that zero redness, zero shedding and zero scaling means zero scarring alopecia disease activity. That’s not quite accurate. However, it sure sounds good. But it’s certainly a really important “first step.”

You see, it could be that for some patients that the redness goes away, and shedding reduces and flaking goes away and still the hair loss continues a little bit. That’s why photos are so important! I would encourage everyone with scarring alopecia to take photos or have someone take them for you.

I often get referrals from doctors who ask me to help the figure out if their patient’s disease activity is zero or not. If I don’t see much activity on the scalp when I perform a scalp examination, I reply to the patient and referring doctor by saying “things seem quiet today but I’ll give you my final answer in two years.”

I’ll take a photo now and then again 6 months, 12 months, 18 monks and 2 years. Sometimes we will take even more photos. If the photos look the same over a 2 year period of careful observation and there has been no further loss at all … then the scarring alopecia disease is deemed inactive.

I will point out at this juncture that the word inactive is not the same as burnt out. Inactive means the disease is quiet but it could be that the use of medications brought it to that state. Burnt out means the disease is completely over. One can take away all medications from true burnt out scarring alopecia and the disease still stays quiet.

Is your disease active?

You are only a few months into hydroxychloroquine treatment. It could be that the medication has slowed your LPP disease activity down or it could be that the medication has completely stopped the disease. We won’t know for sure a while. For some patients, it takes just a matter of months to see that the hair loss has in fact still continued. For others, it will take a full 1 or even 2 years to really get an appreciate that the hair loss is still continuing. It just depends one the speed of the hair loss.

If one’s LPP is progressing along fast, I can tell in 1- 2 months if the disease is still active

If one’s LPP is progressing along moderately fast, I can tell in 4-6 months if the disease is still active

If one’s LPP is progressing along moderately slowly, I can tell in 9-15 months if the disease is still active

If one’s LPP is progressing along really slowly, I may need 18-24 months to tell if the disease is still active

So I would encourage you to take lots and lots of photos every 3-6 months. When it comes to treating scarring alopecia, photos are so so important.

Of course, you’ll want to check in sooner with your doctors than 2 years in order to figure out how well you are doing on your treatment. In fact, you’ll probably want to be checking in with your doctors every 4-6 months. I’m glad you have no side effects with hydroxychloroquine but do keep in mind that some side effects with hydroxychloroquine happen after 1-2 months (ie changes in blood counts or liver enzymes) and some side effects don’t really become all that common until 5-10 years have gone by (ie retinopathy) So, if you do stay on this medication, be sure to have periodic follow up to monitor side effects.

If you find that hair loss seems to be continuing when when see your doctors at the 4-6 months follow up or the 1 year follow up, then that means you may want to bring on board other treatments to help the hydroxychloroquine. There are many treatments for LPP.

Sometimes, a patient keeps losing hair despite the fact that the every doctor thinks the scarring alopecia is quiet. In some cases, the scarring alopecia is not quiet and the impression of the doctors is wrong. In other cases, the scarring alopecia is, in fact, really quiet but other types of hair loss are present in the patient too that nobody has picked up on.

For example, if a patient’s scarring alopecia has been brought under good control but they have a telogen effluvium present from some other medication they recently started then guess what? Hair shedding is going to continue and hair density is not going to get better. Every hair loss condition needs to be addressed!

If a patient has both a scarring alopecia and a telogen effluvium, then both the scarring alopecia and the telogen effluvium need to be properly treated. If a patient has scarring alopecia and androgenetic alopecia, then both the scarring alopecia and the androgenetic alopecia need to be properly treated in order to maximize regrowth. If a patient has scarring alopecia and a telogen effluvium and androgenetic alopecia (all three), then a treatment plan needs to be created that addresses all three of these conditions.

Conclusion

Thanks again for the great question. I am glad things have improved. I would encourage you to take photos as this issue going to be the best way to get a really good sense of how well you are doing in the long run. I am always encouraged when patients report they are improving but what matters most to me is really how well a person is doing over a very extended period of time.

Doctors and patients can sometimes debate about whether they are better or not after a few months. However, there is absolutely no debate after 1 or 2 years. A photo captures the essence of the disease activity completely.

Can I reduce the dose of minoxidil for treating my AGA and if so, how?

Minoxidil (Rogaine) for the treatment of Androgenetic Hair loss: How soon after starting can I go down on the dose?

I’ve selected this question below for this week’s question of the week. It allows us to the review some key concepts in the treatment of androgenetic alopecia - particularly the need for ongoing lifelong treatment.

Question

I have female pattern hair loss and I’ve been on minoxidil 1/2 cap daily for about 1 year now. It seems to be helping. I was advised this week by my provider that it’s okay to go down to 3 or 4 times weekly. What protocol do you recommend for reducing the dose and how do you taper safely so as to not lose hair?

Answer

Thanks for the question. The answer is simple: If you have androgenetic alopecia and Rogaine is helping you, then this medication probably can’t be tapered to any significant degree without you losing some hair.

If Rogaine has not been helping you all these months and you’ve actually been wasting your time in the last 12 months applying it - you can stop it without any immediate negative effects. The hair won’t mind at all that Rogaine was stopped because it wasn’t helping in the first place.

However, if Rogaine was helping (which I imagine for you it probably must be), it can NOT be tapered without losing hair. I don’t know how this concept has started permeating in this world - I’ve heard it myself. But Rogaine can’t be stopped if it was helping. You can’t go from 7 days a week to 5 without some negative effect on the hair. You can’t go 7 days to 4. You can’t go twice daily to once daily. Sure you might be able to go 7 to 6 but there’s a fine line for what its acceptable.

If all a person is able to do is apply Rogaine 5 or 6 days per week, then I say try to apply it five or 6 days per week. That’s fine. It still has a chance of helping even if it’s not perfectly daily. . But to start at a higher dose and then reduce the dose at a future time just doesn’t work well for most people.

Reducing the dose of Rogaine usually leads to hair loss (if it was helping). Consider the female patient who starts using Rogaine 5% twice daily because she really wants to try to stop her hair loss, or the patient who even uses a full cap instead of the recommended 1/2 cap. Then, imagine that the patient winds up in the clinic of a specialist 12 months later and the specialist says confidently to her“Oh, Rogaine for women only needs to be used once daily at 1/2 cap - so you can reduce your dose”

Guess what happens when the patient goes from a full cap twice daily to 1/2 cap daily?

She loses hair! !!!!!!

Hair is not pleased with a four-fold reduction in the dose.

Summary and Conclusion

All the treatments for androgenetic alopecia are lifelong. If a patient is going to use Rogain to treat their AGA, then they should plan to start it with the intention to use it lifelong. If a patient is going to use anti androgens to treat their AGA, then they should plan to start it with the intention to use it lifelong. If a patient is going to use low level laser therapy to treat their AGA, then they should plan to start it with the intention to use it lifelong. If a patient is going to use PRP therapy to treat their AGA, then they should plan to start it with the intention to use it lifelong.

We would to think that it’s possible to reduce the dose of Rogaine after some time. It sure sounds like a nice plan …. and a convenient one too! It’s just that it doesn’t really work like this and reducing the dose carries a high risk of hair loss.

Now for all the people who are using Rogaine for other types of hair loss besides androgenetic alopecia - the rules are a bit different. If one uses Rogaine for alopecia areata, one can stop Rogaine once the hair grows back. Sometimes (but not always) that’s true for other types of hair loss as well. But for androgenetic alopecia the rules are pretty straight forward. If a certain dose or amount of Rogaine has helped, then that dose or amount needs to bee continued exactly the same way to maintain results. A reduction in dose will likely lead to hair loss.

The following chart is helpful to differentiate the use of Rogaine in these conditions

What is More Accurate for Diagnosing Early Stages of Hair Loss : A Scalp Biopsy or Clinical (Trichoscopic) Examination?

Biopsy or Up Close (Trichoscopic) Examination: What’s better for diagnosing the early stages of hair loss?

I’ve selected this question below for this week’s question of the week. It allows us to the review some key concepts in diagnosing hair loss via clinical scalp examination and through a biopsy.

QUESTION

What is more accurate - a scalp biopsy or a scalp exam with a dermatoscope? My biopsy results said telogen effluvium and androgenic alopecia with the diagnosis of androgenetic alopecia being favored.

As for me, I’m a 30 year old female. My scalp is itchy, likely from seborrheic dermatitis which was diagnosed by a dermatologist. I’ve suffered from alopecia areata in the past (1 small bald patch at a time and treated with cortisone injections) . I have a lot of food and environmental allergies that I’m treating naturally. My hair started shedding excessively at the end of February 2021 after a very traumatic event in December 2020. I’m not on any prescription medications but I do take supplements (iron, vitamin D and C, coQ10, quercetin, probiotic, l-lysine, caprylic acid, and a multivitamin for hair). The shedding has been diffuse and I have lost density. My family members insist that no one would know I’m having issues with my hair. In the past few weeks I have had days with minimal shedding. I have been treating the seborrheic dermatitis with medicated shampoos. I have been treating the hair loss naturally, through dietary changes, lowering stress levels with meditation, etc; I have not used any medications.

The dermatologist that performed the biopsy said it’s “age related” (I’m a 30 year old female) and therefore not even considered an early stage AGA. The second dermatologist I saw (for a second opinion) did a scalp exam with a dermatoscope and said there was “maybe one” miniaturized follicle at the biopsy site on my crown. Throughout the rest of the top of my scalp she said about 1 in 100 follicles are miniaturized. She gave me a diagnosis of just telogen effluvium. So far all of my test results (iron, ferritin, vitamin D, vitamin B12, thyroid panel, and hormone panel) have been normal. I’m very confused and not sure if and what treatment would be best for me. Thank you!

ANSWER

Thank you for the question. In order for me to advise you on what treatment would be best for you, we need a diagnosis.

So what is your diagnosis then?

Well, in order for me to give you a diagnosis, I would need to know a bit more about your story from birth until today, and see your scalp up close myself and review your blood tests. Those are the three key steps in order to make a diagnosis for anyone!. Because I don’t have any of these pieces of information in your case, I can’t actually say what your diagnosis is.

However, there are still some very important points to be aware of and that’s why I’ve selected your question for this week’s question. It’s such a good one with so many things for us to review.

So let’s get to it.

You have what I call early hair loss. You yourself know there is a change, but your friends and family think everything is just fine. Even one of the dermatologists thinks it’s simply a telogen effluvium. This is early hair loss.

As you have correctly outlined, this can often be due to androgenetic alopecia or telogen effluvium …. or both.

As I review all your information about what your biopsy showed and what your doctors actually said, I need to know how reliable each of these three pieces of information are. If dermatologist 2 is a world expert in hair loss and doesn’t think its AGA - does this carry more “influence” as I think about your case than if dermatologist 1 thinks it’s AGA but really has only seen a handful of hair loss patients in his or her career?

Yes it most certainly does.

Your question is really all about the reliability of these three pieces of information - the 2 doctors and the 1 biopsy.

And what if the biopsy was taken from an area on the scalp that is really not so useful for making a diagnosis (like the temples) - am I to trust this result? Well, no.

So, let’s take a look at these four scenarios below in order for us to better understand when a biopsy is better than a clinician’s interpretation and when a clinician’s interpretation is to be trusted more than a biopsy report.

In general, the very early stages of hair loss can be challenging to decipher from one another. The more experience and expertise the clinician has in treating hair loss … the more reliable his or her view will be on the cause of hair loss. The less experience the clinician has, the less reliable his or her view is and the more a biopsy result is to be trusted. However, biopsies are not all the same. The only biopsy result that I really trust is one taken from the correct area of the scalp and interpreted properly by expert dermatopatholgist.

Let’s take a look at the following chart and then we’ll break it down some more.

SCENARIO 1. The practitioner evaluating the scalp is a VERY EXPERIENCED hair loss expert and a 4 mm punch biopsy was taken from a correct area of the scalp and interpretations were done by a VERY EXPERIENCED dermatopathologist.

In this case, both the dermatologist’s opinion and the dermatopathologist’s opinion are fairly reliable. In fact, in most cases, they are fairly equivalent. A highly experienced clinician can examine all areas of the scalp and can determine just how much variation in the caliber of hair follicles (ie “miniaturization”) is seen in the various regions including the front, middle, top and back. If the clinician appreciates that density is slightly different in one area compared to another it’s like their is some androgenetic alopecia going on - especially if the thinner area show a greater degree of miniaturization.

A clinician can also evaluate density in the frontal area and compare this to the back. If there is a subtle increase in “part width” in the frontal and mid scalp compared to the back, this gives a suggestion there could be some androgenetic alopecia going on.

So an astute clinician can look at the scalp, look at the part width, look a the density in various regions of the scalp and look at what the trichsocopy shows and come up with a conclusion.

Clinical examinations of the early stages of hair loss are tricky to interpret. It takes expertise to appreciate subtle changes in hair follicle caliber. It’s not something that is learned overnight. It’s not a result that pops up on any sort of screen when one places a dermatoscope one the scalp. Of course, it one’s dermatoscope its connected to a computer and the caliber of follicles can actually be measured in various areas, this really increases the reliability of the interpretation for less experienced practitioners.

But if a practitioner is less experienced with hair and scalp issues, simply placing a dermatoscope on the scalp and concluding “I don’t see any miniaturization” does not give me a great amount of confidence in diagnosing early hair loss issues.

What about a biopsy? Biopsies in early hair loss can be wonderful! A biopsy taken from the area of androgenetic alopecia can also show a DECREASING terminal to vellus ratio from a normal low 7:1 or 8:1 down to 4:1 or less. In true telogen effluvium, the terminal to vellus ratio stays well above 6 or 7 to 1. An experienced dermatopathologist who interprets a biopsy from a patient with early hair loss and says ‘the T:V ratio is 3.5:1 and sebaceous glands appear enlarged and there is no real shift in catagen to telogen ratios and there is no peribular inflammation” is telling me this is likely androgenetic alopecia. I trust that report if I know the dermatopathologist is experienced.

To summarize, a very experienced practitioner can often make a diagnosis of androgenetic alopecia fairly reliably even without a scalp biopsy. However, if a scalp biopsy is done, the results should be similar trusted as the findings of a very experienced practitioner provided the biopsy is interpreted by an expert pathologist.

SCENARIO 2. The practitioner evaluating the scalp is an INEXPERIENCED practitioner and a 4 mm punch biopsy was taken from a correct area of the scalp and interpretations were done by a VERY EXPERIENCED dermatopathologist.

In this case, the biopsy report is MORE reliable than the view of the clinician. We need to remember here that early hair loss stages are really difficult to diagnose! There is no harm in saying that and I’ll be the first to point that out.

It can take anywhere from 6 months to 5 years from the time some types of hair loss first start before a patient themselves figure out that something is changing on their scalp. So, the early stages of hair loss are tricky to spot. The early stages of hair loss can sometimes look normal. The less experience the practitioner has …. the more the scalp will look normal to them ! That’s just a fact. Any practitioner who takes a quick 5-10 second glance at the scalp and says to their patient ‘your scalp looks fine to me… don't worry” is by definition an inexperienced practitioner. This is pretty much a rule. The early stages of hair loss are hard to spot sometimes and take a bit of poking and prodding in the scalp to see what all the 100,000 hairs are doing and a bit of sleuthing to gather information from the patient as to exactly what’s been happening over the past months.

If a very experienced clinician says ‘This scalp is normal” then it’s pretty unlikely there is any androgenetic alopecia. Not 100% guarantee of course….. but pretty unlikely. If an inexperienced clinician says ‘This scalp is normal” then it carries less meaning. Of course, it could be normal, but I’m a bit more skeptical. I am sent referrals every day of the year that say “ Normal scalp exam. Patient thinks they have hair loss. Please see in consultation.”

What do many of these patients end up having as a diagnosis ? Well, many have androgenetic alopecia !

Suppose I’m meeting up with a friend for dinner and I tell my friend that I have been getting some pretty bad headaches lately. If my friend tells me everything sounds fine, do I believe it? Well, if my friend is a neurologist I’m a bit more likely to trust this information than if my friend is an accountant. The quality of the information makes a difference.

So to summarize, if a clinician is less experienced with diagnosing hair loss but takes a biopsy from a correct area of the scalp (ie where the hair loss is most affected) and the biopsy lands in the hands of an expert dermatopatholgist …. then I would usually trust the dermatopathoglist report over the clinician’s interpretation of what’s causing the early hair loss.

So what’s a good biopsy in your case? Well, in your case this likely means that biopsy was taken from somewhere in the yellow area shown below. I would prefer if the biopsy was 4 mm in size. I would also like if the biopsy was processed with horizontal sections as personally that increases my confidence in these early stages of hair loss. It’s only with horizontal sections that the pathologist can give a measurement of the terminal to vellus ratio. This can’t be done with vertical sections. If your T:V ratio is less than 4:1, we might begin to think there is some androgenetic alopecia present as a diagnosis.

SCENARIO 3. The practitioner evaluating the scalp is an EXPERIENCED hair loss expert and a suboptimal biopsy was taken from an incorrect area of the scalp and/or interpretations were done by an INEXPERIENCED pathologist.

This would be an unusual situation whereby an experienced clinician took a biopsy from a wrong spot. But this situation could be an experienced clinician is trying to decide what diagnosis a patient has and the patient brings in a biopsy report they had at another clinic showing a certain result.

In this case, I trust the result from the clinician any day over the biopsy report. Every day, I see biopsy reports that are taken form the back of the scalp or the sides of the scalp or the temples. These are not the ideal areas to be taking biopsies from if we want determine whether or not the patient has androgenetic alopecia!!!

Sometimes, the doctor does not want to cause a scar…. and so takes it from the sides of the scalp so as to hide any scar. Sometimes, a patient asks the doctor to take it from the temples because that’s where they are most worried and where they see the changes every day of their life when they look in the mirror. These are not where we should be taking biopsies to confidently assess androgenetic alopecia !

If a biopsy returns showing “no evidence of androgenetic alopecia” but was taken from the sides fo the scalp does it mean the patient does not have androgenetic alopecia? No! Not at all,. That biopsy was not helping in making the proper diagnosis.

If a biopsy returns showing “no evidence of androgenetic alopecia” but was taken from the main area of hair loss in the central scalp zone, does it mean the patient does not have androgenetic alopecia? Probably that is the correct interpretation.

SCENARIO 4. The practitioner evaluating the scalp is an INEXPERIENCED practitioner and a suboptimal biopsy was taken from an incorrect area of the scalp and interpretations were done by an INEXPERIENCED pathologist.

A particularly challenging situation is when a less experienced practitioner is not sure what the diagnosis is but proceed to take the biopsy from an area of the scalp which is less than ideal. Typically this is a well meaning practitioner who wishes to take the biopsy from an area that will best be hidden in the future should the area form a small scar. So the biopsy is taken from the sides of back of thee scalp and typically returns showing no evidence of androgenetic alopecia. The only thing that can be interpreted in this situation is that the patient does not have androgenetic alopecia down the sides of their scalp. However, we can’t conclude anything at all about what might be happening in the middle of the scalp - the area where the patient is most concerned about the hair!

I often use the following analogy when I explain the concept to doctors that I teach.

Suppose you have a mold of some kind in your home. The house smells like mold! Terrible, right?

And so you call a mold specialist for help. Unfortunately, all the mold specialists in town are away at a convention so you decide to call a plumber. After all, mold grows in water and damp conditions, and you figure that a plumber knows a lot about water and damp conditions in homes.

The plumber answers the call and says he or she knows how to take mold samples because they learned how to do so in a course they took.

Voila!

You are happy with the answer and invite the plumber to your home to get some help.

The plumber finds a bit of water in the basement and takes some mold samples. It all comes back negative.

You are all relieved there is no mold!

The problem is that the smell continues.

When the mold specialist in town returns from the convention, you invite him or her now into your home. Within a few minutes the source of the mold is located in the attic of the house. Their is a leak in the roof and this is causing the roof to leak and the attic to grow mold !!!! Samples are taken and the mold is finally proven.

Did it matter where the samples were taken? You bet it did!

An experienced specialist is more likely to know where to take the sample .

Conclusion

Your question is really a great one. Thanks again for submitting. It’s difficult, if not impossible for patients to know if their biopsy was taken from the correct spot or whether their clinician really has a lot of experience or not. It’s tough to navigate the medical world sometimes.

The short answer to your question , however, is that a very experienced clinician can often diagnose hair loss with a similar degree of accuracy to a biopsy interpreted by an expert dermatopathlogist. If the skills of the clinician change or the skills of the dermatopathologist now change, this no longer holds true and you’ll need to see the chart about as to which is better.

It is quite likely with your story that at least one of your diagnoses was telogen effluvium that was triggered by the stress of December 2020. With your story, I think it’s really important that someone make sure that your seborrheic dermatitis is under good control and someone keep an eye on the possibility that a diffuse alopecia areata is not part of the reason for your shedding. I think that would be unlikely given that shedding has settled now and that the biopsy did not capture this.

With this one biopsy that you do have I can’t exclude that there is not some degree of androgenetic alopecia present. There certainly is a possibility with this information you’ve given. oOf course, I would need to see the scalp or a photo of your scalp myself to know for sure one way or another.

Please keep taking photos of your scalp to show your doctors. If you feel that your hair returns to full by September 2021 and you are really pleased with the way your hair looks and feels at that time, then it’s pretty unlikely there is any AGA. However, if your hair does not return to full by September, I would encourage you to further explore ways to confirm this diagnosis with certainty one way or another so that you might get connected with the correct treatment in the event you do have androgenic alopecia.

Thank you again for your question.

Do I just need patience or is my hair density not going to fully return?

Is my hair density going to return?

I’ve selected this question below for this week’s question of the week. It allows us to the review some key concepts in the diagnosis of hair loss in the early stages.

QUESTION

I am a 40 year old female. I have always had a lot of hair, and coarse hair. I have always been a shedder, but it never made a difference on how dense my hair was. Until now. I had my "normal to me" hair up until August/September 2020. But, in September/October, I started to see a lot more hair coming out in the shower/brushing afterwards/when blowdrying.

Handfuls would come out in the shower when in the shower. It was definitely the worst/at it's peak in November 2020.

I remember after one shower the entire wall was covered with the hair I collected. By this time I started to freak out a bit. It was definitely making a difference on my head now as far as density. I went to my family doc, and he did blood work. My ferritin came back at 21, but my hemoglobin was ok. I started taking iron supplements at the end of November. At the end of Jan 2021 I went to see a dermatologist. She only had a physical look at my scalp, did not do a biopsy and did not look at my scalp with any sort of magnifying tool or anything. She said based on my story she thought it was either Androgenetic Alopecia or Telogen Effluvium. She had my vitamin D tested. It was a bit low, so I started taking 2000IU of vitamin D daily. The hair shedding continued like this until end of February-ish/beginning of March. (The lost hair was mostly long hairs, some medium length, barely any short hairs)

In March/April 2021 the hair fall slowed down a lot, and now I would say it is back to a normal amount with each wash.

But, I can definitely see a difference on my head. It is most noticeable on the top/sides of my head, and down the back of my head (I have weird parts all along the back of my head). It also sort of looks like I lost hair at the nape of my neck. My part has not gotten wider at all, but sparser. I do have a lot of new growth at the top and back of my head, but it doesn't seem like enough to make a difference in terms of overall thickness, even when it grows longer.

My scalp hurts often, as if it has been in a super tight ponytail, even though it has not. Sort of hurts to move it around. My scalp can be quite dry/itchy at time (always has been like this, even before hair loss)

I am still taking iron supplements, as when I was re-tested in February my ferritin had only gone up to 30. I am also still taking the vitamin D daily. I should mention I take 2.5 or Ramipril daily.

My question is … would Androgenetic Alopecia happen that quickly and then taper off that quickly? And, if it is Telogen Effluvium would I expect to have more re-growth by now? Or, is there any chance I could have some sort of diffuse Alopecia Areata, based on what is happening at the nape of my neck and the weird parts down the back of my head? I have attached some photos. I am trying to be patient, as I know hair takes a long time to grow.

Thank you for your input!!

Image 1. Hair density in the central part.

Image 2: Hair density in the crown.

Image 3: Hair regrowth.

Image 4: Hair regrowth.

ANSWER

Thanks for the great question. The short answer is that many diagnoses are possible for you. I’ll get into these in just a moment.

I would need to see your scalp and know more about your full story to tell you which diagnosis (or diagnoses) you actually have…. but the 6 possibilities are outlined below. Each of these possibilities has different probabilities for being your actual diagnosis. If I was to see your scalp, these ‘estimated’ probabilities would change. However, with the information provided, we have six scenarios. The most likely is scenario 1 and 2 followed by scenario 3.

Six Possible Scenarios for Your Hair Loss

There are six possible scenarios for your hair loss. The most likely is scenario 1 and 2 followed by scenario 3.

Scenario 1) You have a telogen effluvium due to low iron or low vitamin D. This has now been fixed and you need to give it until October/November in order for your density is going to come back.

Scenario 2) You have a telogen effluvium for some other reason (other than simply low iron and vitamin D) and it has now somewhat resolved and you need to give it until Oct/November in order for your density is going to come back. Causes of telogen effluvium that could be relevant for you would include stress last summer 2020, low iron (which you might have), thyroid problems, medications started last summer, weight loss last summer, COVID infection last summer. Other causes are possible too.

Scenario 3) You have actually had a hint of subtle “subclinical” androgenetic alopecia for a while and this recent telogen effluvium has “unmasked” the subtle androgenetic alopecia. Your density is going to improve by the Fall 2021 now that your telogen effluvium is resolving but you might or might not get back all your density - but you may come pretty close.

Scenario 4) You have an inflammatory scalp condition that has been present for a while and is now acting up to give periods of hair shedding. The iron and vitamin D are unrelated in this particular scenario and are simply a true red herrings. Your inflammatory scalp condition has now settled again but you need to give it until November/December to see if things will fully settle. Such inflammatory condition could include seborrheic dermatitis, psoriasis, scarring alopecia or contact allergy (ie to some ingredient in a shampoo, conditioner, hairstyling product or dye). This scenario number 4 carries a risk of flare again.

Scenario 5) You have an inflammatory scalp condition that has been present for a while but it’s not enough to give hair loss. A new telogen effluvium has come along that will resolve and time will tell whether the inflammatory scalp condition also settles fully. If the inflammatory scalp condition is a low grade scarring alopecia, density won’t come back fully but still will improve to some degree when the current telogen effluvium resolves.

Scenario 6) You have an inflammatory scalp condition that has been present for a while but it’s not enough to give hair loss. You also have a subtle amount of androgenetic alopecia that has now been unmasked by the new telogen effluvium. If the inflammatory scalp condition or androgenetic alopecia is active enough it may prevent density from coming back to your full normal by Fall 2021. 

Detailed Review of the INITIAL Situation (August 2020 to Dec 2020)

Let’s go further into the situation that you describe in your question. Before we do, let me point out that there are three stages of hair loss for most people. At least that’s a helpful way that I view hair loss. These stages are important to appreciate because it impacts how I approach your question.

In “stage 1” of hair loss, the patient has hair loss but doesn’t really know it. For all practical purposes, the patient feels the hair looks the same as it always did and feels the same as it always did. Perhaps when they look at a photo from years gone by they might say something like “Wow, I can’t believe how much hair I had back then!” Otherwise stage 1 of hair loss is unrecognizable by anyone - patient, doctor, specialist or hairstylist.

In “stage 2” of hair loss, patients themselves realize they have hair loss - but others around them don’t believe it or don’t realize it. The patient feels the pony tail is smaller or the scalp is more see through or something is just not the same. A spouse, sister, parent, daughter, son, barber, hairstylist or friend usually say the same thing - “You’re exaggerating ! Everything looks fine to me! Sometimes that sentence is delivered by the doctor or other hair expert that has been asked to help.

Stage 2 is sometimes frustrating and lonely and anxiety provoking. Patients feel something is wrong but the world around them says repeatedly that everything is just fine.

Now, some patients in stage 2 resolve their hair loss and go back into stage 1 and so they do end up feeling they were exaggerating because everything resolves itself. Some patients stay in stage 2 and eventually find an answer to their hair loss issues. If specialist A does not believe them, they move on to specialist B. If specialist B does not believe them, they move on to specialist C.

Some patients in stage 2 do progress on to stage 3 of hair loss where hair loss becomes more noticeable to others. With hairstyling and camouflage a patient in stage 3 might still be able to hide their hair loss. With treatment of course, a patient may be able to return to stage 2 or even stage 1.

With these stages in mind, let’s delve a little further into this situation you have mentioned in your question.

There are two main scenarios that may have been present before you noticed hair loss in August. The first is that your hair density was completely normal and the same as it was when you were 20. You then lost hair in the August - December period and the density went down. In other words, you went from no hair loss to stage 2. This is shown below.

The second scenario is that you felt that your hair density was completely normal but it was not, in fact, completely the same as it was 20 years ago. You then lost hair in the August - December period and the density went down. In other words, you went from stage 1 of hair loss into stage 2. This is shown below

Both of these situations above would appear identical to you. In the first situation, you had normal hair to start and then you lost density. In the second situation, you had (what you thought was) normal hair to start and then you lost hair. The only difference is that in the second sitatution you actually didn’t have quite normal hair - it just seemed that way to you (and everyone else).

Detailed Review of the RECOVERY (April 2021 to Dec 2021).

Your hair loss is now in a recovery phase. Your shedding has stopped. You are sprouting hair everywhere!

Let’s spend some time looking at the recovery of your hair loss and how the hair might respond over the next few months. The most likely are the following 2 scenarios.

If you don’t have any underlying issues that are affecting how hair grows, then it’s likely that this telogen effluvium will continue to settle and a you’ll get a return to full growth by the end of the year. In other words, you’ll go from stage 2, into stage 1 and back to full hair. The chapter on hair loss will be closed

Even if you do have some kind of “subclinical” hair loss situation happening in your scalp, there is still a good chance that you’ll recover your density by the end of the year and you’ll return feeling that your hair feels ‘full’ to you. In other words, you’ll move from stage 2 into stage 1. Stage 1 of hair loss looks just as good of having no hair loss at all so for all practical purposes it does not matter.

What happens if my density does not recover by the end of the year?

The final scenario is a bit trickier to explain. If you did in fact have some sort of subclinical hair loss situation going on in the scalp before August 2020 and this condition got a little bit worse from August 2020 through summer 2021, then you might not find that you have a full recovery by the time the Fall 2021 comes around. This could be due to several situations including

a) you had some subclinical androgenetic alopecia prior to August 2020 and the androgenetic alopecia got a bit worse from August 2020 to August 2021.

b) you had some subclinical scarring alopecia prior to August 2020 and the scarring alopecia got a bit worse from August 2020 to August 2021.

c) you had some subclinical psoriasis or contact dermatitis prior to August 2020 and the inflammatory issues got a bit worse from August 2020 to August 2021.

In these situations, it’s possible you stay in stage 2.

This final scenario is the least likely but a proper scalp examination and full review of your story is going to help me decide just how likely it is in your specific situation. For now, I estimate it as unlikely (but not zero).

What you can see here in these examples above is that you really need some definite diagnoses. If you allow time to help you with a solid diagnosis then that’s one good strategy. For example, if your density comes back perfectly to normal by the end of the year, then there’s probably no real hair issues at all that need treating or need any kind of workup. In other words, if your density returns back to full by December 2020 (and you enter stage 1 or no hair loss), it’s pretty unlikely there’s any other hair loss issue going on.

But if density does not return, I strongly believe that you need to have some formal diagnoses put on paper for BOTH the hair loss and the scalp symptoms. The reason we need different diagnoses is because every hair loss condition is treated differently. Unless we have a diagnosis, we can’t formulate the right treatment plan.

My Final Comments

Thanks again for the great question.

I’m really glad you are seeing all this hair growth sprouting everywhere as it’s a really good sign. The hairs are about 5-6 cm so it seems that the telogen effluvium you had in Aug/Sept 2020 is settling down. It could be that the iron and/or vitamin D is helping or that could just be a coincidence. It’s difficult to prove.

I do feel your scalp symptoms (dry, itchy, hurts to move) needs a formal diagnosis. Your scalp symptoms need a name of some kind. Now, keep in mind that the diagnosis of that situation might not be anything concerning given how long you have had it, but it still needs a formal diagnosis. If nobody is sure of what to call your itching and soreness, then you need a scalp biopsy. That is pretty clear in my mind. There is flaking present in some of your photos so there is some kind of inflammatory issue present. I would need to see the scalp up close to give a diagnosis. Please be sure to follow up on that.

I am glad you are taking photos as that will be key over the next 6 months. If you feel by November/December 2021 that you are really happy with your hair and how the density has returned, then this chapter of your hair story is likely done: you had a telogen effluvium and it resolved. It went away. In this situation, it’s unlikely there is some subclinical androgenetic alopecia present but it does not really matter much. I wouldn’t treat hair loss if you go back to feeling good about your hair. I’d simply repeat photos in 1 year. Put the shedding episode behind you for now.

If your density does not return to normal by the end of the year, then there is a good chance that there is some androgenetic alopecia that has entered the picture. No, it’s not 100% but that becomes increasingly likely. There’s very small chance that another diagnosis besides androgenetic alopecia is responsible but that’s pretty rare. Of course, the itching and tender issues on your scalp need to be diagnosed properly. That may or may not have any role here. But someone needs to give it a name.

But if you are pleased with your density in November/December 2021 and your shedding is completely back to normal (and stays normal), and your scalp symptoms are not worrisome to you and your doctors …I would put it all to rest and simply take a photos again in 1 year. It’s helpful to have your doctors follow you closely but nobody really knows their hair better than you. If you feel your hair has not returned back to normal, then you have remained in stage 2 and need a solid convincing diagnosis.

I hope this helps.

Many thanks for the question.

Hair Breakage and Hair Growth in Central Centrifugal Cicatricial Alopecia (CCCA)

CCCA: How do I overcome my hair breakage?

I’ve selected this question below for this week’s question of the week. It allows us to the review some key concepts in the management of central centrifugal cicatricial alopecia (CCCA) and the importance of hair breakage in patients.

QUESTION

I recently was officially diagnosed with CCCA. I am a 35 year old black woman. I started having hair breakage on the vertex of my scalp since around June of last year. I stumbled across your papers, watched your seminars on youtube etc etc. and I had a strong suspicion that I had a diagnosis of central centrifugal cicatricial alopecia (CCCA).

I went to see the physician but by that time, my hair was growing back in that area (I had to wait several months to see a specialist) so the specialist did not think it was CCCA and diagnosed me with another hair condition called Trichorrhexis Nodosa as there were nodules on my hair shaft and I had a positive pull test.

Long story short, my hair seemed to be doing relatively well for awhile but around the end of March of this year, what seemed like overnight, I had hair breakage in my vertex again with the hair shaft super short. Basically I had a peach fuzz in that area. So I immediately called my dermatologist again and pushed for a biopsy. Three weeks later I was diagnosed with an inflammatory scarring alopecia, with the differential being CCCA.

This is what my biopsy said:

Microscopic Examination: There is concentric perifollicular fibrosis and the level of the isthmus, with associated patchy perifollicular lymphocytic inflammation. There are decreased sebaceous glands and focal interface dermatitis involving follicular epithelium. The features are of a lymphocytic inflammatory scarring alopecia, with the differential including lichen planopilaris and CCCA. Clinical correlation is recommended.
- Final Diagnosis SKIN BIOPSY SCALP: INFLAMMATORY SCARRING ALOPECIA"

So, now to my question.

I do not have any external scarring....as in I am not bald on any area of my scalp. I just have a small island maybe the size of a golf ball of short hair while the surrounding hair is significantly longer. At the end of March when I noticed the breakage, it was a peach fuzz. Since getting the biopsy and waiting on the results it has grown a little. It is now measured at a little less than 1.5 inches. So the hair in that area seems to be growing. However, will it grow continuously OR will it grow to a certain point and break off? I have internal follicular scarring at the level of the isthmus and my dermatologist told me that that is irreversible (though I want to explore the 10% metformin in Lidoderm that is hypothesized to reverse scarring).

So, assuming I had CCCA since last year, I am afraid that I will go through a cycle of hair growth to a couple inches and then breakage even if I am able to get the inflammation under control with the oral doxycycline and topical clobetasol that I was prescribed. I assume that the follicular fibrosis at the level of the isthmus has probably affected the formation or structure of the hair shaft and that's why some patients experience hair breakage early on in the disease? So, in your experience, have you seen continuous hair growth when CCCA is caught at the hair breakage stage or did it go through a cycle of grow and break?

Also, should I be taking clobetasol breaks? My dermatologist prescribed it once a day, every day indefinitely. Well, I suppose we will reassess when I see him again in 4 months but I remember reading on your site that you suggest steroid holidays every couple weeks. I use very little in that area daily as I am aware of, and afraid of any side effects.

ANSWER

This is a great question.

Hair breakage is very common in CCCA. In fact, hair breakage can be one of the very first clues that a patient has to the disease process. Hair breakage can happen prior to hair loss and prior to the appearance of ‘patches.’ You may wish to review a previous article I wrote:

Hair Breakage in Black Women: Not to Be OverLooked!

It’s true that “trichorrhexis nodosa” is associated with the hair breakage as you write - but the reason the hair is breaking in these situations is partly due to the underlying scarring alopecia. Heat and chemicals and hair styling might still have a role in some so that needs to be investigated in your case too. You and your dermatologists can review that.

The pattern that you describe of these short hairs that don’t seem to grow very long is very typical of CCCA. Usually these areas on the scalp are about the size of a tennis ball, although sometimes the area is bigger and sometimes smaller.

Hair breakage is common in CCCA and may appear as small patches about 2- 6 cm in diameter that simply fail to grow longer. Proper treatment of the CCCA reduces the inflammation under the scalp and sometimes helps the hairs to elongate and areas to fill in more normally.

This hair breakage issue is so important to recognize because it can be a sign of very early CCCA (or what I term subclinical CCCA).

Will my hair grow longer?

These areas of short hair might grow longer - yes! It’s possible that’s for sure. However, the overall chances this area will regrow is higher if you choose to aggressively treat your scarring alopecia than if you choose to less aggressively treat your scarring alopecia. By “aggressive treatment”, I mean the use of a plan that really works to chase away inflammation. This plan might include periodic topical steroids with steroid injections and oral doxycycline. You and your doctors can decide what is right for you and if you have any specific contraindications to these medications (ie reasons why you should not use). Topical 10 % metformin is an option too but no it’s not a “first line” treatment. It is a newer treatment and it’s not clear how many it helps. Maybe someday it will be first line treatment, but it’s not right now. Topical metformin does not reverse scarring, that would not be correct. Nothing reverses scarring - that’s permanent. However, topical metformin most certainly can help with stopping inflammation and getting hairs to sprout back up. There is a big difference between helping with hair growth and reversing scarring. Many treatments for early staged scarring alopecia can get hairs growing and help the patient achieve improved density. But that’s not because it reverses scarring.

To review the treatments for CCCA, you might wish to review the prior article but I’ll go into it a bit more here to review.

CCCA: Diagnosis and Treatment

It could be that topical steroids like clobetasol alone (as the sole treatment) might be sufficient to treat CCCA but for many women with CCCA, clobetasol alone is not enough to stop the disease. An aggressive approach might involve use of topical clobetasol with periodic steroid injections and a 3-6 month course of oral doxycycline. I am also a big fan of topical tacrolimus ointment as well in treating CCCA and it can be used with the clobetasol. How exactly these are used depends on the patient and her story and how much inflammation seems to be present. Treatment might initially involve daily clobetasol in the morning and tacroliumus in the evening or clobetasol three times weekly (Monday, Wednesday and Friday) and then Tacrolimus the other days. This is always re-evaluated every 3-5 months. No treatment is forever, except perhaps minoxidil if the patient also has a diagnosis of androgenetic alopecia.

I’m all very much a big fan of reducing heat and chemical as much as possible for at least 6 months. I know it’s not always possible but it does seem to help a great deal during this period where the hair is really weak. Your hair will be better able to tolerate heat and chemicals in the near future if we can get rid of the inflammation.

The ‘gold medal’ or first line treatments for CCCA are shown below together with second line (silver medalist) and third line treatments (bronze medalist):

You can see from the list above that 10 % metformin is certainly an option, but jumping on board with this as the first step would not be considered “first line”. There are only a small number of patient around the world treated with topical metformin so if that’s the route you want to take that’s fine. But know ahead of time that you are going at this without the backup of thousands upon thousands who have used the other first line treatments. It still could be a good option.

It may take 3-5 months to see changes but the patient often sees less breakage, less itching, less tenderness and this is followed by some degree of improvement. Early stages of CCCA are more likely to have some degree of improvement in terms of a bit of hair regrowth. Late stages usually do not.

I do feel that periodic breaks in using steroids are needed. I like my own patients to initially treat as aggressively as they are comfortable with. This means topical steroids daily for 4-6 weeks and then a 2-3 week holiday whereby no topical steroid are applied. This ‘holiday period’ is a great time for applying tacrolimus ointment as tacrolimus does not thin the skin and has very little in the way of absorption. After the two week clobetasol drug holiday is over, I might advise the patient to do another 4-6 weeks. However, if things are going well, we’ll often drop down to using clobetasol 3-4 days per week (and possibly use the Tacrolimus on some of the other days). So, to answer your question, use of clobetasol is not lifelong for patients with CCCA. Clobetasol is used until the point in time that we feel we don’t need daily treatment any more because of how good the scalp looks or feels or how well things are growing. But for those who need it, I have no issues with using clobetasol longer term provided we have some “steroid holiday” periods mixed in there.

It’s okay to be afraid of side effects, but periodic topical clobetasol, steroid injections, tacrolimus, and topical metformin are very well tolerated for the vast majority. Even doxycycline is well tolerated for most, although you’ll want to be comfortable with all the side effects of doxycycline if you go down that route.

All patients with CCCA need blood tests for CBC, TSH (thyroid studies), ferritin (iron), and 25 hyroxyvitamin D, glucose and hemoglobin A1c. If any of these are abnormal, they need to be addressed.

I hope this helps. If you treat the inflammation and limit injury to hairs for the next 6 months, you can break this hair breakage cycle.

Thank you again for the question.

Reference

Callender V et al Hair breakage as a presenting sign of early or occult central centrifugal cicatricial alopecia: clinicopathologic findings in 9 patients. Arch Dermatol. 2012 Sep;148(9):1047-52.

Should I stop my immunosuppressants when I get my COVID vaccine?

Do patients with immune mediated hair loss who use immunosuppressants need to stop their medications when they get a COVID 19 vaccine?

I’ve selected this question below for this week’s question of the week. It allows us to the review the decisions that go into stopping (or not stopping) medications after getting a COVID vaccine.

QUESTION

My daughter is 16 years old and was prescribed methotrexate for her alopecia areata. The treatment is working extremely well and she has had full hair for 9 months. She is planning to have her COVID vaccine in a few weeks and we are trying to get a sense as to whether she is supposed to stop her methotrexate or not before she gets her shot. Our various doctors have mixed views on what to do!

What are your recommendations for your patients?

ANSWER

Thanks for the great question. It’s an important one!

Short answer - it’s probably okay to continue !

Let me begin by saying that at present, there are still no clear-cut, definite and universally agreed upon guidelines on what to do for patients with alopecia areata (or other immune based hair loss conditions). We only have guidelines from other medical organizations that then need to be interpreted for hair loss patents.

There is one recommendation, however, that is pretty clear - keep the appointment for the vaccination! That’s a far more important decision for your daughter than the decision to stop the methotrexate or not!

Let’s get into the key part of the question - should your daughter stop methotrexate or not?

I’d like to point out that there are many different types of immune-mediated hair loss conditions for which immunosuppressive medications are prescribed. These include alopecia areata and patients with various scarring alopecias like lichen planopilaris, frontal fibrosing alopecia, discoid lupus, etc.

Methotrexate, cyclosporine, mycophenolate, TNF inhibitors, hydroxychloroquine, JAK inhibitors, oral steroids are all immunosuppressive medications that may be used by patients with immune-mediated hair loss. I prescribe them every day.

So does being on an immunosuppressive make it any more difficult for a patient to mount a full and normal immune response after getting a vaccination?

For some immunosuppressive medication that answer is a “yes.”

The Famous Park et al Study from South Korea

We know from data in the past that rheumatoid arthritis patients using the drug methotrexate had antibody responses to the influenza vaccine that were “slightly worse” when patients were told to continue their methotrexate compared to when they were told to stop taking the methotrexate for 2 weeks. This well known study has prompted many physicians to consider withholding methotrexate (if possible) before giving the influenza vaccine.

Let’s look at the study in more detail.

The South Korean study by Park and colleagues involved 156 patients with rheumatoid arthritis who continued their methotrexate before getting their influenza vaccine and 160 patents who stopped their methotrexate for 2 weeks AFTER getting their influenza vaccine. 75.5 % of patients who paused their methotrexate had satisfactory vaccine responses compared to 54.5 % of patients who kept taking the methotrexate. In addition, it’s important to take note that there was no change in disease activity between the groups and patients who took paused methotrexate for two weeks did not experience a disease “flare.”

The question then arises as to whether our hair loss patients who use immunosuppressive medications should withhold their treatment before or after getting COVID vaccine. The challenge with answering this question is we don’t have any good data on antibody responses in patients with specific autoimmune “hair loss” conditions. We have some guidelines for how patients on various drugs for rheumatologic disease should proceed with vaccination. In addition, we have some recommendation on how patients with skin diseases like psoriasis should proceed. However, we don’t have any studies or advice to specifically guide hair loss patients.

Being a hair loss doctor, these sorts of answers are important to me!

Should a 16 year old on methotrexate for alopecia areata stop her methotrexate for a period of time after getting a COVID vaccination?

Should a 16 year old on methotrexate and 10 mg prednisone for alopecia areata stop her methotrexate for a period of time after getting a COVID vaccination?

Should a 16 year old on methotrexate and 40 mg prednisone for alopecia areata stop her methotrexate for a period of time after getting a COVID vaccination?

Should a 16 year old on methotrexate for alopecia areata stop her methotrexate for a period of time after getting a COVID vaccination if her hair is thick and full and has been full for a long time?

Should a 16 year old on methotrexate for alopecia areata stop her methotrexate after getting a COVID vaccination for a period of time if her hair only started growing back last month?

Should a 21 year old on tofacitinib for alopecia areata stop her tofacitinib for a period of time after getting a COVID vaccination?

Should a 41 year old female using methotrexate for lichen planopilaris stop her methotrexate for a period of time after getting the COVID vaccine?

Let’s review some key stuff.

Recommendations from the Rheumatology Field

Rheumatologists frequently use immunosuppressive medications for treating autoimmune diseases so we frequently turn to the rheumatology field for guidance on how we might treat autoimmune hair loss. Various rheumatology organizations have put forth broad recommendations to help patients and their doctors. These organizations often recommend stopping some mediations for one week and rarely two weeks. We’ll take a look at some key studies and then we’ll take a look at their formal recommendations. Then, we’ll jump over to recommendations from other fields of medicine (other than rheumatology).

The Giesen and Colleagues Study

A study by Giesen and colleagues examined if patients with chronic inflammatory disease who use immunosuppressive medications mount good antibody responses after COVID vaccination and whether these vaccines flare underling disease. The researchers studied 42 healthy controls and 26 patients with inflammatory disease (including psoriasis, psoriatic arthritis, lupus, rheumatoid arthritis, spondyloarthropathy). Antibody responses at week 1 were good in patients with chronic inflammatory disease who were using immunosuppressives although antibody titers were about 20 % less than controls. The main conclusion of the Giesen study was that patients with various immune mediated diseases still mount pretty good antibody responses and the authors proposed these antibody responses should still be fairly protective. That wasn’t studied in the research study so it’s a bit of a best guess.

The Deepak and Colleagues Study

Preliminary data from the Washington University in St. Louis and the University of California, San Francisco suggests that immunosuppressive medications blunt the antibody responses in patients who get the COVID mRNA vaccine. The authors found that oral steroids and B cell depleting agents (i.e. rituximab) are most likely to impair antibody responses but that drugs like tofacitinib and methotrexate can also impair antibody responses - but to a lesser degree. The use of TNF inhibitors had only minimal effects.

To provide more detail, the authors found that compared to immunocompetent controls, there was a three-fold reduction in anti-S IgG antibody titers (P=0.009) and SARS-CoV-2 neutralization (p<0.0001) were observed in immunosuppressed patients. Patients using B cell depleting therapies and corticosteroids had a 36- and 10-fold reduction in humoral (antibody) responses, respectively (p<0.0001). Janus kinase inhibitors and antimetabolites, including methotrexate, also blunted antibody titers (P<0.0001, P=0.0023, respectively). For methotrexate , there was an average a two- to-three-fold reduction in antibodies and neutralization. For JAK inhibitors, it was approximately 4.5 fold reduction. Other targeted therapies, such as TNF inhibitors, IL-12/23 inhibitors, and integrin inhibitors, had only modest impacts on antibody formation and neutralization.

The American College of Rheumatology recommends STOPPING some (but not all) immunosuppressive medications for 1 week after vaccination in order to help improve the effectiveness of the vaccine. This is mainly for those with well-controlled disease who have low chances of flaring when the drug is stopped.

a) Mycophenolate - skip for 1 week after each vaccine dose

b) JAK inhibitors - skip for 1 week after each vaccine dose

c) Methotrexate - skip for 1 week after Pfizer or Moderna (skip 2 weeks after J&J)

d) Hydroxychloroquine (Plaquenil) - no need to stop the drug

The ACR also recommends that patients have the exact same vaccine the second time if they are having an mRNA vaccine. In other words, if a patient gets the Pfizer vaccine for his or her first dose, they should get the Pfizer vaccine for his or her second dose. The ACR does not recommend switching up vaccines depending on availability.

The Canadian Rheumatology Association has published helpful guidance. Their recommendations are different than the American College of Rheumatology. The Canadian group recommends that only two drugs should really change how vaccines are given. Those are high dose prednisone (more than 20 mg per day) and rituximab (which is not used in treating hair loss). Other drugs can be continued including

a) TNF inhibitors - no need to stop after getting the vaccine

b) Azathioprine - no need to stop after getting the vaccine

c) Cyclosporine - no need to stop after getting the vaccine

d) Hydroxychloroquine - no need to stop after getting the vaccine

e) Methotrexate - no need to stop after getting the vaccine

f) Prednisone (20 mg or less) - no need to stop after getting the vaccine

The European Alliance of Associations for Rheumatology (EULAR) advises that most drugs can be continued in those undergoing vaccination. The only exception is the drug rituximab (which is different than Ruxolitinib so readers should not confuse the two!)

The Korean College of Rheumatology has recommended withholding MTX for 1-2 weeks and to consider withholding tofacitinib and JAK inhibitors one week (but recognize that data for JAK inhibitors is less clear than for methotrexate).

The British Society of Rheumatology has recommended that everyone get vaccinated “regardless of treatment regimen or underlying diagnosis”

Other researchers have put for recommendations to stop methotrexate up to 2 weeks after vaccination.

Recommendations from the Psoriasis Field

The National Psoriasis Foundation (NPF) does NOT recommend that patents with psoriasis stop most medications before getting the vaccine. The only exception is the Ad26.COV2.S (Johnson & Johnson or “J&J” vaccine in which case the NPF recommends possibly stopping the J&J vaccine for 2 weeks if the patient is older than 60, has at least one risk factor for poor COVID outcomes, and his or her psoriasis is stable and his or her doctor agree with this plan.

This seems to be the only exception in the psoriasis field. It’s important to point out that we don’t actually know if stopping makes any difference to improve vaccine responses. But this has been the take on the NPF’s recommendations.

Summary of Study Results to Date in the World Regarding Vaccines, COVID Vaccines and Immunosuppressive Medications

The following is a helpful summary of the main key findings of data so far:

1. Current vaccines reduce the chance of developing COVID 19.

2. Current vaccines reduce the chances of developing severe disease even if one does get COVID 19.

3. Some protection against COVID 19 in better than no protection.

4. We still have no clear cut idea about what antibody level after vaccination signals that a person is protected. Fortunately, most people do have pretty good protection after vaccination (but not all).

5. If at all possible, vaccinate patients when their immune disease is quiet.

6. Younger patients have better vaccine responses than older patients.

7. Some immunosuppressive drugs reduce the amount of antibodies that are formed to the Sars-COV-2 virus. Rituximab (which we don’t typically use in any hair loss condition) impairs antibody responses the most - and second highest are the oral steroids. In one study, JAK inhibitors like tofacitinib impair antibody responses 4.5 times and Methotrexate reduces responses by 2-3 fold. There is no good studies yet to suggest these antibody reductions mean the patient is more likely to get COVID19 disease.

8. Organ transplant patients on various immunosuppressant medications don’t mount very good antibody responses to the COVID vaccine. A study from John Hopkins found that only 15 % of patients had good antibody responses after 1 dose and just over one half had good responses after two doses.

9. Doses of prednisone of less than 10 mg daily seem to be associated with good antibody responses. Ideally, patients should not be vaccinated if possible until the doses of prednisone fall below 20 mg.

10. Sulfasalazine, hydroxychloroquine, azathioprine and leflunomide may reduce vaccine antibody titers but have not been shown to inhibit a seroprotective response to the pneumococcal or influenza vaccines. Most of the main world medical organizations suggest these drugs NOT be stopped when patients go for their vaccine.

11. TNF inhibitors probably don’t affect the vaccine response all that much. Most of the main world organizations suggest these drugs not be stopped when patients go for their vaccine.

12. In organ transplant patients, mycophenolate was shown to reduce antibody titers after vaccination but not below the threshold for protection. In one study of mycophenolate users, only 27 % of 11 patients using mycophenolate had good antibody responses. Some organizations like the American College of Rheumatology (ACR) suggest stopping 1 week. Other organizations do not.

13. JAK inhibitors impair vaccine response slightly after various types of immunizations. It’s not clear if this really reduces antibody responses below a protective level after COVID 19 vaccinations or not. Holding it one week could make sense in a stable well controlled patient. This is the view of the American College of Rheumatology and the view of the Korean College of Rheumatology
    

Final Summary: Should patients with alopecia areata pause any of their drugs?

Now that we have reviewed some of the key guidelines in other fields of medicine we can come back to the question raised in the beginning. Should the 16 year old patient in this question stop her methotrexate?

There’s probably no need to stop. However, I would need a bit more information in order to really feel confident that tis the right answer for your daughter. . That’s why it’s so important that you and your daughter have a thorough discussion with her doctor. For some 16 year olds the answer will be “yes - stop it” and for some it might be “no- don’t stop it.” For most of my patients right now the answer would be not to stop. However, there is more to the answer than a simple yes or no. Also, there is still no consensus agreement across the world so I can understand that there will be mixed views from all your doctors.

Let me offer the following important pieces of information:

1. Until new formal guidelines come out, I would generally NOT recommend stopping methotrexate for “most” of my 16 year old patients who take methotrexate and have alopecia areata. There are however, still some patients in my practice that I probably would stop for 1-2 weeks, but these are exceptions right now rather than rules. This could change as more and more studies come in and guidelines get updated. This will happen.

2. I would probably be inclined to consider stopping for 1 week for children and adolescents with alopecia areata who also have obesity, diabetes, asthma or chronic lung disease, sickle cell disease, as these groups of children may be at increased risk for severe illness from COVID-19. This too is not a yes or no answer but this needs a bit of discussion with the doctor. I’d probably be on the side of favoring stopping for a week.

3. I would be inclined to consider stopping methotrexate for 1 -2 weeks for children and adolescents who also are using any amount of oral steroids. ideally, however, I would wait until the oral steroid are finished before vaccinating - if the use of oral steroids will be a short term thing.

4. I would be more inclined to consider pausing methotrexate for 1 -2 weeks if a patient’s alopecia areata has been completely stable with full hair regrowth being present for more than 5 months. In fact, I would also consider meeting with the patient to discuss even reducing the dose of methotrexate in a few monthsbecause it could be that the patient does not need this high dose any more. For methotrexate, less medication is better (if it’s at all possible and does not trigger hair loss again).

5. I would be more inclined to consider pausing methotrexate for 1-2 weeks if a patient lives with someone at very high risk. Should we stop methotrexate for 1 week if the 16 year old patient lives I the same house with a terminally or chronically ill parent or grandparent at high risk for severe COVID disease? There are no guidelines, but I’d likely say yes. Once we get better data, this answer could change.

6. For other immune based hair conditions, similar thoughts apply. Patients with extremely stable (i.e. 100% inactive) immune mediated hair loss such as alopecia areata or scarring alopecia who have been completely inactive for more than 6 months probably can skip 1 -2 week of immunosuppressants (especially methotrexate and possibly tofacitinib) without issue. Again, if a patent is super stable, stopping these drugs for 1-2 weeks should not have a big effect for most. If patients have inactive hair loss issues but are obese, or have other chronic diseases, such a stable patient probably should strongly consider skipping the dose. However, the guidelines in other fields would suggest that patients with autoimmune and immune mediated hair diseases who are less stable can probably keep taking their medications and simply go in and get the vaccine whenever their chance comes up. In other words, if there is any worry that hair loss will flare if medications are stopped, it’s probably a reasons to keep taking them and no stop.

7. For patients who are immunosuppressed, checking antibody titers after vaccination (anti S antibody titers) is something that should be strongly considered. More guidance will be needed from regulatory bodies about how best to do this. We don't yet know exactly what antibody titer means a person is protected so routine antibody testing is not something that has become mainstream

8. Further studies will be needed in the future to determine if patients on certain types of immunosuppressants need more frequent booster vaccinations that those who do not used immunosuppressive drugs.

I hope this helps. Thanks for the excellent question.

Reference

Adler et al. Protective effect of A/H1N1 vaccination in immune-mediated disease–a prospectively controlled vaccination study. Rheumatology 2012;51:695–700.

Deepak P et al. Glucocorticoids and B Cell Depleting Agents Substantially Impair Immunogenicity of mRNA Vaccines to SARS-CoV-2. medRxIv 2021 (preprint)

Fischer et al. Pneumococcal polysaccharide vaccination in adults undergoing immunosuppressive treatment for inflammatory diseases - a longitudinal study. Arthritis Res Ther 2015;17:151.

Fomin et al. Vaccination against influenza in rheumatoid arthritis: the effect of disease modifying drugs, including TNFα blockers. Ann Rheum Dis 2006;65:191–4.

Franca et al. Ribeiro ACM, Aikawa NE et al. TNF blockers show distinct patterns of immune response to the pandemic influenza A H1N1 vaccine in inflammatory arthritis patients. Rheumatology 2012;51:2091–8.

Gabay C et al. ; H1N1 Study Group. Impact of synthetic and biologic disease-modifying antirheumatic drugs on antibody responses to the AS03-adjuvanted pandemic influenza vaccine: a prospective, open-label, parallel-cohort, single-center study. Arthritis Rheum 2011;63:1486–96.

Geisen et al. Immunogenicity and safety of anti-SARS-CoV-2 mRNA vaccines in patients with chronic inflammatory conditions and immunosuppressive therapy in a monocentric cohort. Annals of Rheumatic Disease. 2021;0:1–6. doi:10.1136/annrheumdis-2021-220272

Keshtkar-Jahromi M et al,. Argani H, Rahnavardi M et al. Antibody response to influenza immunization in kidney transplant recipients receiving either azathioprine or mycophenolate: a controlled trial. Am J Nephrol 2008;28:654–60.

Park et al. Impact of temporary methotrexate discontinuation for 2 weeks on immunogenicity of seasonal influenza vaccination in patients with rheumatoid arthritis: a randomised clinical trial. Ann Rheum Dis. 2018 Jun;77(6):898-904.

Increased Shedding: Should I start treatment for Male Pattern Balding?

Does increased shedding indicate that a male should start finasteride?

I’ve selected this question below for this week’s question of the week. It allows us to the review the diagnosis and work up of increased hair shedding in males.

QUESTION

I am a male, 30 years old who has been monitoring his hair for quite some time as I don't want to lose my hair to androgenetic alopecia (AGA). I have been counting the hairs that I shed in the shower since around 2016. Since I have usually midlength to long curly hair I stretch out the days I wash my hair, otherwise it gets dry. I have always shed around 210/220 hairs when showering every third day. This has increased to 280 since a few weeks now.

Since I said every third day this means the average on a day was: 210/3=70 . Now it has become 280/3=93 a day, for the last month or so. I know that 100 hairs a day is normal, but considering that the number I was shedding was consistently around 70 for years I am a little worried. The majority of the shed hairs look healthy and thick and long. My hairline, crown and density are still the same. Could this be temporary and could the shedding go down within the next few months?

When should I start finasteride? As soon as I see recession / lessening in density / thinning?

In short, is a little increase in shedding a reason to go on treatment?

ANSWER

Thanks for submitting this question.

I’d like to discuss several important things in the question you ask and the information you have submitted.

Before we do go further, I’d like to point out that the ideal way to diagnose hair loss is using what I termed the ”Diagnostic S.E.T.” I refer to these as the diagnostic “set” because theses 3 aspects all go together. These 3 items include:

1) the patient’s story

2) the findings uncovered during the process of the scalp examination including trichoscopy

3) the results of relevant blood tests. 

The first letter of each of the three words 1) story, 2) examination and 3) tests spell out the word “S.E.T.” - again a helpful reminder of how the information obtained from reviewing each of these 3 aspects helps solidify a proper diagnosis. I don’t have a full story in your case and I don’t have photos (or a chance to examine the scalp) and I don’t have the opportunity to review any tests …. so I am limited to some degree in my helpfulness. Nevertheless, I do think the discussion here will be helpful.

The main phenomenon you are describing is increase shedding. You have gone from 70 hairs per day of shedding to 93 hairs per day . Although both are considered within the realm of normal, I would agree that in your case this likely represents a true increase in shedding. This does not necessarily mean that this will be long term shedding or that it will actually translate into a loss of hair density or thickness. There are some unknowns here.

There are 3 potential considerations for why you are shedding more hair in the last month:

a) a telogen effluvium has occurred

b) the initiation of androgenetic hair loss has taken place

c) an autoimmune mimicker of telogen effluvium is present rather than telogen effluvium

d) combination of the above

Let’s take a look at these in more detail.

a) Is this a true telogen effluvium and if so what is the cause?

It’s quite possible that you are having a minor telogen effluvium. Hair shedding does not need to be over 100 hairs per day to have a telogen effluvium - it just needs to be more than one’s original shedding rates. If a person shed 38 hairs per day before and now sheds 68 - it’s abnormal. In your case, your shedding from 70 to 93 is abnormal. Of course, there is a big difference between something being abnormal and something being serious. Your hair shedding may not be serious and might only be temporary. We’ll get to that in moment. But this shedding suggests a potential diagnosis of telogen effluvium. As we’ve reviewed in the list above, a diagnosis of telogen effluvium is not the only cause of shedding. So it would be a mistake to assume otherwise.

A variety of ‘triggers’ are responsible for telogen effluvium. These triggers include stress, low ferritin levels, thyroid problems, medications, weight loss, seborrheic dermatitis, scalp psoriasis, immunizations, infections and internal illness inside the body.

You and your doctors really need to go through each of these potential triggers step by step very carefully to see if anything fits with your story. If your shedding started at the beginning of April, then you’ll want to go back to January or February (2-3 months prior) and ask yourself if something changed in your life. If this is a telogen effluvium, that’s probably when the body felt some sort of a trigger.

So, you and your doctors will want to evaluate that answers to the following

1) Did you experience higher stress levels in January or February?

Stress in January can trigger shedding 8-12 weeks later.

2) Did levels of any of your key blood test parameters change in January or February?

Clearly, blood tests are going to be needed if you really want to get to the bottom of why you are shedding more. There are over 75 blood test abnormalities that can trigger shedding. Fortunately, most of those 75 are rare and we don’t go about even ordering them. The ones we mainly check are iron (ferritin levels) and thyroid (TSH test) along with basic hemoglobin level and 25 hydroxy vitamin D level. However, your doctor will need to review your story from start to finish and examine your scalp and ideally perform aa physical examination too. If there’s anything that crops up as a concern, more blood tests besides just ferritin and TSH might be needed. For example, patient who has lost 25 pounds in 2 months and has no idea why they are losing so much weight is likely going to need an extensive work up.

3) Did you start any new medication or vitamin or supplement in January or February?

Starting medications can sometimes be a trigger - and the same is true for some supplements, herbal medications, teas, and vitamins. This all needed to be reviewed.

4) Did you stop any sort of medication or vitamin in January or February?

Stopping medications can sometimes be a trigger - and the same is true for some supplements, herbs, teas, vitamins. This all needed to be reviewed. In addition to stopping medications. sometimes even changing brands can be an issue. For some people, a change in drug A from brand name to generic is enough to trigger a shed. You can see that we’re going to need aa pretty detailed understanding of what’s been happening in your life to determine why you area shedding.

5) Did you receive any sort of immunization in January or February?

Immunizations are not common causes of shedding but that does not mean they are not on the list. Immunizations of all kinds have a slight chance to trigger some temporary shedding. COVID vaccination rarely does too. I don’t know if you received a vaccine or not, but your doctors will need to review this carefully. If you were vaccinated in January or February, it most certainly could give a shed now. Fortunately, it’s pretty rare - but we’ve seen it.

6) Did you get any kind of infection in January or February?

Infections of any kind can trigger shedding. Granted, severe infections associated with someone being quite ill are more likely overall to trigger shedding than less severe infections. But even minor infections can trigger shedding. Tooth infections, flus, COVID 19, all can trigger shedding. Many patients who have been infected with COVID 19 do not even know they had COVID 19 but some still get shedding. In fact, about 10 % of patents with hair shedding due to COVID 19 didn’t really have any COVID 19 symptoms. You and your doctors are going to want to evaluate that carefully and whether there is any possibility of an asymptomatic COVID 19 infection happened in January or February. Antibody tests can help address this question in some patients.

Other infections may also be relevant to ask about. Again, over 300 infections can cause shedding but most of the time, none are all that relevant for the patent in front of the doctor. But a variety of bacterial, viral, protozoal infections can cause shedding. In some of my patients from outside of North America, Dengue fever (spread by dense virus) is a common cause of shedding. There are estimated to be 390 million Dengue viral infections every year in the world. Sometimes we test for infections like HIV and syphilis in patients with risk factor who have chronic shedding. So depending on your story, more broad testing could be needed. For most people, we don’t need much in the way to these sorts of tests.

7) Did you develop any kind of illness inside my body in January or February?

Any illnesses inside the body can trigger shedding. Most often these are illnesses that a significant impact on the body. For example, an illness that causes diarrhea or a bad cough or an intensively sore joint that affects the motion in the joint all have the potential to cause shedding.

8) Did you have any kind of surgery or procedure in January or February?

Any proper evaluation for shedding examines whether or not the patient had any type of surgery or hospitalization in the months leading up to the shedding. Medications used in surgery, blood loss during surgery are well known triggers of telogen effluvium.

In summary, you can see that if you want to get to the bottom of what is happening with your hair, you are going to need a proper history and examination and you are going to need blood tests. Whether you get blood tests now or simply wait a month or two if things don’t improve is a clinical decision that is left to you and your doctors. But the only way right now to be sure that an abnormality in some blood test is not the reason why your shedding went from 70 to 93 is to order these blood tests.

Three Important Patterns of Telogen Effluvium

Before we leave the concept of telogen effluvium, it’s important to mention a few more points regarding the patterns of shedding that you might see. There are a few scenarios that might happen. If the diagnosis of your hair shedding is telogen effluvium and there is some well defined trigger that happened to you in January or February and then went away you will have some shedding in April through July but then the months of August September and October will be associated with less shedding and things should return to normal by November or December (assuming you don’t have genetic hair loss). If you do have genetic hair loss, that’s a bit of a different story as patients who are en route to slowly developing genetic hair loss may not find there shedding goes back completely to normal once the trigger of the telogen effluvium is fixed. We say in this case that the TE precipitated or unmasked an androgenetic hair loss.

Let’s take a look at scenario 2 now. If the diagnosis of your hair shedding is telogen effluvium and there is some well defined trigger that happened to you in January or February but is not going to end up being fixed until July then you will have a bit more prolonged shedding. This could be a scenario whereby an individual went on a diet from January to July or had intense stress from January to July or developed a thyroid problem in January and could not get into the doctor until July to get it fixed. If scenario 2 applies in your case, you will not slow your shedding quite as quickly. You will have some shedding in April through July but then the months of August September and October will be associated with less shedding and things should return to normal by November or December (assuming you don’t have genetic hair loss). If you do have genetic hair loss, that’s a bit of a different story as patients who are en route to slowly developing genetic hair loss may not find there shedding goes back completely to normal once the trigger of the telogen effluvium is fixed.

Let’s take a look at scenario 3 now. If the diagnosis of your hair shedding is telogen effluvium and there is some well defined trigger that happened to you in January or February but it simply goes unfixed then you will have a prolonged shedding and it’s not going to stop. This could be a scenario whereby an individual developed a chronic illness like inflammatory bowel disease in January and does not get connected with the right treatment because either the diagnosis has not yet been even uncovered or the medications are not working. Another example would be a patient who experience high stress starting January because they are caring for a terminal ill member of the family and the stress just continued to run high. Another example is patient who develops an unknown chronic illness in January but just can’t get the right diagnosis and shedding just goes on and on because the issue is not addressed.

If scenario 3 applies in your case, you will not slow your shedding at all until the problem is fixed. You will have some increased shedding starting in April but then it will persist. Only when the trigger actually gets fixed will you shedding resolve.

b) Is this the start of androgenetic hair loss?

You are very wise to consider the possibility that your increased shedding is actually a reflection of androgenetic alopecia arriving on the scene. Very wise. More hair specialists and patients need to get into the frame of mind that hair shedding means potentially so much more than simply a diagnosis of telogen effluvium. What’s the most likely cause of chronically increased shedding in a healthy 30 year old male with normal blood tests? Androgenetic alopecia is the answer.

Now, are you a 30 year old male with chronically increased hair shedding and normal blood tests? No, you are not. You are a 30 year old male with acutely increased shedding (just a few weeks so far) and I have no idea what your blood tests show.

So you could have the early stages of endogenetic alopecia and this diagnosis becomes more and more likely if your shedding does not reduce as time goes on and more and more likely if all your blood tests come back normal.

Is now the right time to start finasteride?

You have asked a great question - is now the right time to start finasteride? In my opinion, a male should only every consider finasteride if five conditions are met. Interested readers can read more about these in a previous article that I wrote last year.

Criteria 1: The individual has a proven (confirmed) diagnosis androgenetic alopecia

Criteria 2: The individual does not have any contraindications to finasteride

Criteria 3: The individual accepts the potential side effect profile of this drug

Criteria 4: The individual has considered the other treatment options but feels they are not better than finasteride as a starting point (topical minoxidil, oral minoxidil, laser, PRP)

Criteria 5: The individual plans to use the medication lifelong.

A little bit of shedding that is due to AGA is certainly a reason to consider starting treatment but it does not necessarily mean it has to be with oral finasteride. It could be topical minoxidil, topical finasteride, laser or PRP . There’s nothing wrong with being conservative in the early stages and seeing if the AGA can be halted with minimal coaxing.

Before leaving the topic, let me reiterate how important criteria one actually is. If you had some major stress in January or February and telogen effluvium is actually the cause of your shedding rather than a diagnosis of androgenetic alopecia, starting finasteride would not be the right step, If you are shedding 93 hairs because your diet is poor and you have a micronutrient deficiency, starting finasteride is not the right step, However, fixing the diet or starting a vitamin in the meantime would be .

c) Is this a mimicker of telogen effluvium ?

There are many conditions that look like telogen effluvium, sound like telogen effluvium but aren’t telogen effluvium. Unfortunately, they can be tough to spot for even clinicians. Fortunately, they are not common. Alopecia areata incognito is not common but presents with shedding. Trichoscopy is needed for the diagnosis (or a biopsy). It’s usually not so perfectly symmetrical as seen with AGA but it can be of course. It responds to topical steroids and Rogaine. Lichen planopilaris and folliculitis decalvans are scarring alopecias that can mimic AGA in some cases. They generally have associated itching, burning or scalp tenderness. Some patients have all three symptoms and some have only two and some have no symptoms at all .

The other common mimicker of classic TE is seborrheic dermatitis and scalp psoriasis. These are common in the population so every hair specialist needs to know everything there is to know about scalp seborrheic dermatitis and scalp psoriasis because these are common concerns. . About 5-10 % of people have seborrheic dermatitis and 2-3 % of all people have psoriasis. In mild cases, seborrheic dermatitis and psoriasis don’t give much in the way of shedding. In moderate to severe cases, they most certainly do. These can mimic a telogen effluvium.

Conclusion

Thanks again for your great question. I hope this helped.

In summary, it’s likely your shedding is abnormal but it could be temporary. A full exam together with review of your story and completion of some key blood tests would be part of an ideal plan. Taking photos every 3 months is probably the most helpful thing you can do for yourself. If your shedding settles but density seems to be dropping off it’s likely there is some AGA present and starting one of the treatments is a good idea if your goal is to halt hair loss. If your shedding stabilizes in the next few months and density stays high, watchful waiting is probably the way to go. This later situation probably means you had some form of telogen effluvium.

Combination Treatments for Frontal Fibrosing Alopecia

Can acitretin and finasteride be combined for the treatment of FFA ?

I’ve selected this question below for this week’s question of the week. It allows us to the concept of combination treatments for frontal fibrosing alopecia and specifically address whether finasteride and acitretin can be combined.

QUESTION

I am 49 years old (female) and the clinical diagnosis was initially FFA, but the biopsy was ‘inconclusive’. It is thought that I probably have a combination of telogen effluvium and FFA.  I am still losing hair and the front hairline has receded more than half an inch. So far I've only taken a mild topical steroid for 4 months and then Dermovate for 4 months. I am on HRT and on Lipitor {statin} for high cholesterol, and on cod liver oil.

My doctor suggests either Acitretin or finasteride. It is up to me to decide which I will take.

My question: could I combine both medications?

You have always suggested combination treatments, but I don’t actually recall having read about the combination of Acetrin and Finasteride. 

Also, my doctor suggests 1mg Finasteride – however, some medical articles mention a dose of 2.5mg.

Would you suggest I start with a higher dose and if necessary, decrease it in case of side effects? 

QUESTION

Thanks for the question.

Yes, finasteride and acitretin can be used together by a great number of post-menopausal patients with FFA - but I am not usually a big fan of starting a large number of treatments together on day 1. I generally like starting one treatment and then adding another in the near or distant if at all possible. In other words, if I can “stagger” the start dates, I prefer that for my patients. I’ll go more into that in just a minute. Sometimes we do need to be more aggressive with treatment than other times and need to combine drugs from the start. That’s a clinical judgment. Even when we do start drugs together, I still like to stagger by 2-4 weeks in the event one causes any sort of rare side effect (i.e. rash, nausea, etc) when starting.

But the short answer to your question is that provided you don’t have any contraindication to using finasteride and provided you don’t have any sort of contraindication to using acitretin, you can use them together.   These two treatments are amongst the most effective treatments for FFA and I’m glad you have been considering them. I refer to these as the gold medal or first line treatments for FFA.

You and your doctor can review all the contraindications to these drugs and confirm whether or not you have any contraindications. Women with past or present depression, or past or current breast cancer may not be good candidates for finasteride and similarly women with high cholesterol or any sort of issue related to dryness  (dry lips, dry eyes, vaginal dryness) may not tolerate high doses or acitretin. You have high cholesterol treated with statins. It does not mean you can’t start acitretin but it does mean you are susceptible to cholesterol numbers bumping up. You’ll simply need to follow the numbers with repeat lab tests if you do start. Most are fine.

It always needs to be emphasized for readers that both of these drugs cannot be used in pregnancy and strict attention to contraception is needed in women who still have menstrual cycles.

You are correct that I combine treatments very often when treating scarring alopecia. But I’m not usually one to just pile on the drugs and send someone out the door with 37 prescriptions. If my patient needs only one drug to control the disease, then why use two drugs? If one can get some good control of the disease with one oral medication along with a course of steroid injections or topical calcineurin inhibitors there is no need to use 2 oral medications.  As mentioned above, it’s not always so simple and sometimes clinical judgment tells us that we need to hit the emergency button and pull out all the stops.   Sometimes we don’t even need pills at all and use of topical finasteride, steroid injections and topical minoxidil might be a good plan. Again it comes down to clinical judgment and of course - shared decision making with the patient.

In FFA, we can get a good sense of how well any newly initiated treatment is working in about 3-6 months. So periodic re-evaluation is key and often more important than the first appointment. (A second appointment is often more involved than the first and decisions can become trickier). Remember though that we might be looking for at the follow up appointment might simply be stopping hair loss as our main goal or we might be looking for some hair regrowth as our main goal. It just depends on the specific patient and the exact details of their FFA so far. Not everyone with FFA regrows any hair back - but some of course do. However, stopping the disease from getting worse is the main goal for everyone. 

In cases where I am a bit more worried or situations where past experience tells me one drug is not going to be enough, I might add 2 drugs. So unfortunately there are no definitive rules to treatment of scarring alopecias. I might start finasteride 2.5 mg at a frequency of 3-7 times per week with isotretinoin or acitretin 10 mg daily or isotretinoin or acitretin every other day. In other situations, I will prefer to start one drug and review how the skin and hair is doing in 3-6 months and adjust accordingly.

At the follow up appointment in 3-6 months, we might go up on finasteride if we started 3 times weekly or stay the course with the dosing we used. Similarly, once I review the mandatory blood tests I like to see for anyone with FFA on acitretin , we may similarly go up or down on the dose of this drug. If we just started finasteride at a past appointment, we might add isotretinoin or acitretin at the follow up if we did not start the drug at the first appointment. But if things are going well on finasteride and the other treatments we started (topicals, injections) .. I might not add acitretin at all. 

Finasteride should be at 2.5 mg rather than 1 mg and use of the drug is 3-7 times per week.  Now, before we leave the topic of finasteride it’s probably worth noting that the related drug dutasteride may be slightly more effective than finasteride in treating FFA. More good studies are needed to definitely prove how different each drug is bit that is important to keep in mind. Sometimes I start a patient on 2.5 mg finasteride daily and depending on how things go I might alternate finasteride 2.5 mg daily with dutasteride 0.5 mg daily in the future or switch completely from finasteride to dutasteride. Dutasteride has a very long half-life so if I have any worry about side effects or potential side effects I might start finasteride rather than dutasteride. However the reality is that for most women with FFA these two drugs are very well tolerated.  

As another example, some women find dutasteride and finasteride worsen hot flashes and so if I am worried about this as a side effect in someone already dealing with hot flashes, I might start finasteride 2.5 mg 3 times weekly not dutasteride daily. Of course, depending on the clinical situation, I might not even start it at all - or might prescribe topical finasteride instead.

Sometimes we need to go higher on acitretin or isotretinoin dosing than 10 mg daily. Whether we do depends on how the patient is tolerating the drug and whether they have side effects. A patient with the side effect of unbearable dry lips or dry eyes is not a patient that we are going to want to increase the dose of acitretin or isotretinoin. In fact, we may even go down on the dose or stop and bring on board a silver medal (second line treatment) like hydroxychloroquine.   Similarly, if cholesterols is jumping up (ie LDL cholesterol or triglycerides), we may want to go down one the dose and bring on board another treatment that won’t impact cholesterol.

 

The Treatment of FFA: Combination Examples

The treatment or scarring alopecia requires a lot of decisions based on what the patient sitting in front of me feels about these treatments and the past health of the patient and the activity of the disease currently. If you dig through the charts of patients with FFA in my practice you’ll see a lot of different treatment plans:

a) some use no pills only creams (steroid or calcineurin inhibitors) and/or steroid injections 

b) some use dutasteride or finasteride and creams +/- steroid injections 

c) some use dutasteride or finasteride with doxycycline and/or hydroxychloroquine plus creams +/- steroid injections 

d) some use oral doxycycline +/- oral hydroxychloroquine alone and creams +/- steroid injections 

e) some use dutasteride or finasteride with creams and isotretinoin or acitretin +/-steroid injections 

f) some use dutasteride or finasteride with acitretin or isotretinoin with creams  +/- steroid injections   +/- hydroxychloroquine 

g) some use acitretin or isotretinoin with creams  +/- steroid injections   

h) some use acitretin or isotretinoin with creams  +/- steroid injections   +/- oral hydroxychloroquine 

i) some use topical finasteride in place or oral finasteride or dutasteride in the above

j) some also have oral minoxidil, topical minoxidil, laser therapy, mycophenolate mofetil, methotrexate, cyclosporine, apremilast, tofacitinib added into various patterns of the above examples

Variations on the Same Theme.

It is important to note that within each example there can be hundreds of variations.  Consider two patients who say, “I take dutasteride, hydroxychloroquine and isotretinoin.” 

One  patient might be on dutasteride 4 times each week PLUS at 10 mg isotretinoin 2 times per week PLUS hydroxychloroquine 200 mg daily.

The other patient might be on dutasteride 7 times per week PLUS at 10 mg isotretinoin 3 times per week PLUS hydroxychloroquine 200 mg 4 times per week.

Combinations that Are Not Permitted.

 I have reviewed a lot of the common combinations above in how we manage FFA. Some treatments cannot be used together due to side effects. Common examples are doxycycline with isotretinoin or hydroxychloroquine with cyclosporine. 

I hope this helps. Thanks for submitting the question.

REFERENCE

[1] Acitretin Handout for Patients with Scarring Alopecia

[2] Finasteride Handout for Women

Drug Induced Alopecia Areata: Can Drugs Cause Alopecia Areata?

Can medications cause alopecia areata ?

I’ve selected this question below for this week’s question of the week. It allows us to discuss the concept of drug induced alopecia areata.

Drug induced Alopecia Areata: 14 drugs to date have been implicated in the development of alopecia areata. The association is still considered very rare even in those who take one of these medications.

QUESTION

Hi Dr Donovan,

I am a 29 year old female and developed alopecia areata in late January 2021. I first developed a patch at the top of the scalp on Jan 23rd and then a second at the back of the scalp on Feb 8. They have fortunately both now grown back with steroid injections using Kenalog.

I am trying to understand this condition and what might have caused it. There is nobody in my family with this condition so I am perplexed. I am quite healthy, eat well and exercise 5 days per week. I have mild asthma and take puffers only very rarely. I developed a urinary tract infection in December and was treated with the antibiotic trimethoprim/sulfamethoxazole (Septra). I’ve been wondering if this could be the cause.

I have been researching if medications can cause alopecia areata but I’m not sure that medications are really all that commonly implicated.

Can you tell me if some medications are strongly connected with developing alopecia areata?

ANSWER

Thanks for submitting your question.

The short answer is no. Mediations are not really all that strongly connected with developing alopecia areata. That’s not to say that some medications have not been linked - it’s just the chances are very low and the vast majority of medications are not strongly associated with development of alopecia areata.

To date, there have only been about 25 patients reported in the medical journals with suspected drug induced alopecia areata. Could it be that there are more? Absolutely. But one thing is likely that drugs are probably not all that commonly connected with alopecia areata.

A nice research paper published in the journal called Clinical and Experimental Dermatology looked at these 25 patients so far who were felt to have ‘drug induced alopecia areata.’ The average age of patients with this condition was 42. Alopecia areata developed about 3-4 months after the drug was started.

Features of Drug Induced Alopecia Areata

Here are some of the key features of “drug induced alopecia areata”:

 1) There can sometimes be an itchy widespread skin rash on the body plus an itchy scalp eruption that precedes the alopecia by 2-3 weeks. Unlike many drug rashes, the patient here has no fever or joint pains. This itchy rash might not always be present.

2) The hair grows back very rapidly when the drug is stopped and further recurrences of patches of alopecia areata are unlikely to occur provided the drug is avoided.

3) Patches of alopecia areata occur again within weeks when the drug is restarted.

4) Blood tests for autoimmune tests, organ function, etc are normal.

What drugs have been implicated in drug induced alopecia areata so far? 

So far, most cases of drug induced alopecia areata that have been published in the medical journals have been with new so called monoclonal antibodies. In fact,  ¾ of cases involve a monoclonal antibody. The list of implicated drugs include 14 medications.

The monoclonal antibodies include:  Adalimumab, Denosumab, Sulfasalazine, anti PDL 1  inhibitors, Alemtuzumab, Nivolumab, Dupilumab and Secukinumab. The others include Lansoprazole, Rifampicin, Phenobarbital, Acitretin, Abacavir, and Carbocysteine.

Summary

Thanks again for your question. About 2 % of the world will develop alopecia areata during their lifetime and it seems that for 99.999% of patients with alopecia areata a drug is not the cause. But for some it could be. The list of drugs will certainly grow beyond the 14 listed above as we continue to understand this concept of drug induced alopecia areata. Perhaps it’s even a bit more common now than we even realize.

But this diagnosis is so much more complex than simply “I took a drug and then got alopecia areata.”

It’s actually closer to “I took a drug and got an itchy skin rash and then got alopecia areata and then stopped and I did not have a patch of alopecia areata at all until I chose to take the drug again.

But for most people, the chances of developing alopecia areata was present the day they were born into the world. There’s a number of genes that increase the risk of developing alopecia areata. So these are really the key factors. But there certainly are environmental factors (exposures) that cause the alopecia areata to develop in someone with the right genes. We don’t understand all these environmental factors but the factors that are being studied are include infections, viruses, stress and others. it’s possible drugs are on that list for now.

What’s striking about drug induced alopecia areata is how fast hair grows back when the drug is stopped. Now, we very rarely decide to give the drug again so it’s hard to know in many cases about criteria number 3 (hair loss occurs when drug is restarted). But if hair loss does occur rapidly when the drug is restarted, it really increases the odds that the drug is implicated.

Taken together, trimethoprim/sulfamethoxasole is not on the list of drugs currently implicated in drug induced alopecia areata. That does not mean it can’t be but there is no really convincing evidence. If a person had a rash when using this drug and developed a patch again with the use of this drug it could support a connection. But if there are patches of alopecia areata that develop when a person is completely off the drug, it really makes it less likely that a drug induced alopecia areata is the correct diagnosis.

REFERENCE

Murad A et al. Drug-induced alopecia areata? Clin Exp Dermatol. 2021 Mar;46(2):363-366.

Do I have AGA? Everything thinks I am Crazy!

Why am I losing hair ?

I’ve selected this question below for this week’s question of the week. It allows us to discuss the diagnosis of hair loss in the early stages and the use of the 5 day modified hair wash test.

QUESTION

Dear Doctor Donovan,

I'm a 27 year old female. I've seen a lot of dermatologists over the years but none of them could solve my problem and I'm desperate!! It's been three years that I'm losing hair. It started during a stressful period in 2018 with a significant amount of shedding (300-400 hair a day).

The shedding stopped for 4 months and then the shedding started again until now. The only thing I noticed during these years is that hair loss is focused on the side of the head and temples and hair always grows back, even if I have less. The dermatologists have all said the diagnosis is telogen effluvium or chronic telogen effluvium (CTE) because in their opinion I still have a lot of hair and no miniaturized hair (but I can see them!)

In 2019 I decided to starting using minoxidil 2% because I was losing my mind and I was scared to go bald. My mother uses it for AGA. I suffer from hypothyroidism, I have regular periods but low levels of ferritin. I'm also losing hair in different lengths (short, long, thick, thin).

I am afraid I have AGA. Nobody believes me and they think I'm crazy!.

Thank you very much for listening.

ANSWER

Thanks for submitting this very interesting question.

I’d like to discuss several important things in the question you ask and the information you have submitted.

Before we do go further, I’d like to point out that the ideal way to diagnose hair loss is using what I termed the ”Diagnostic S.E.T.” I refer to these as the diagnostic “set” because theses 3 aspects all go together. These 3 items include:

1) the patient’s story

2) the findings uncovered during the process of the scalp examination including trichoscopy

3) the results of relevant blood tests. 

The first letter of each of the three words 1) story, 2) examination and 3) tests spell out the word “S.E.T.” - again a helpful reminder of how the information obtained from reviewing each of these 3 aspects helps solidify a proper diagnosis. I don’t have a full story and I only have a trichoscopy photos from one area and I don’t have the opportunity to review all tests …. so I am limited to some degree in my helpfulness. Nevertheless, I do think the discussion here will be helpful.

In the early stages of hair loss, nobody can tell you have hair loss. So, when people tell you they think your hair looks normal, they are being honest. You know you hair the best.

What are the Most Likely Diagnoses in this Case?

We are deciding here between three situations:

1) Do you have androgenetic alopecia (AGA) and telogen effluvium (TE) ?

or

2) do you have telogen effluvium (TE) only ?

or

3) Do you have both of these conditions?

I think there is little doubt in your story that telogen effluvium has been present at some time in the past. Whether it is still present NOW (today) is a bit more challenging to say as we will see in a while. I will explain in a moment how we can better distinguish between the two diagnoses.

It’s fairly unlikely that other diagnoses like alopecia areata incognito are present this long and similarly the photos don’t really lead me to believe we’ve dealing with other diagnoses. Of course, a full examination can confidently exclude that. But it’s unlikely.

What do I see in the photos?

The photos seem to show less density ‘now’ compared to 2018. This simply tells me you have some type of hair loss. It’s true that the part width is wider in these photos but without a sense of the part width in the back (to compare to part width in the front) it would be a mistake to conclude that this widened part width equates to AGA. The temples have some subtle changes but we see these minor changes in AGA and TE. The changes in the temples do not allow me to determine the diagnosis.

The trichoscopic images you have included here are great quality. However, I don ’t know where on the scalp they are from. It’s really important when fully interpreting trchoscopy to know where the images are from.

Trichoscopy IMAGE 1

The top image appears pretty normal. Is it from the back of the scalp from more posterior regions on the head? Hairs in the first image are grouped in groups of 3 and 4 hairs. There are really no single hairs. There is slight variation in caliber of hairs but this is just a few percent that show this. It is nowhere near the 10-20 % variation in caliber of hairs that’s needed to make a diagnosis of AGA. There are no upright regrowing hair seen. The scalp is pretty healthy other than than some minor redness.. There is a bit of scale but that’s what a scalp looks like.

Trichoscopy IMAGE 2

The second image is different than the first which makes it important to know where exactly where it’s taken from. Whenever we interpret trichosocpy we need to know where it’s taken from or else we can’t say all that much. What stands out to me in image 2 is that it’s slightly different than image 1. This could be important but again I would need to know where on the scalp it is from. There are more single hairs seen in image 2 and the density is subtly less compared with image 1. If image 2 was from the front of the scalp and image 1 was from the back I’d be of the opinion that there was at least some good evidence for androgenetic alopecia. But I don’t know where these were taken from so I can’t say very much. However, the fact that the two images look slightly different makes me wonder about pattered hair loss - the most common being andrgoenetic hair loss.

Key Questions I Would Want to Know and Why I Would Need this Information

There is lots more to your story that I need to know if order to help determine the diagnosis in a convincing way. We need to determine if there is evidence for androgenetic alopecia and we need to determine if there is evidence for a telogen effluvium. I would want to know the answers to the following questions::

PART 1: IS THERE EVIDENCE TO SUPPORT A DIAGNOSIS OF ANDROGENETIC ALOPECIA?

Q1. Where does it feel the thinnest?

It would be helpful to know from your perspective where the hair feels the thinnest. Does it simply feel thinner “all over” (diffusely) or does one area of the scalp feel more than another? Most patients with classic TE feel that the hair is thinner all over and can’t usually point to a single area that is thinner (EXCEPT maybe the temples). In AGA, the central scalp often feels a bit thinner although some women do have a diffuse pattern or loss.

Q2. Is the part width similar in the back of the scalp as it is in the front of the scalp?

Why do I need to know? Le't’s talk now about the physical examination of the scalp and the steps your doctors would take when examining the scalp. it’s critical to know if the part width in the frontal region is the same as in the back or whether it’s different. You’ve shown a very good photo of your central part in the FRONT which allows me to see that there is more hair loss than 2018. However, what I am not able to tell now is what the part in the BACK OF THE SCALP looks like. If it’s quite similar “width” to the frontal region, that’s not really very supportive of AGA and is more supportive of TE. However, it it’s clear that you have lost more hair in the frontal region that would be more consistent with androgenetic alopecia.

Q3. What was the exact timing of starting minoxidil ?

Why do I need to know? There is evidence of regrowth on the scalp. As I see in the photos, there is considerable growth of 12-15 cm hairs which means that these hairs in the middle of the scalp started growing well about 1 to 1.5 years year ago. It would be helpful to know if this is where minoxidil was applied and if it was late 2019 rather than early 2019 that minoxidil was started.

Q4. Is that 12-15 cm regrowth seen just in the middle of the scalp or is that seen everywhere equally.

Why do I need to know? When your doctors examine the scalp, it’s going to be really important to determine if this growth of these hairs is truly everywhere or just I the central scalp where I imagine you would be applying minoxidil. If the hair regrowth is just central and these 12-15 cm hairs are not found so easily in the back of the scalp, then it’s more suggestive of an early androgenetic alopecia that is present that is responding well to minoxidil.

Q5. Is the hair density today less than 1 year ago or about the same as one year ago?

One of the most important questions in this case is whether or not you are still losing hair density. Here I am not referring to shedding but rather density and how thick your hair feels overall. Is it less thick? …. or just as thick as it used to be. I understand that you are still shedding but that is a bit different from whether you are still losing density. If you are still losing density and you feel that you have less hair on your scalp today than 1 year ago, that would be slightly more suggestive of possible AGA than TE. If you are still having problems with shedding but don’t actually feel your density is getting less and less, then TE still remains a very likely diagnosis.

Q6. Do you have acne or excessive hair growth elsewhere?

As we evaluate hair loss, it important to get a sense if there are clinical signs of hyperandrogenism (high androgens). Having hyperandrogenism does not necessarily mean the patient has AGA but does increase the odds just that much more.

Acne and hirsutism are two of the more important signs to enquire about. If there is any clinical evidence of hyperandrogenism, it will be important to have blood tests for testosterone and DHEAS. Only 10 % of women with AGA have hyperandrogenism so the finding of normal hormone levels still makes AGA possible. In addition, many women with hyperandrogenism do not have AGA at all so this is just a fact that gets considered as part of the bigger picture.

PART 2: IS THERE EVIDENCE TO SUPPORT A DIAGNOSIS OF ONGOING TELOGEN EFFLUVIUM?
It’s clear that a telogen effluvium was present in the past for you. The key question now is whether there is some kind of ongoing TE. The causes of telogen effluvium include stress, low iron, thyroid problems, medications, diets, systemic illness. So we need to understand more about these potential issues or ‘triggers’ for anyone who is shedding. In CTE, shedding can occur without a clear trigger.

Q7. Did you start and stop other medications or supplements?

Why do I need to know? Other medications and supplements can trigger shedding. Even taking some medications and herbal medications can give an ongoing shedding. I’m assuming in this scenario that minoxidil is the only product used. Clearly, if other products are used they need to be considered.

Q8. Have you had eyebrow changes, eyelashes changes, body hair changes, nail changes?

Why do I need to know? Eyebrow and eyelash changes and body hair changes don’t occur as part of AGA but can occur in TE. They can also occur in other immune based conditions. I am not suspecting any immune based issues but certainly it would be quite unexpected if you were experiencing a lot of body hair loss. If there was any eyebrow or eyelash loss, the key is to figure out if it affects both the right and left side symmetrically or whether one side is affected more. Eyebrows and eyelashes can reduce in density from telogen effluvium, alopecia areata, trichotillomania, seborrheic dermatitis as well as cicatricial alopecia (and other conditions). It would not be surprising if you have some minor eyebrow changes over the last 3 years but it should be quite symmetrical. If you do have eyebrow changes, some of the eyebrow changes could be due to the hypothyroidism.

Similarly, if there was an increase in body hair this too would be unexpected here and a possible sign of increased androgens. Increased hair on the thighs, abdomen and nipples can be a sign of hyperandrogenism and raise suspicions for PCOS (even if periods are regular). I would think that it issei's quite unlikely you would report this to be the case. This would be information that your doctors should confirm.

Q9. Have you had weight loss or weight gain? What is the current weight?

In the setting of a likely telogen effluvium, it’s important to know whether there has been weight loss that could be triggering a telogen effluvium. In addition, we need to make sure that your current weight is high enough (i.e. BMI is above 18) otherwise the result can be an ongoing TE from poor nutritional status.

In addition, weight loss and weight gain can be reflective of underlying medical conditions. So, if weight has fluctuated either way, it could be important.

Q10. Do you have any scalp itching, burning or tenderness?

Scalp symptoms are important to know for every single patient. Your scalp looks quite healthy so I would be surprised to learn there is any itching or burning or tenderness. I’m usually not too worried about a slight among of itching from time to time, but if there was burning or tenderness in the scalp, that would be worrisome. I don’t think this is very likely to be relevant here for your case but we need to always keep in mind that there are conditions that mimic telogen effluvium.

Q11. Do you feel you are getting hair breakage?

I am not appreciating much in the way of hair breakage, but it’s important to inquire about. Some patients confuse hair breakage with actual new growth so what you are seeing on the top of the scalp appears to be new growth. It’s not uncommon for patients to exclaim - “look at all my hair breakage!” In your case, this is not breakage from what I can see. However, if you felt there truly was increased breakage that would need further exploration. Breakage can come from heat and chemicals and can give the feeling of ongoing shedding and loss. A proper examination can completely exclude breakage, but I would be surprised if that’s even an issue here. your scalp and hair are healthy.

Q12. How low your ferritin dropped over this period ?

I understand that you have a history of low ferritin. It will be important to know what your ferritin level is right NOW. That is what will be relevant to ongoing shedding. A ferritin of 10 is likely associated with hair loss. A ferritin of 40 is probably not. Therefore, it will be important to know what the ferritin level is now and how it’s been changing over the last few years.

is it possible you’ve had a ferritin of 22 and it’s been responsible for your shedding for three years? Perhaps. The higher your ferritin level - the less likely it is that your iron is the culprit in your hair loss. But you have not given me the number so I don’t know the current level.

Certainly, if you have a ferritin less than 15, it’s probably a problem and probably one of the reasons why your hair is shedding. Taking iron supplements in these situations has a high likelihood of helping. However if your ferritin is currently 40, 50 or 60, it’s less likely that you currently have an iron problem.

Most women need ferritin levels in the 30-40 range for healthy hair. However, some women definitely need those levels to be higher than that and into the 50 - 70 range. If you have a history of low ferritin, it will be important for your doctors to review why you have low ferritin and how the levels have been changing over time and what they are now. Many women have low ferritin levels. However, when low ferritin is combined with low hemoglobin (which we call iron deficiency anemia) I’m much more concerned. Excessive bleeding from menstrual cycles, poor diet, celiac disease, gastrointestinal issues all need to be explored.

The following table gives an estimate of how likely it is that taking iron supplements will help your hair according to the ferritin levels.

Q13. When did you start thyroid medications? Have your thyroid levels (TSH) changed during this time? What is the exact reason for the thyroid disease (Is it autoimmune Hashimoto’s?)

It would be helpful to understand when your thyroid disease was diagnosed and whether the TSH has been changing over this period. Some patients occasionally have fluctuation TSH levels which give shedding. Also, it would be important to know if you are on thyroid medications NOW and when this started and whether the dose has been changing over time. It is important to know the exact causes of the thyroid disease.

Q14. Were your periods always regular?

It’s always reassuring to know that your periods are regular at the present time. It would be important to know if they have always been regular of whether they have become regular just recently. It would be important to know exactly what each patient means by regular periods. Are some cycles considerably longer and some shorter than others? Having regular periods does not make it impossible to have an endocrine issue but does make it less likely. Having regular periods does not necessary mean these are ovulatory cycles but for most women they, of course, are. ovoluatory cycles.

Q15. Has your density ever come back to normal or has it just become less and less?

It would be important to know whether you feel your density and thickness ever came back to normal. When the shedding stopped for four months, did density return? Do you know the reasons why the shedding stopped for those 4 months? Was it that your iron levels finally came up? Was it that that your thyroid levels were brought back to normal? Was it that stress was reduced? Was that the period that minoxidil was started?

If your density did return completely to normal, this makes AGA much less likely during those times. It does not mean that it could not have happened or developed later but we would not expect your density to come back to 100 % normal in the setting of AGA.

Q16. Do you have other symptoms like joint pains, headaches, fatigue or rashes?

In situations like this, it’s helpful to know if the patient has any other symptoms that could suggest a systemic cause for a telogen effluvium. Issues like going pains, chronic headache, unusual fatigue or rashes on the body could prompt further work up and evaluation.

Q17. What other conditions run in the family?

it’s helpful to know what conditions run in your family. I understand your mom uses minoxidil so that tells me there is a family history of AGA. It’s helpful to know what the hair density is like in other males and females in your family. It’s also helpful to know what other diseases or medical conditions run in the family. These would include issues like psoriasis, lupus, inflammatory bowel diseases, arthritis, alopecia areata, diabetes, multiple sclerosis, early menopause, infertility and polycystic ovarian syndrome.

What Would I Recommend Next?

1. The answers to these questions above are going to be helpful and so is an evaluation of the frontal part width and back part width. That could be really informative in this case. If the part is wider in the frontal regions than the back, this suggests a possible diagnosis of AGA. If not, it still could be but TE becomes more likely.

2. Comparative trichoscopy of the middle of your scalp compared to the back of your scalp is going to be very very helpful in reaching the proper diagnosis. If the two are really different with more single hairs in the frontal and more variation in caliber noted in the frontal regions, then AGA becomes a likely diagnosis.

3. Current blood tests from ferritin and TSH and CBC are going to be important. I suspect you’ve had these tests done many times. If your ferritin is not high enough, it could be that you are shedding chronically in part from iron deficiency. The history will guide if other blood tests are helpful.

4. Finally, 5 day modified hair wash test (MHWT) is likely going to be the most helpful and least invasive next steps. Of course, a scalp biopsy can also be done but I think a modified hair wash test is probably going to be better in this case. The five day MHWT is fairly easy to do and you can do it yourself at home if you are so motivated to do so. The hair must not be washed for five days before doing the test. A 5 day modified hair wash test (MHWT) is a standardized means of assessing and quantifying hair shedding and provides information on the type of hairs being shed. It is a non-invasive method to measure hair loss by counting and identifying rinsed out (shampooed) hairs. To begin the test, a gauze is placed in the sink and hair is shampooed normally and the hair is rinsed in order to collect and trap all shed hairs on the gauze. The hair can be shampooed and rinsed repeatedly in order to remove all hairs that need to come out.

The following is helpful diagram illustrating the key steps in the 5 day hair collection.

After gently lifting the gauze from the sink, the gauze is then dried for 3 days and then counted. In our clinic, patients who do this test mail the hairs to us, but patients can also go about counting hair. It is important that the gauze not be disturbed while drying or mailing as this gauze has dozens of small fine barely detectable hairs that must be included in the analysis. The final number of hairs as well as the proportions of 3 cm or less hairs, provides information on the relative proportions of androgenetic alopecia as well as telogen effluvium.  The proportion of broken hairs and the proportion of abnormal hair gives us a sense of the possibility of an autoimmune issue such as diffuse alopecia areata. 

The number of hairs collected in the MHWT can give a good sense of excessive shedding. Ideally, results need to be interpreted by a dermatologist who is familiar with the performance and interpretation of this test but as mentioned patients can count hairs.

a) Patients with 10% or more of hairs 3 cm or shorter and who shed fewer than 100 hairs are diagnosed as having androgenetic alopecia (AGA).

b) Patients with fewer than 10% of hairs that were 3 cm or shorter and who shed at least 100 hairs are diagnosed as having chronic telogen effluvium (CTE).

c) Patients with 10% or more of hairs that were 3 cm or shorter and who shed at least 100 hairs are diagnosed as having AGA + CTE

d) Finally patients with fewer than 10% of hairs that were 3 cm or shorter and who shed fewer than 100 hairs are diagnosed as having CTE ‘in remission.’

Final Summary

Thanks again for sending in your question. I hope this was helpful. A few more details in this history together with a good scalp examination is going to go a long long way here in getting to the correct diagnosis (or diagnoses in the event there are two).

IFor you, I think that a 5 day modified hair wash test is going to really help give the evidence that you need to move forward with the right diagnosis. If there is any doubt, then a biopsy could further clarify but I doubt it will be needed.

The use of minoxidil could complicate things a bit in this case but only slightly. If one were to stop minoxidil and find that significantly worse shedding happens 4-6 weeks later I do think this would also be proof of some component of AGA being present.

Post COVID 19 Hair Shedding (Sars-CoV-2 Telogen Effluvium)

How common is hair loss after COVID 19 infection? 

I’ve selected this question below for this week’s question of the week. It allows us to discuss the issue of hair loss after COVID 19 infection.

QUESTION

Hi Dr. Donovan !

I have recently recovered from COVID 19 and was pretty sick. I have read about hair loss in people who had COVID 19 and I am terrified that I might experience hair loss. I would like to know my chances of getting hair loss.

Can you please offer some guidance as to the likelihood of all this happening?  How likely am I to get hair loss?

Thank you very much.

ANSWER

Thank you for your question. I hope you are feeling well. Let’s look at this in a bit more detail. 

There are a variety of symptoms and signs that can persist or develop long after the SARS-COV-2 virus has left the body. When symptoms or complications are present more than 4 weeks after the onset of symptoms of COVID 19 this is revered to as “Post-acute COVID 19 syndrome.” Many people who have such long lasting symptoms after COVID 19 refer to themselves as “long haulers.” Other names such as “long COVID” and post-acute COVID syndrome (PACS) have been applied to this situation as well.

It is common to have symptoms in the weeks and months after being diagnosed with COVID 19. Carfi and colleagues showed in their publication in JAMA that most people still have one or more symptoms at day 60 of recovery. specifically, the authors of this study showed that 87.4 % of patients had at least one symptom and fatigue and shortness of breath were the top symptoms. 

Patients with post-acute COVID 19 syndrome can experience a wide array of persisting symptoms. These include fatigue, chest pain, shortness of breath, heart rhythm problems, brain fog, headaches, poor sleep, loss of smell, anxiety, depression, joint pains. Quality of life is reduced in many people even after the infection has cleared the body. Patients with post-acute COVID 19 syndrome may have lung issues, kidney issues, hematologic issues, blood clotting issues, cardiovascular issues, endocrine, psychiatric and neurological issues and therefore may be referred to a variety of different medical specialists. 

Hair Loss in COVID Survivors

Hair loss is one of the most common dermatologic issues that develops in patients who recover from COVID 19. It has been estimated that about 1 in 5 patients (20 %) of hospitalized who survive COVID 19 will have hair loss. We don’t know exactly what the numbers are patients with milder forms but it could be slightly less. Hair loss typically happens 8-12 weeks after infection and can even happen in those without any symptoms of COVID 19 at all. Let’s take a look at some of the important studies. 

The Huang Study, 2021

Huang and colleagues studied patients with confirmed COVID-19 who had been discharged from a hospital in China between Jan 7, 2020, and May 29, 2020. In total, 1733 patients completed questionnaires about their health status after leaving the hospital. Hair loss was reported in approximately 22 % of patients. Interestingly, the incidence of hair loss did not seem to differ in patients with greater degrees of illness compared to patients with less degrees of illness. For example, 22- 24 % of patients who required oxygen or mechanical ventilation during their hospital stay had hair loss compared to 22 % of patients that did not require oxygen.

The Garrigues Study, 2020

Garrigues and colleagues from Paris France examined health status of patients with COVID 19 after being discharged from hospital. They included 120 patients in their study, of which 96 were admitted to a hospital ward and 24 were more ill and needed to be admitted to the intensive care unit. Hair loss was reported in 20 % of patients overall. Further analysis showed that hair loss occurred in 25 % of ICU patients and 18.8 % of hospital ward patients. In this small study, these differences did not meet statistical significance indicating that hair loss is not seem to matter much according to how ill the patient was. 

The Akama-Garren Study, 2021

Akama-Garren and colleagues used the electronic health records from Mayo Clinic to examine whether certain terms were more common in patients before they were diagnosed with COVID 19 or more common after they were diagnosed with COVID 19. The authors showed that the term “hair loss” was much more commonly found in charts in patients after diagnosis with COVID 19 than before COVID 19 (OR 2.44, 95% CI 2.15-2.76, p=8.45x10-3). Other terms that also appeared more frequently were those related to kidney disease and coagulopathies. Hair loss seemed to be much more of a concern unique to females in this study rather than males. In addition, concerned about hair loss spiked dramatically at around day 100 after a diagnosis of COVID 19 which is what we would expect in a telogen effluvium.

The Miyazato Study, 2020

Miyazato and colleagues from Japan interviewed patients following discharge from hospital. 58 patients were asked about hair loss. Fourteen (24.1%) of 58 patients reported hair loss. . Of the 14 patients, 5 were women and 9 were men. Hair loss developed approximately 58.6 days ( 8 weeks) on average after symptoms of COVID 19 firsts began. Of the 14 patients, there were only 5 patients who had been studied long enough to get a good sense of how long hair loss lasted. Nevertheless, of these 5 patients, hair loss lasted on average 76.4 days ( 10 weeks). 

The Morenes-Arrones Study, 2020

I’ve talked about the Morenes-Arrones study before. This was a study of 214 patients with proven SarsCOV2 infection. 13. 6% were asymptomatic, 77% needed medical treatment and 21 % needed hospitalization. Hair shedding occurred after an average of 57.1 days ( 8 weeks) similar to the results from the Miyazato study reviewed above. 

Conclusion and Summary 

Thanks again for the great question. If you were hospitalized for your COVID 19 infection, we can say that there is approximately a 20 % chance you’ll get hair loss. we don’t know with great confidence that chances of hair loss in patients with more mild symptoms of COVID19 but there is a chance that the chances of hair loss are under 20 %. The only good data we have so far is in patients who were released hospitalized. 

Overall, the data together indicate that there is a much better chance that you won’t get hair loss than you will get hair loss. But if you do get hair loss, it will occur most likely around week 8 to week 12 after your COVID symptoms first started. Shedding will last about 10 weeks before the stopping. Complete hair regrowth would be expected in a large proportion of patients. 

I hope you recover well and feel back to yourself soon if you are not already.

REFERENCE

Akama-Garren et al. Hair loss in females and thromboembolism in males are significantly enriched in post-acute sequelae of COVID (PASC) relative to recent medical history. medrxiv.https://doi.org/10.1101/2021.01.03.20248997

Carfì, A., Bernabei, R., Landi, F. & Gemelli Against COVID-19 Post-Acute Care Study Group. Persistent Symptoms in Patients After Acute COVID-19. JAMA 324, 603–605 (2020).
Huang, C. et al. 6-month consequences of COVID-19 in patients discharged from hospital: a cohort study. Lancet 397, 220–232 (2021).

Garrigues, E. et al. Post-discharge persistent symptoms and health-related quality of life after hospitalization for COVID-19. J. Infect. 81, e4–e6 (2020).

Miyazato et al. Prolonged and Late-Onset Symptoms of Coronavirus Disease 2019. Open Forum Infect Dis 2020 Oct 21;7(11):ofaa507.

Moreno-Arronnes OM et al. SARS-CoV-2-induced telogen effluvium: a multicentric study. J Eur Acad Dermatol Venereol. 2021 Mar;35(3):e181-e183. doi: 10.1111/jdv.17045. Epub 2020 Dec 9.

 Nalbandian et al. Post-acute COVID-19 syndrome. Nature medicine 2021; 27: 601-614.

What is the reason for my hair loss?

Why am I shedding ?

I’ve selected this question below for this week’s question of the week. It allows us to discuss shedding issues in women with hair loss.

QUESTION

Hi!

I am a 42 year old women and have been shedding about 200 hairs a day since March, 2020. I have seen 4 dermatologists and my General Practitioner and they have different diagnoses from TE to FPHL or a combination of both. Prior to March, 2020 I was under extreme stress which started in November 2019. In March 2020 my hair loss was sudden and I have had diffuse shedding since then for the past 10 months. I have always had full, thick and healthy hair and no issues with my hair until the past 10 months. There is no family history of hair loss and my bloodwork came out normal.

Increased hair shedding.

I have been taking vitamins, biotin and Lysine (since June 2020) daily. I am washing my hair every other day, air dry my hair and do not use styling or heating products and eat healthy. I am also taking spirolactone since December 2020 (one month as of today). My dermatologist suggested I take spirolactone (50 mg twice a day) because I have irregular periods. My hair loss slowed down in September 2020 to about 100 hairs a day and went back up to 200 plus in November 2020. I am experiencing itchiness, pins and needles sensation on my scalp and my hair texture changed from straight to wavy for the past 10 months. My hair is also now flat, dull and I have some dandruff that comes and goes. My middle part is widening (compared to pre-March 2020 before the shedding) and with the ongoing shed the part has somewhat looked the same since March.

I lost about 30% of my hair and cannot style it the way I used to because of the thinning in the front. The last two dermatologists I saw performed a pull test and scalp examination and one of them said it is CTE and that there is nothing I can do but wait it out. The other doctor said it's FPHL and that she can tell just by looking at the front of my hair because of the way its thinning. I do see hair growth and my hair is full of static with short hairs coming out but I am also losing a lot of hair in all different lengths including short ones every day. I am frustrated because it has been 10 months and my shedding is not stopping. I do not know which diagnosis is right and what treatment I should start. Also It would be great for the itching and "pins and needle" feeling on my scalp to go away...

Thank you for reading and I'm so happy to find this website.

ANSWER

Thanks for the question.

I’d like to discuss several important things in the question you ask and the information you have submitted.

Before we do go further, I’d like to point out that the ideal way to diagnose hair loss is using what I termed the ”Diagnostic S.E.T.” I refer to these as the diagnostic “set” because theses 3 aspects all go together. These 3 items include:

1) the patient’s story

2) the findings uncovered during the process of the scalp examination including trichoscopy

3) the results of relevant blood tests. 

The first letter of each of the three words 1) story, 2) examination and 3) tests spell out the word “S.E.T.” - again a helpful reminder of how the information obtained from reviewing each of these 3 aspects helps solidify a proper diagnosis.

There is lots more to your story that I need. I would want to know exactly what your lab tests showed and which ones were tested. In about 20 % of patients who tell me they had blood tests and all came out normal, the labs are either insufficient (more are needed based on their story and examination) or the labs are not in fact really normal. I always like to see the labs. I would want to know about other symptoms like joint pains, headaches, fatigue, weight loss, eyebrow changes, eyelashes changes, body hair changes, nail changes, and rashes.

I strongly suspect that androgenetic alopecia with seborrheic dermatitis are part of the diagnoses. The 2 key questions here in your case are:

1. Do you have really have telogen effluvium as well ?

2. What really is the reason for the ‘pins and needles’ sensation ?

Let’s look at a few key points.

POINT 1. Androgenetic alopecia (female pattern hair loss) appears to be at least one of the diagnoses.

I do think that at least one of the diagnoses here is androgenetic alopecia (also called female pattern hair loss, FPHL). The widening of the part does not itself mean the diagnosis is AGA. however, the pattern of the part widening is not the same front to back. There is a slight increase in thinning noted in the mid scalp and crown compared to the frontal one third of the scalp. This leads me to believe there is a patterned nature of the hair loss. I’m open to the possibility that some of the hair loss is diffuse in nature (ie all over) but some is likely not. In other words, I don’t think this is entirely a diffuse type of hair loss.

Also, when I look up close at the images, it’s clear that some follicles are thinner than others. This is a phenomenon called anisotrichosis and is a feature of AGA. Some hair follicles are miniaturization (getting thinner).

Women with AGA often experience shedding of hair in the early stages and shedding can fluctuate in intensity. Other hair loss conditions can cause shedding as well so we’ll address that in just a moment. Women with AGA often notice that the texture of hair changes. There are many such patterns of texture change and a change from straighter to curlier is quite common as you too have described.

The fact that you note increasing numbers of short hairs is not confirmatory for a diagnosis of AGA but certainly is supportive of this diagnosis.

POINT 2: Seborrheic dermatitis/dandruff is likely another diagnosis.

I agree with you that dandruff (or its close cousin called seborrheic dermatitis) is likely present. Flakes are noted in some of the photos. I’d need to perform trichoscopy to confirm this diagnosis but it appears to be a component of the issues present. Mild dandruff is not usually a cause of hair loss but it certainly can cause all sorts of scalp symptoms. To eliminate the possibility that dandruff or seborrheic dermatitis is contributing to symptoms, I often encourage my own patients to aggressively treat their seborrheic dermatitis so we can remove this as a factor. Shampoos with zinc pyrithione, ketoconazole, selenium sulphide or ciclopirox can be used 2 times per week and left on 90 to 120 seconds before being rinsed off. The duration that these shampoos are left on the scalp can certainly be increased but I don’t recommend that to start with as many antidandruff shampoos can be drying and then the dryness starts causing itching and symptoms. I often recommend to my own patients that 5-10 drops of betamethasone valerate lotion 0.1 % can be applied in the scalp after their hair is shampooed and dried. This is a weak steroid and can be safely used for 2 week periods to help settle itching. If the use of shampoos settles the itching, tingling and pins and needles, then it’s not needed.

POINT 3: Telogen effluvium could be present.

Telogen effluvium is one of those conditions that can come and go. Sometimes it’s easy to prove a TE is present and sometimes it’s a bit more challenging. It could be that a TE was present when your AGA first started. You were under extreme stress in November 2019 and yes this could most definitively give shedding in March 2020. Telogen effluvium usually follows 2-3 month after some kind of trigger and can last 3-6 months or more. Other causes of telogen effluvium are low ferritin levels, thyroid issues, medications, diets, weight loss and internal illness. I don’t really have enough information to evaluate these other issues so I’ll go with your assessment that your blood tests were normal. Hopefully you had a reasonable set of tests including TSH, ferritin, CBC. With your irregular periods you describe it would make sense to have FSH, DHEAS, testosterone. One needs to consider whether you are entering a perimenopausal transition and how this could contribute to hair shedding and AGA. With any pins and needles sensation, it’s nice to know that liver enzymes (AST, ALT) are normal and that kidney function is normal (creatinine).

Telogen effluvium can sometimes precipitate or accelerate an underlying AGA. This is a well accepted phenomenon. it does not happen to all women with AGA. However, women with shedding who have AGA that is about to begin (ie very early onset AGA) often find that the AGA component of the hair loss gets sent into a more rapid speed of development if a TE is present. This could be a feature here.

With your normal blood tests, it’s unlikely that a TE is still driving hair loss all this time. Not impossible of course, but unlikely. What is more likely is that AGA is not fully being treated. Spironolactone helps but does not fully suppress AGA in all women at 50 mg twice daily. Sometimes higher doses are needed OR other treatments for AGA are needed (other anti androgens, laser, minoxidil, etc)

POINT 4: If you want to assess the degree to which AGA and TE are present, you could have a biopsy or 5 day modified hair wash test (or a proper trichoscopic examination). I don’t think these are really needed.

For your physicians/specialists who think that AGA is not a diagnosis here for you, a biopsy or 5 day modified hair wash test could help prove them wrong (… or prove them right!). This is a wonderful test but adds to the stress of collecting hairs so I’m not always in favour of it. Biopsies leave scars but if interpretted by a knowledgable dermatapathologist, they can be very helpful.

But, let’s be clear. A biopsy showing a terminal to vellus hair ratio of less than 4:1 taken from your mid scalp area puts to rest any argument about whether AGA its present of not. End of discussion. A 5 day modified hair wash test (done properly !) showing less than 100 hairs and more than 10% hairs being tiny 3 cm hairs also points to an underlying AGA.

Of course, simply examining the scalp with trichoscopy can also confirm this diagnosis but not all specialists are skilled with trichoscopy. If a specialist knows how to use a handheld dermatoscope, we don’t even need biopsies or hair collections to diagnose AGA. If they don’t then yes, we need to go to the extra effort to prove it.

POINT 5: The ‘pins and needles’ is a bit trickier given how many conditions can cause this.

There are a very large number of conditions that can cause pins and needles in the scalp. Stress can cause it. AGA can cause it. TE can cause it. Alopecia areata can cause it. Dandruff can cause it. Scarring alopecias cn cause it. The list is long and includes issues even outside the scalp like cervical spine disease.

I would need to know more about your story and carefully examine the scalp and eyebrows and eyelashes and nails to get a sense of what is causing this.

For pins and needles sensations, I usually advise treating any dandruff or seborrheic dermatitis and using a few drop of betamethasone lotion as outlined above. If it’s still there and the patient has AGA, I usually recommend treating the AGA more aggressively. This often help stop pins and needles. Low level laser, minoxidil and other antiandrogens can be considered.

Conclusion/Summary

Thanks for the question. I hope this helps you in your search for answers and helps with further discussion with your doctors. I think it’s really important for you and your doctors to feel confident with the diagnosis and not proceed with any sort of “maybe.” It would appear that AGA is a component of the issues here but if there is any doubt, a trichoscopic examination, biopsy or 5 day modified hair wash test can help confirm this.

Photos are really important moving forward to document changes - hopefully for the better.

if spironolactone is not fully helping then you and your dermatologists might discuss together whether or not to increase the dose or whether other treatments need to be considered. These include topical minoxidil, oral minoxidil other topical or oral antiandrogens and low level laser. PRP can be considered too. The important thing to note about minoxidil, laser and PRP is that if there is any amount of chronic shedding issue present these treatments can help promote more normal shedding patterns. This is assuming all your blood tests are normal. If any of your blood tests are abnormal and if, in fact, you have not had a proper work up then those issues need to be addressed first. it sounds like you’ve had a good set of blood tests through all the doctors you have seen.

Thank you.

Daily Shedding... with high DHEAS.... What should I be doing?

Why am I still shedding ?

I’ve selected this question below for this week’s question of the week. It allows us to discuss shedding issues in young women with high DHEAS.

QUESTION.

Dr. Donovan, I'm hoping you may be able to shed some light onto my hair shedding situation. I started experiencing increased hair shedding 6 months ago. Prior to the shedding, I'd started a birth control pill (low androgen) 2.5 months before, and Spironolactone 5.5 months before (for hirsutism). I experienced mild stress but it was nothing out of the ordinary. A month into the shedding, I began to experience tingling, crawling, and pain in my scalp. 1.5 months after the hair loss started, I went off of Spironolactone, and 2.5 months into the shedding, I went off birth control. My scalp became itchy as well.

I went to 3 dermatologists, all of whom diagnosed me with telogen effluvium. I recently had a biopsy done that stated telogen effluvium as well. I was also diagnosed with seborrheic dermatitis (which I've never had before in my life). I tried ketoconazole shampoo. I've had blood work done that stated my thyroid was normal, ferritin within normal range, (was 95 in October due to brief supplementation and then 26 in January), and I was deficient in vitamin D. My vitamin B12 level was too high, I'm not sure what that means.

I have symptoms of androgen excess (acne and excess hair growth on my face / body), dating back to my teen years (17), I'm 21 now, soon to be 22. The facial hair growth appeared in November of 2019 at age 20. I have elevated DHEAs (512), and had an ultrasound ruling out PCOS (no irregular periods, no polycystic ovaries).

Photo of the patient’s scalp.

Since the hair shedding began, I experienced massive emotional stress as a result. I was diagnosed with anxiety and depression - which I'm sure I've had for years but got extremely bad once my hair started to fall out. I am thin (weighing only 104lbs) but lost 10 pounds presumably due to stress of the hair loss. I've had two episodes of what was probably telogen effluvium in the past - one was related to low iron (ferritin of 7) back when I was 15, and one episode when I was 18 most likely due to a bad case of the flu. Those episodes only lasted 3-6 months and I grew all of my hair back.

This time, I've been consistently shedding for 6 months with no sign of improvement. My scalp is very tender, sensitive, flaky and itchy still. On an average day, I used to shed maybe 5-10 hairs, now I am shedding roughly 50-150 hairs - which is not normal for me. I'm at a loss for what could be causing this and what I can do about it. Any advice would be greatly appreciated

ANSWER

Thanks for the question.

I’d like to discuss several important things in the question you ask and the information you have submitted.

Before we do go further, I’d like to point out that the ideal way to diagnose hair loss is using what I termed the ”Diagnostic S.E.T.” I refer to these as the diagnostic “set” because theses 3 aspects all go together. These 3 items include:

1) the patient’s story

2) the findings uncovered during the process of the scalp examination including trichoscopy

3) the results of relevant blood tests. 

The first letter of each of the three words 1) story, 2) examination and 3) tests spell out the word “S.E.T.” - again a helpful reminder of how the information obtained from reviewing each of these 3 aspects helps solidify a proper diagnosis.

There is lots more to your story that I need. I would want to know about other medications you have started and stopped. I would want to know about other symptoms like joint pains, headaches, fatigue, weight loss, eyebrow changes, eyelashes changes, body hair changes, nail changes, and rashes.

The 2 key questions here in your case are:

a) Is the diagnosis ONLY telogen effluvium … and …. if so what is the trigger?

b) Is this a telogen effluvium with the starting stages of androgenetic alopecia?

Let’s go further into your story.

POINT 1. Many people who take birth control pills shed for the first few months.

First, I think there’s little doubt that at least one of your diagnoses is telogen effluvium. We don’t actually need to debate that. The debate we will get into in a moment is whether anything else is going on.

You have several reasons why you could have a telogen effluvium, including starting the birth control pill and starting spironolactone. A large proportion of women shed when starting these treatments, especially birth control pills. The shedding starts 2-3 months after taking the first pill and the shedding lasts 3-6 months provided the pill is continued every day. A lot of women shed when stopping these pills too, especially the birth control pill. The shedding starts 2-3 months after stopping the pill and the shedding lasts 3-6 months provided the pill is not restarted.

So what would I expect to hear from a 21 year old woman who starts spironolactone and then starts a birth control pill? Shedding.

And what would I expect to hear from a 21 year old woman who starts spironolactone and then starts a birth control pill and then stops these pills? Shedding.

What is your story? Shedding.

So in some ways, it’s possible this is entirely consistent with your story.

POINT 2: All patients with hair loss, acne and hirsutism and androgen excess need a proper work up. A work up should be done off birth control.

You have DHEAS 512 (which is 13.9 umol/L in SI units). Any female age 21 with DHEAS 512 and acne and hirsutism and hair loss needs a thorough endocrine work up in my opinion. We need to rule out PCOS and late onset CAH.

With the limited information you have provided here, it would be false to say that you “don’t” have PCOS.

The correct way to say it is more likely “you have a low likelihood of having PCOS.”

Women with PCOS who are thin with low BMI often have regular periods and often have no cysts visualized on ultrasound examinations … but still have elevated androgens. This is a bit more advanced type of knowledge, but I think it’s important especially since you have hyperandrogenism. Anyone who claims there is zero chance you have PCOS is wrong. Anyone who thinks there is a very low chance you have PCOS is correct. I have seen many women with your story exactly who go from being thin to being heavier in their 20s and 30s and ‘develop’ PCOS. I’m not saying that is your case, but sometimes weight gain brings about insulin resistance that then promotes a fuller PCOS clinical presentation.

So what work up do you need? Well, I would advise a proper work up on day 3-5 of your cycle for my own patients that come to see me with a story like yours. The fact that you are off birth control again is a good time to do this. We can’t do these tests when women are on birth control.

The tests that I order on day 3-5 of the cycle for my patients with similar stories are: LH, FSH, estradiol, testosterone, free testosterone, SHBG, glucose, insulin, hemoglobin 1A1c, AM cortisol, prolactin, androstenedione and 17 hydroxyprogesterone, AST, ALT, and cholesterol. These should be done fasting and day 3-5 of the cycle. You have already had your DHEAS measured so there is not a lot of good reason to do this again unless someone suspected levels could be climbing. I would probably include it again for completeness.

What am I looking for in these tests?

a) a high 17 OHP level on day 3-5 that would lead us to a diagnosis of late onset congenital adrenal hyperplasia

b) a high testosterone, high fasting insulin, high LH that would point is towards a PCOS like state

c) A normal prolactin and AM cortisol that reassures us that no other issues are present

In your case, I would want more blood tests if I was your doctor. I would want to know if there is any evidence of insulin resistance that would push me towards PCOS. I would want to know if the other hormones were normal. I would want to know your free testosterone and SHBG. I would want to know your 17 OHP levels to rule out late onset congenital adrenal hyperplasia before moving on.

POINT 3: When it comes to ultrasound examinations, there is a lot that patients don’t realize.

When I hear that a patient had an ultrasound that showed no cysts, my first response is usually that I’m glad to hear that news. But there are a few points to keep in mind. First, it depends on whether the ultrasound examination was a transabdominal ultrasound or transvaginal. There is a big difference in the quality of the studies and what it all means. Transvaginal studies with modern ultrasound techniques are the most helpful. Many people don’t have these studies done. Transvaginal studies can pick up a lot of cysts that the transabdominal can not. Of course, it’s very unlikely this is even an issue with your story but it’s something that we need to keep in mind.

With your ultrasound, I would want to know where it was done (what center? what clinic?) and whether it was transabdominal or transvaginal? What was the volume of the ovaries noted in the report ? Were any ovary measurements more than 10 mL ?

POINT 4: In the early stages of hair loss, TE and AGA can look the same and have the same story. Rarely, they can have a similar biopsy too.

When I look at your photos, I immediately say to myself :

Could this person have AGA?

Could this person have TE?

Could this person have both conditions?

(Also …. whenever we use the word TE, we need to immediate shout out hey could this be diffuse alopecia areata …. but I don’t think that’s what this is. But I include this for completeness of this write up).

In the early stages TE and AGA look the same. Of course, an up close examination with use of trichoscopy is going to help in your situation. In fact, it’s critical this be done! If the back of the scalp is convincingly thicker than the front of the scalp, I am pushed more towards thinking this could be AGA (with your TE). If the back and front areas are similar density, we are more likely thinking about a sole diagnosis of isolate TE. If there is no evidence of “follicular miniaturization” or variation in the caliber of your hairs when your scalp is examined with trichoscopy, we are likely dealing with an isolated TE. If there is a convincing variation in the caliber of hairs, it could be an early AGA.

Biopsies can be tricky. There is so much more to doing a biopsy than just doing it and so much more to interpreting a biopsy than just reading the information that comes printed on report. My ability to accurately interpret a biopsy depends where on the scalp it was taken from!. It depends how it was processed (horizontal vs vertical section). It depends who read the biopsy (dermpath vs general path). If a biopsy was taken from the sides or the back or somewhere just to prevent the patient from having a visible scar, then the biopsy is often useless. Biopsies in your case need to come from the top.

Here is where I would need your biopsy to have been taken from for me to feel better about the situation:

Also, if someone is going to tell me all you have in your biopsy is a telogen effluvium, I’m going to hope that horizontal sections were used. It’s a huge stretch to diagnose a telogen effluvium confidently from vertical sections. In horizontal sections, the pathologist gets to see 20-40 hairs in order to give their best guess about what could be going on with the rest of the scalp. With vertical sectioned biopsies, they just get to see 3-6 hairs. I don’t want to leave my patient’s hair loss diagnosis to interpretations as to what is seen with 3-6 hairs.

POINT 5: TE and seborrheic dermatitis (and sometimes even AGA) give tingling and symptoms.

With the biopsy result you have in your possession, I’m much much less worried about the tingling, crawling and pain. Of course, I wish you did not have it. But I’m not suspecting anything inflammatory that would make me want to act with a much different course. This is assuming your biopsy came from an area that was tender) I’m always worried when a patient says they have scalp pain. But this worry evaporates to a large degree when the biopsy from that area shows non-scarring alopecia. If your biopsy was from a random area and not from a tender area, then it becomes more difficult to interpret what it means.

Pain and tingling in your case can come from seborrheic dermatitis. it can come from TE, It can come from depression. It can come from allergy or irritation from a current shampoo. it can come from irritation of allergy from other cosmetics.

We still need to keep an eye on this pain. I often encourage my patients to commit to treating their seborrheic dermatitis with a rotating schedule of shampoos. Zinc pyrithione one day. Ketoconazole the next regular shampooing day and selenium sulphide shampoo the next shampooing day. Shampooing must be done 2-3 times per week and left on 2 minutes. I advise my patients to not over do the time as this often just dries the hair and scalp out further. Also, putting a prescription topical steroid on the scalp like betamethasone valerate lotion 0.1 % aa few times per week right after showering is often helpful (of before bed). 10 drops to 15 drops of betamethasone valerate lotion two times per week for a few months is very safe and anyone who says otherwise has little understanding, knowledge or training in the area.

If the pain is still present in 3-5 months, this needs to be looked into further.

POINT 6: What to do next depends on the blood test results and your prior response to spironolactone.

What exactly to do next and how do help your shedding depends partly on your next set of blood test results. If you have elevated 17 OHP on your blood tests, you may want to see an endocrinologist. If you have high LH or evidence of insulin resistance you’ll want to see a really experienced endocrinologist for evaluation of PCOS. Not all women with PCOS are overweight and in fact, women with PCOS who are thinner or have low body mass index often have regular periods and no cysts on ultrasound.

If you tolerated spironolactone well (in the past) and tolerated birth control well, it may even be an option to return to these and stay on these. Did it control your acne? Did it stop hirsutism? Did you feel good on it? Anyone starting these medications has a chance to get shedding so I’m not necessarily worried by a story of shedding. You stopped too soon to really get any sense what the long term outcome was. If there is any evidence of AGA with an up close examination, this could be a good option again. If not, you might want to treat your acne and hirsutism differently - perhaps topically.. The other option is to wait longer in hopes the TE resolves. Continuing iron and vitamin D and shampooing your hair diligently with these anti dandruff shampoos is going to be important no matter what is going on up on the scalp.

Finally, with any TE, we need to always keep in mind that maybe we have not found the trigger. If your ferritin was low and your hemoglobin was low (less than 12.0), a work up could be important. I often test for example a celiac panel in patients with BOTH low HGB and low ferritin. I’m not worried about your high B12. I would want to know about other medications you have started and stopped. As mentioned above, I would want to know about other symptoms like joint pains, headaches, fatigue, weight loss, eyebrow changes, eyelashes changes, body hair changes, nail changes, and rashes. Sometimes we consider ordering autoimmune tests in women with shedding but only if the history points us to ordering these. Ordering these tests ‘just to cover all bases’ is usually not a good idea.

Summary

I can instantly tell by your question that you’ve read a lot and thought a lot about your issues and what all this information means. Congratulations for that. That is important. You need to figure out if late onset CAH is a possibility or not ….. and whether insulin resistance/PCOS its truly off the list or not. In my opinion, these blood tests on day 3-5 are important to you. I’m glad you are off the birth control pill now because it allows you to get these tests done.

If your biopsy was taken from the area I have noted above, then that’s probably very helpful provided it was analyzed in the lab with horizontal sections. . The key point now is figuring out if there is any possibility of an evolving androgenetic alopecia that just could not be picked up in the early stages with the work up you had. A biopsy with horizontal sections and a good trichoscopic examination by a specialist who understands hair loss will uncover these answers.

Regardless, photos should be taken every 3 months. Not every day and not every week. If there is any kind of evolving pattern of hair loss, a photos will also capture these changes over time.

If TE is truly what you have and there are no underlying concerns, doing minimal additional things could be the best plan. However, if your hyperandrogenism is part of a bigger endocrine issue (like PCOS or CAH), getting advice from an endocrinologist would be a good way to proceed. These blood tests will be a really important guide. Some women just have elevated DHEAS and some women with elevated DHEAS develop AGA but some don’t. I never recommend patients start treatment because of what the labs say - treatment is started because of what the skin or hair is doing.

Thanks again for sending in the question. I hope this helps you are your team of specialists.

Acitretin, Isotretinoin and Minoxidil for Patient with FFA & AGA: What if they cause shedding?

Retinoids for Patient with FFA & AGA: Do they cause hair shedding that worsens hair loss?

I’ve selected this question below for this week’s question of the week. It allows us to discuss the use of retinoids and minoxidil in FFA .

QUESTION

I am a female age 67. My diagnosis is frontal fibrosing alopecia (FFA) - with a new diagnosis of underlying androgenetic hair loss (AGA). My dermatologist originally planned to put me on Acetrin for FFA but she now says that the shedding usually caused by retinoids will in cases with underlying AGA not be temporary, but will precipitate permanent hair loss, and therefore she does not want to prescribe it.

For review, I have itching all over scalp at different times [behind ears; frontal hairline, crown, temples]. Rosacea [onset only after topical clobetasol ]; thinning all over scalp with exception of crown; hair already thinning at age 50; eyebrow thinning at age 35/40. medicated since April 2020 by first Betnovate, then Dermovate [Clobetasol], then topical Pimecrolimus with Lymecyline. Other medications: HRT [estrogen only], statins [Rosuvastatin], ARB [Candesartan, as the only BP medication that is not linked to alopecia]; in the past decades [but now discontinued because of links to alopecia]: sun blockers and retinol creams.

I do not understand why underlying AGA should make a difference in prescribing this medication. However, I am concerned about hair follicles affected by FFA. I worry that the hair near my hairline, once shed, will not grow back because in FFA, the follicles that still produce hair may not generate new hair after the shedding, as more and more follicles become affected by FFA. I don't know if hair follicles, once affected by FFA, (but not yet dead) continue their cycle from catagen to anagen until such time when they are truly dead.

I have the same concern with Minoxidil, in particular as it was confirmed by another hair clinic that they do not advise the use of Minoxidil in patients with FFA, as Minoxidil stimulates initial shedding and FFA affected follicles would not produce new hair after that. - I would be very grateful if you could give me your opinion on the use of Minoxidil and Acetrin in a case of FFA with AGA.

Many thanks for your help and kind regards

ANSWER

Thanks for the great question. There is a lot to discuss, so let’s get to it.

First, let me say how relevant this question is. A very large proportion of women over 50 years of age with a diagnosis of FFA have a diagnosis of AGA in my opinion. I’d put the number around 55 % to even as high as 70%. So the most common scenario is treating both. Do I worry that any of my treatments are going to worsen the AGA? Not all that much. Is it possible? Sure. Do I see it? Yes, but I’d say less than 1 in 150 women. This is my experience in treating large numbers of patients with FFA.

POINT 1. The Question is Important Because Retinoids are among the Most Effective Treatments for FFA

Retinoids like isotretinoin and acitretin are among the most effective treatments for FFA. They are what I called “gold medal” treatments or first line treatments. Retinoids together with 5 alpha reductase inhibitor drugs are the most effective treatments for FFA. There is still a bit of debate about which drugs are actually better in treatment FFA. A 2017 study by Rakowska and colleagues suggested retinoids are the clear winner. Other studies by Vañó-Galván and colleagues suggested that finasteride and dutasteride (especially dutasteride) are the top treatments.

Here are the treatments that I consider top treatments:

POINT 2. Acitretin and Isotretinoin Can not be Used with Lymecycline

I’m not sure from your story if you are still on Lymecycline or not. It’s important to be aware that these two drugs can’t be used together - ever. So that’s not an option. But if you are off lymecycline, acitretin could be an option provided your cholesterol is under good control with the statin. If you are still on lymecycline and feel that it’s helping, you might decide to continue it and look to other options like dutasteride, finasteride or hydroxychloroquine. Acitretin won’t be possible. These are all discussions that you would want to have with your dermatologist. For some patients with FFA, they are good options - but not everyone.

POINT 3. Shedding can occur with Acitretin but is Not Common on Small Doses used in FFA.

Let’s come back to acitretin. Acitretin can cause shedding in 3 -5 % of users at the typical doses used in treating various diseases. The issue is that in FFA, I normally use much smaller doses - like 10 mg daily or even every other day to start. The risk of shedding is a lot less than 3-5 %. Do we have a number to quote you? Not really but I’d estimate it’s around 1 % and probably less.

How do I know? Well I have a large number of patients with FFA and AGA with on retinoids and I am not answering emails and phone calls very often about shedding issues. It still happens.

Provided you are not on Lymecycline, you certainly could consider going slowly on the dose if that issue something you want to discuss with your dermatologist again.

There are other options too - especially dutasteride (and finasteride). If your dermatologist is worried about shedding and won’t use, then dutasteride is an option. Do these drugs cause shedding? Sure, sometimes. Anything can. Fortunately, it is just not common either. shedding is less likely with dutasteride than acitretin but fortunately both are fairly uncommon. Sometimes, I prescribe acitretin and dutasteride together.

So, to summarize. It’s not impossible to have shedding from acitretin. It’s just not so common at the doses we use in FFA.

POINT 4: If shedding does occur, shed hair is not necessary gone forever.

There is an assumption that is wrong here - and that is that any shed hair is guaranteed to be gone forever. That’s just simply not accurate. You are shedding hairs all the time - and some are going to pop back up through the scalp. The more active the FFA is the less likely the hair is to come back up - but a lot still does even in active FFA. If the FFA is only mildly active - then probably a good deal of the hairs are going to return.

Granted, you are correct that we don’t want shedding if we don’t have do.

But if shedding is going to occur it will be mild most likely and happen around 6-8 weeks after treatment . You’ll have a few week window to stop. So I said that shedding is not common with 10 mg acitretin and I’ll point out that even if shedding does occur, it’s usually not common to massive shedding. So we have two “not commons’ in a row.

The risk of massive chaos with the hair is low.

Is it zero? Well no. But it is low.

Do be sure to review with your dermatologist the role of dutasteride too. Now, you might have contraindications to the drug so that is something you’d need to review with your doctors. I don’t have enough information. But often in situations like this I might consider starting dutasteride 0.5 mg 3 times weekly with acitretin or isotretinoin 10 mg three times weekly (along with steroid injections and topical pimecrolimus) and see where things are at in 4 months. We can go up on dutasteride dosing or up on acitretin dosing. That’s often my plan in situations like this but it may or may not apply to your situation.

POINT 5. Minoxidil is a common treatment for FFA.

Minoxidil can cause shedding. Sure. Is there a big risk that if you get shedding, the hair is not coming back? No. Is there a small chance it’s not coming back? Sure, but it’s small.

Minoxidil can be an important part of managing FFA sometimes. It can also play a key role in helping androgenetic alopecia.

Many of my dermatology colleagues who treat FFA like I do also use minoxidil. It’s not off the table as a treatment. I consider it a silver medal treatment - meaning that I might not start it right away in everyone but I often add it down the road. Some hair specialists use minoxidil immediately in treating FFA. I don’t but some do. I use it as an “add on” in many patients.

Conclusion and Summary

Thanks again for the question. I hope this helps. Minoxidil is commonly used in treating FFA and even in those who have AGA. Is it a first treatment to reach for? Not in my opinion but it’s a good option for many once things are coming a bit more stable. Minoxidil is worked into many patient’s treatment plans for FFA - even if they have AGA.

The acitretin is a good option for many (provided you are not still on Lymecycline or any sort of tetracycline antibiotic). In my opinion there are three treatments that a really need to be discussed for anyone with FFA - the retinoids (acitretin, isotretinoin), the 5 alpha reductase inhibitors (dutasteride or finasteride) and steroid injections. Those discussions are worth having with the dermatologist.

I’m not sure exactly why the other clinic you went to did not want you to use minoxidil. You can read my previous article on “The Six Reasons Why My Practitioner Won’t Start the Treatment You Were Hoping” - the answer certainly lies in one or more of these 6 reasons.

Thank you again

Hydroxychloroquine (Plaquenil) for Frontal Fibrosing Alopecia

Hydroxychloroquine (Plaquenil) for FFA

I’ve selected this question below for this week’s question of the week. It allows us to discuss the use of hydroxychloroquine (Plaquenil) in FFA as well as the rare cardiac effects of hydroxychloroquine.

QUESTION

I am a female in my late 70s with frontal fibrosing alopecia, confirmed by a scalp biopsy. It is being treated with clobetasol .05%, one application per day. I have read that this is not a very effective treatment when used alone. What would you suggest might be used with it?

My dermatologist suggested hydroxychloroquine (plaquenil), but I read that this might have an adverse effect on people with heart disease. Do you agree? The first symptom about six months ago was drastically thinning eyebrows. I am in the third month of treatment and hair loss around the hairline is not yet apparent. I have cardiomyopathy and atrial fibrillation, for which I am taking a blood thinner (Eliquis) plus daily irbesartan, bisoprolol and spironolactone. Do you think any of these drugs might be the cause of my FFA?

ANSWER

Thanks for the great question. I’d like to discuss several important points in the question you ask and the information you have submitted.

Before we go further, I’m going to assume here in your question that the diagnosis is correct. Can I be 100 % sure you have FFA? Well no - not at all. I haven’t seen your scalp and eyebrows and I don’t know all the details of your story. You might reply to me that you have already told me you had a biopsy. Well, biopsies are not 100% either. Nevertheless, it sure sounds like many aspects of your story do, in fact, support a diagnosis of FFA. So I’ll proceed with this assumption. If you do have FFA, this answer then helps. If the diagnosis is not correct, then the answer has helpful points nevertheless for others with the condition.

Let’s look at some aspects of your question:

a) How good is hydroxychloroquine in FFA?

Hydroxychloroquine is helpful in some patients with FFA. I tell my patients it’s a silver medalist. In other words, it can be helpful, it’s just that other treatments are probably better. We will get into that a bit later. That does not mean hydroxychloroquine is useless as a treatment. Not at all. For some patients with FFA, hydroxychloroquine does help. It does not help everyone that is for sure.

Let’s look at some helpful studies from the past evaluating the effectiveness of hydroxychloroquine in FFA treatment.

in 2013, Ladzinski and colleagues proposed that hydroxychloroquine had some benefits in about 50 % of patients,

In a much larger study conducted in 2014, Vano Galvan et al showed that a 15 % of patients with FFA using hydroxychloroquine had some improvement in their disease. 59 % had their disease stabilized. For about one quarter of patients, the drug did nothing helpful at all.

in 2018, Strazzulla and colleagues found that about 70 % of patients had some benefit with hydroxychloroquine - with results being more or less the same ass doxycycline.

A 2010 study by Samroa and colleagues found that hydroxychloroquine reduced redness and inflammation in FFA patients.

Treatment Options for FFA

Before we leave the subject of hydroxychloroquine for treatment of FFA, let’s look at the options for treatment. Every single type of hair loss has treatment options. The thing that is often forgotten is that not all treatments are the same. Some are good. Some are not so good. Some are good but crazy expensive. Some are good and not so expensive. Some are good and fairly safe and some are good and incredibly risky. I divide every disease into gold, silver and bronze medal treatments. 

I personally like this analogy of categorizing treatments because it reminds us of a couple of key things. First, not all treatments are equal. We select treatments by balancing benefit and risk and take into account the safety, affordability, feasibility and effectiveness of treatment (what I have previously termed the "S.A.F.E." Principle. )

The second reason I like the analogy of gold and silver and bronze medal treatments is because it reminds us that this is not always going to be the order. The athlete that received the gold medal in the recent Olympics may not be the athlete that gets the gold medal in the next Olympics. Of course, if the athlete is really good - he or she will probably be up there one the podium in the top spot again in 4 years. The same is true with hair loss treatments. 

As new treatments come out and as they are studied more and more, a certain treatment might just rise into the gold medal spot and push out other treatments that are there now down into silver or bronze positions. Sometimes, a treatment gets removed from the market entirely just as some Olympians get disqualified from the Olympics. They disappear entirely.

In the diagram below, I outline what I consider the gold, silver and bronze treatments for FFA. In FFA, Plaquenil is a silver medallist. It’s not useless. It has reasonable safety (although I will discuss the heart issues next). It’s relatively inexpensive (Plaquenil is about $1300 USD per year whereas Apremilast is $ 18,000 USD per year). It’s easy to use. It’s somewhat helpful. In terms of the SAFE principle, it’s an okay option to keep in mind for many.

b) Does hydroxychloroquine have effects on the heart?

Hydroxychloroquine can have effects on the heart. Fortunately, they are not common but risks do increase with advancing age. In fact, physicians need to be much more on alert for eye, muscle, heart side effects in patients over 65 compared to those under 65. Of course, side effects of this nature can happen at any age - but they are more common with advancing age. Hydroxychloroquine cardiotoxicity is non common - but it is a serious side effect.

Plaquenil “cardiotoxicity” (potential toxicity on the heart) has best been studied inn patients with the autoimmune disease lupus who take the drug and also to seem degree in patients with rheumatoid arthritis. Could it be that a these groups are more likely to experienced heart muscle side effects with Plaquenil? Could be, but more studies are needed. For now, it’s a potential side effect that needs to be considered in everyone. There’s nearly 100 reports in the medical journals now of hydroxychloroquine induced heart toxicity. When it does occur, the patient usually develops a restrictive or dilated cardiomyopathy or has conduction system abnormalities including atrioventricular block and bundle branch block. Studies by Costedoat-Chalumeau showed that when cardiomyopathy is present other signs of toxicity are often present as well - eye toxicity, nerve toxicity, and muscle toxicity.

So who is more likely to get hydroxychloroquine induced cardiomyopathy ? Risk factors are currently proposed to include older age, female sex, longer duration of therapy (>10 years), higher doses of the drug, pre-existing cardiac disease, and renal insufficiency (kidney disease). It’s important to remember that most patients who develop hydroxychloroquine cardiotoxicity have been on the drug a long time - ie 10 years or more. Of course, there are reports in the medical journals of those who have been on it just a few months before developing side effects.

The Lane and Colleagues 2020 Study

Finally, I’d like to tell you about an important study by Lane and colleagues. This was recently published. This was a study of almost 1 million ( 956,374) hydroxychloroquine users so it’s a massive study. Massive studies of this size are important because they allow us to get a better sense of the risk associated with certain drugs. Lane’s study focused non patents with rheumatoid arthritis (not FFA) so we need to always keep that in mind. The researcher showed that long-term hydroxychloroquine use increased cardiovascular mortality 1.65 times compared with control treatments There are some limitations of the study (as there are with any study). nevertheless, it points to the fact that there may be a slight increase risk of heart related effects with long term use of hydroxychloroquine - at least in patients with rheumatoid arthritis. Fortunately, side effects of this nature are still quite uncommon.

In conclusion, there are some small risks with hydroxychloroquine use in your case. This is something you’d certainly want to review with your heart doctors too. Depending on the degree of heart issues (class of heart failure, etc), it may be something they agree with at a low dose, or something they advise against.

c) What would you suggest might be used with clobetasol?

This is actually a very involved question. If you find that use of clobetasol in the manner described and recommended by your doctors stops further hair loss completely - then you don’t need to use anything else. The key to treating FFA is not to pile on more and more drugs but rather to use the safest and simplest approach possible that stops the disease. if clobetasol stops your FFA 100% - then you need not look for anything else.

Is it likely that clobetasol stops your disease 100%? Well, no. But again - it’s not impossible that it does. It’s a silver medallist.

There are some 20 other options available. Again we follow a logical approach to deciding on which other treatments to use. We select treatments that have good evidence from good studies as well as treatments that have good safety.

You may want to review with your doctors other options like topical calcineurin inhibitors (like Pimecrolimus) as well as low doses of steroid injections (2 mg per mL) every few months. Topical clobetasol is going to give atrophy after a few months of daily use so you and your doctors are going to need to decide when to start reducing that dose.

You can also review options like topical anti androgens (topical finasteride) or even oral dutasteride. Starting two times weekly could be something that you are your doctors discuss. You’ll want to carefully review if you have any contraindications to its use (depression, cancer risks, osteoporosis). Adding acitretin once weekly or twice weekly may also be something you discuss.

d) I am taking a blood thinner (Eliquis) plus daily irbesartan, bisoprolol and spironolactone. Do you think any of these drugs might be the cause of my FFA?

Some drugs do contribute to the development of FFA. For example, the antiestrogen tamoxifen is one of them. The drugs on your list have not been implicated to date in the development of FFA. However, some can cause hair loss - just not FFA.

I’ll make a few additional comments at this point. First, your patterns of hair shedding are going to be important in giving you the fullest answer possible. Your story is interesting in that it seems that you have eyebrow loss without scalp frontal loss yet. Yes, that sure sounds like FFA but again I can’t say much more because I don’t know much about your story and haven’t seen your scalp. If your hair shedding is markedly increased the question must be posed to your health care team as to whether there is any component of telogen effluvium as well. All the drugs on your list can cause telogen effluvium - fortunately that’s still really unlikely overall. Most people have no issues of the sort.

Now on to the tricky part. it’s not possible to 100% say that the drugs you are taking had nothing to do with the development of FFA. Beta blockers (like bisoprolol), angiotensin II receptor blockers (like irbesartan) and spironolactone have rarely been involved in skin rashes known as “lichenoid” drug eruptions. There is some similarity between lichenoid drug eruptions and the lichenoid eruption that is part of the pathology of frontal fibrosing alopecia. Have any of the drugs you are taking been convincingly implicated in the development of FFA? No. It is possible there is some link in those with some sort of predisposition to this disease ? Yes.

Conclusion and Summary

Thanks for submitting your question. I do hope this will be helpful in the discussions you have with your doctors. I’ve included references below in the event they too are helpful. I wish you the best of health.

Reference

August C, Holzhausen HJ, Schmoldt A, et al. Histological and ultrastructural findings in chloroquine-induced cardio- myopathy. J Mol Med (Berl) 1995; 73: 73–77.

Baguet JP, Tremel F and Fabre M. Chloroquine cardiomypathy with conduction disorders. Heart 1999; 81: 221–223.

Clark C, Douglas WS. Lichenoid drug eruption induced by spironolactone. Clin Exp Dermatol. 1998 Jan;23(1):43-4

Costedoat-Chalumeau N, Hulot JS, Amoura Z, et al. Cardiomyopathy related to antimalarial therapy with illustra- tive case report. Cardiology 2007; 107: 73–80.

Fesssa et al. Lichen planus-like drug eruptions due to β-blockers: a case report and literature review. Am J Clin Dermatol 2012 Dec 1;13(6):417-21.

Ladzinski et al. Frontal fibrosing alopecia: a retrospective review of 19 patients seen at Duke University. J Am Acad Dermatol. 2013 May;68(5):749-55.

Lane, J. C. E. et al. Risk of hydroxychloroquine alone and in combination with azithromycin in the treatment of rheumatoid arthritis: a multinational, retrospective study. Lancet Rheumatol. (2020).

Massa MC, Jason SM, Gradini R, Welykyj Lichenoid drug eruption secondary to propranolol. Cutis. 1991 Jul;48(1):41-3.PMID: 1831116

Nord JE, Shah PK, Rinaldi RZ, et al. Hydroxychloroquine cardiotoxicity in systemic lupus erythematosus: a report of 2 cases and review of the literature. Semin Ann Rheum Dis 2004; 33: 336–351.

Pfab et al. Lichenoid drug eruption due to an antihypertonic drug containing irbesartan and hydrochlorothiazide. Allergy 2006; 61(6):786-7

Samrao A et al. Frontal fibrosing alopecia: a clinical review of 36 patients. , Chew AL, Price V.Br J Dermatol. 2010 Dec;163(6):1296-300.

Schön MP, Tebbe B, Trautmann C, Orfanos CE. Lichenoid drug eruption induced by spironolactone.Acta Derm Venereol. 1994 Nov;74(6):476.

Strazzulla LC et al . Prognosis, treatment, and disease outcomes in frontal fibrosing alopecia: A retrospective review of 92 cases.. J Am Acad Dermatol. 2018 Jan;78(1):203-205. doi: 10.1016/j.jaad.2017.07.035.

Vano-Galvan S. Frontal fibrosing alopecia: a multicenter review of 355 patients. J Am Acad Dermatol . 2014 Apr;70(4):670-678.

Yogasundaram H, Putko BN, Tien J, Paterson DI, Cujec B, Ringrose J, Oudit GY. Hydroxychloroquine‐induced cardiomyopathy: case report, pathophysiology, diagnosis, and treatment. Can J Cardiol 2014; 30: 1706–1715.

Hair Loss and Hidradenitis Suppurativa:

Hair Loss in Hidradenitis Suppurativa

I’ve selected this question below for this week’s question of the week. It allows us to discuss the important topic of hidradenitis suppurativa and what associations is has with hair loss.

QUESTION

I am a 23 year old female and was diagnosed with androgenetic alopecia at age 16 and treated with Rogaine and Spironolactone. I also have polycystic ovarian syndrome and prediabetes and have seen an endocrinologist for several years. Everything seemed to be going okay until recently. Lately, the pattern of hair loss is changing and my scalp is becoming intensely itchy and sometimes quite red and scaly. I am shedding a lot more and seen to have hair loss in many areas of the scalp whereas it used to be mainly on the top. Strangely, I am getting very itchy in several other areas recently including the underarms, thighs, private area and breasts. These areas are lumpy and tender and occasionally drain some small amounts of fluid. It’s getting pretty bad and is so so embarrassing for me. It makes be extremely sad. I am generally healthy although I am overweight and have depression and high blood pressure. I take metformin for prediabetes. I take citalopram for depression. Both fo these drugs sstarted about 1 year before these issues began. I am not on medications for blood pressure yet as my doctor increased by spironolactone from 100 mg to 200 mg to see if this will help.

My questions for you are :

1) Can polycystic ovarian syndrome causes cysts outside of the ovary like on the areas stated here?

2) Is PCOS also associated with scalp itching ?

Any insights into this could be helpful as it is severely affecting all and every part of my life!!!!!

ANSWER

Thanks for the question. I can understand how difficult many of these issues are so I’m glad you’ve submitted this question.

I’d like to discuss several important points in the question you ask and the information you have submitted.

Before we do go further, I’d like to point out that the ideal way to diagnose hair loss is using what I termed the ”Diagnostic S.E.T.” I refer to these as the diagnostic “set” because theses 3 aspects all go together. These 3 items include:

1) the patient’s story

2) the findings uncovered during the process of the scalp examination including trichoscopy

3) the results of relevant blood tests. 

The first letter of each of the three words 1) story, 2) examination and 3) tests spell out the word “S.E.T.” - again a helpful reminder of how the information obtained from reviewing each of these 3 aspects helps solidify a proper diagnosis.

There are several important issues in your scenario. The first key question here in your case is what exactly is the reason for your scalp symptoms and hair loss. The only way I can really confidently determine that is with an up close examination. The second important issue is whether you had a systemic issue (full body issue) to explain the lumps. The most important to consider with your doctors is a conndition called hidradenitis suppurativa.

Let’s go further into your story.

Your Scalp Issues

I can’t say exactly what you have without examining your scalp myself (or at very least seeing photos). It does seem that there is a new issue going on on the scalp that is very different from androgenetic alopecia that you were diagnosed with in the past. I would encourage you to see a dermatologist as soon as you can for an up close examination. Common issues like seborrheic dermatitis and psoriasis and contact dermatitis need to be considered. These can cause itching and scaling. However, other issues also need to be thoroughly evaluated - including various types of scarring alopecia.

Many of these conditions can be diagnosed with a proper examination and trichoscopy. If there is any remaining doubt, a scalp biopsy can be considered. Blood tests are always needed for anyone with shedding including thyroid studies, iron studies (ferritin), CBC. Issues like thyroid diseases or low iron can give increased hair shedding but would not give the intense itching you described. That would be caused would be something else.

Your Lumps

I would also urge you to bring up the issue of the lumps you have in the armpits, thighs, private area and breasts to your dermatologist. There could be a few reasons for this but a condition called hidradenitis suppurativa needs some careful consideration by your doctors. There are other issues that cause lumps too although with your story the diagnosis of hidradenitis suppurativa needs prompt consideration before moving on to other diagnoses.

Hidradenitis suppurativa (HS)

Hidradenitis suppurativa (HS) was once considered rare. We know now that it’s not rare and in fact up to 1-4 % of the population an be affected when mild cases are taken into consideration. HS is a dermatological condition that is associated with painful draining lumps in the underarm area (axillae), groin area and buttocks and under the breast. The lay public often refers to such lumps as “boils” - and patients affected by hidradenitis often describe their disease as one of multiple draining boils in the armpits, groin and buttocks regions. The condition can be emotionally and physically disabling.

Hidradenitis suppurativa is thought to be a disease of hair follicles. It has been proposed that there is some initially plugging of follicles that then leads to the eventual rupture of these follicles. Better and better treatment options have arisen in the last decade.

Hair Loss Conditions Associated with Hidradenitis Suppurativa

Not all patients with HS have hair loss. But when they do have hair loss, a variety of reasons need to be considered. Some of the reasons are unrelated to the HS and some are related to th HS. Patients with HS seem to have an increased risk for psoriasis, alopecia areata, Telogen effluvium, dissecting cellulitis and lichen planopilaris. Of course, patients with HS can have hair loss conditions that anyone can get.

See Prior Article “Risk of Alopecia Areata and Lichen Planopilaris Increased in Hidradenitis Suppurativa”

I am not completely sure if you have HS - as that would require a proper examination. However, as I reflect on your question, it’s important to consider issues like psoriasis, lichen planopilaris and dissecting cellulitis as being causes of your hair loss. . These can cause redness, and itching. Alopecia areata does not cause this kind of itching but if you had alopecia aerate with seborrheic dermatitis or alopecia areata with psoriasis it certainly could. Fortunately, a proper examination by your dermatologist can usually distinguish between these issues. If not, a biopsy is going to be key.

Systemic Issues Associated with Hidradenitis Suppurativa

There are several systemic (internal) diseases that occur more frequently among patients with a diagnosis of hidradenitis suppurativa. PCOS is one of them. Psoriasis is another one. Prediabetes (and diabetes) is another and depression is another. I think it’s really important that you review your health issues again with your dermatologists and endocrinologist.

When I teach doctors about Hidradenitis Suppurativa in the clinic, I really want them to remember all the conditions that patients with HS can develop. I not only want them to remember them - but I want them to ask the patient about them. There are many issues to discuss. The memory tool “PIMPLES” helps medical practitioners remember many of the key issues to ask about. The list does not include all the associatioss - but does include the key ones.

Many Hidradenitis Associations Have Been Well Studied

A number of good studies have been done to date which allow us to understand the strength of the various associations that can occur in patients with HS. These are outlined in the table below. PCOS is increased two fold and metabolic syndrome and depression are increased about 2-3 fold in patients with HS. If you do end up being diagnosed with HS, you will want to review these associations with your doctors.

Summary

Thank you again for your excellent question. Hidradenitis suppurativa affects so many people and my hope is that this answer will provide information and open up dialogue between you and your physicians. The cysts you are experiencing are different than the cysts in the ovary. A proper evaluation can confirm if these lumps are the cyst-like eruptions seen in hidradenitis. The HS issues could be separate form the hair loss or could be related. A biopsy is going to be helpful if there is any doubt as to what’s causing your scalp issues.

Good luck & thank you.

Reference

Andersen et al. Psoriasis as a comorbidity of hidradenitis suppurativa. Int J Dermatol . 2020 Feb;59(2):216-220.

Dessinioti C, Katsambas A, Antoniou C. Hidradenitis suppurrativa (acne inversa) as a systemic disease. Clin Dermatol. 2014;32(3):397-408.

Fauconier M et al. Association between hidradenitis suppurativa and spondyloarthritis. Joint Bone Spine. 2018 Oct;85(5):593-597.

Gonzalez- Vellanueva et al. Hidradenitis Suppurativa is Associated with Non-alcoholic Fatty Liver Disease: A Cross-sectional Study. Acta Derm Venereol. 2020 Aug 18;100(15):adv00239.

Horissian M et al. Increased risk of alopecia areata for people with hidradenitis suppurativa in a cross-sectional study. J Am Acad Dermatol 2019

Patel KR et al. Association between hidradenitis suppurativa, depression, anxiety, and suicidality: A systematic review and meta-analysis. J Am Acad Dermatol. 2020 Sep;83(3):737-744.

Pescitelli et al. Hidradenitis suppurativa and associated diseases.G Ital Dermatol Venereol.. 2018 Jun;153(3 Suppl 2):8-17.

Phan et al. Hidradenitis Suppurativa and Thyroid Disease: Systematic Review and Meta-Analysis. J Cutan Med Surg . Jan/Feb 2020;24(1):23-27.

Phan et al. Hidradenitis suppurativa and polycystic ovarian syndrome: Systematic review and meta-analysis. Australas J Dermatol. 2020 Feb;61(1):e28-e33.

Phan et al. Prevalence of inflammatory bowel disease (IBD) in hidradenitis suppurativa (HS): systematic review and adjusted meta-analysis.Int J Dermatol. 2020 Feb;59(2):221-228.

Rodriguez-Zunga et al. Association Between Hidradenitis Suppurativa and Metabolic Syndrome: A Systematic Review and Meta-analysis. Actas Dermosifiliogr . 2019 May;110(4):279-288.

Tannenbaum et al. Association Between Hidradenitis Suppurativa and Lymphoma. JAMA Dermatol . 2019 May 1;155(5):624-625.

Thanh-Lan Bui et al. Hidradenitis suppurativa and diabetes mellitus: A systematic review and meta-analysisJ Am Acad Dermatol. 2018 Feb;78(2):395-402.

Vazquez BG, Alikhan A, Weaver AL, Wetter DA, Davis MD. Incidence of hidradenitis suppurativa and associated factors: a population-based study of Olmsted County, Minnesota. J Invest Dermatol. 2013;133(1):97-103.