The Risk of Lichen Planopilaris in Patients with Oral Lichen Planus

What is my risk of lichen planopilaris if I have oral lichen planus?

I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in oral lichen planus.

Question

I have oral lichen planus and I’m wondering what my risk of LPP is. Am I likely to develop LPP in the future? I’m feeling terrified about the whole thing actually.

Answer

Thanks for the question.

The short answer is that you probably won’t develop lichen planopilaris. The risk is not zero that you’ll develop LPP - but it’s really really low. Actually, it’s really really really low. I hope you get the point.

Oral lichen planus is a condition that develops in the 30s and 40s. Women are slightly more affected than males. F:M ratio of 1.4 to 1. Oral lichen planus affects about 1-2 % of the population. There are many different forms of oral lichan planus inlcuding variants such as the reticular, papular, plaque-like, erosive, atrophic, and bullous variants. The inner sides of the cheeks (buccal mucosa), tongue and gums are the most commonly affected.

In contrast, lichen planopilaris affects about 0.03% fo the population or roughly 1 in every 3000 to 5000 people. Most people with oral lichen planus don’t have lichen planopilaris at the time they are diagnosed with oral lichen planus and most never go on to develop it! So if you forced me to bet, I would bet you will not develop lichen planopilaris. The odds are dramatically stacked in my favour.

Most people with oral lichen planus never develop LPP. On the contrary, the risk of a person diagnosed with lichen planopilaris developing oral lichen planus is probably 1-2 %. This number is probably similar to the general population risk of 1-2 % or possibly a very slight amount higher. Good studies have not been done to really convincingly know if patients with LPP have a higher risk of oral lichen planus than the general population or not. It’s possible they do but large studies that generate good data just haven’t been done.

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.

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.

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.

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

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.

What is normal shedding? A Closer Look at SEVEN Key Points.

Is my shedding normal?

I’ve selected this question below for this week’s question of the week. It allows us to discuss some of the finer aspects of shedding and why 7 main considerations matter when it comes to evaluating shedding:

Here is the question….

QUESTION

I have been keeping track of my shed hairs as closely as possible for 70 days.  My 30 day moving average is a steady 40 hairs per day and my 5 day moving average ranges from 38 to 42 or so.  However, my daily shed is unstable and can range from 20 to 60 with periodic days of 70.  The 60 and especially the 70 hairs a day concern me. Is it normal for your daily shed to fluctuate this much even though your averages are stable?
I am a 37 year old female.

ANSWER

Thanks for the question. There’s a lot to discuss with your question, so let’s get to it!

Before we 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 and

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’d like to know a lot more about this story ideally but of course the magic of the “question of the week” is that I tackle questions with limited information. We’ll review 7 key questions in a moment. Other questions may also be helpful. I’d like to know what blood tests were done in your case and what the results were. I’d like to know if your menstrual cycles are now regular. I’d like to know if the person asking the question has any medical issues or takes any medications. I’d like to know about stress levels? I’d like to know her family history of hair loss. I’d like to know if the patient has lost any brows or lashes. I’d like to know if her weight has been stable? I’d like to know if the density is the same as 6 months ago or actually worse? I’d like to know if the patient has any headaches, joint pains, skin rashes, dry eyes, dry mouth, thirst, abdominal pain, fatigue, changes in libido, or ulcers the mouth. All these things matter in fully answering these questions.

With that behind us, let's return to our question of the week again!

With the information given in the question submitted, one can not get to the diagnosis. That requires a more full review of your story from A to Z …. and it requires examination of the scalp or at least photos. But let’s explore how we get to the answer.

It’s possible that the shedding here is just a variation of normal. We need to keep that in mind. Many people with your story have normal shedding. If you feel your hair density at age 37 is the same as age 25 and if you feel that your shedding rates are pretty similar now to what they were like at age 25, then it’s likely this is a variation of normal ! If not, then more work is needed for you and your doctors to get to the answer as to whether your shedding is normal or not. Hair loss conditions such as androgenetic alopecia and telogen effluvium are very much a possibility too. Conditions such as chronic telogen effluvium, alopecia areata incognito and scarring alopecia are possible with anyone with the story given in your submission, but the chances of these are pretty low overall. Statistically speaking, most likely a person with your story has either a normal variation or has androgenetic alopecia or has telogen effluvium or has BOTH androgenetic alopecia and telogen effluvium. An astute hair specialist can help you solve the mystery once they gather from you more information, examine your scalp and review some key blood tests with you.

If you really want to understand more about your shedding and what it means, you may wish to review things in detail with your dermatologist. He or she might order a 5 day modified hair wash test. This test takes time and patience to perform yourself at home, but it gives a wonderful amount of information. You can read more about it in the link above. A scalp biopsy is not advised in most cases of someone asking about shedding because the diagnosis can be determined by using the principles discussed above (the SET principles).

As well, as you think about your own shedding, you and your hair specialists can refer to the helpful table below.
Let’s take a look at this table and let’s review some key things we can learn from it.

1. First - Normal shedding ranges from 20-80 hairs per day. Of course, if once shampoos every 2 days then that means the number is 40-160. If every 3 days then up to several hundreds hairs may be quite normal to be lost in the shampoo day. We lose more hair on the days we shampoo than on the days we don’t shampoo. It’s true that some lose up to 100 hairs per day but the reality is that if you average if out over a long time, it works out to under 100 hairs for most. This is the daily rate assuming one shampoos every day. If a person shampoos once per week, then they may lose 500 hairs easily that day without me even being concerned. shedding can vary across the menstrual cycle - especially after ovulation and in the days leading up to one’s period. This is normal. Other patterns are also possible.

2. Second - shedding can occur in other hair loss conditions and that rate of shedding can range from fairly normal to quite profound. Some individuals with telogen effluvium shed a little bit more than normal. However, some with TE shed massive amounts of hair. Generally speaking the rate of daily hair shedding in androgenetic alopecia is mild - but it must never ever be forgotten that AGA is one of the most common causes of slightly increased shedding in women with hair loss. Far too often we jump to the conclusion that a person with shedding has a diagnosis of telogen effluvium - nothing could be further from the reality. AGA must be on that list for women.

3. Third - the lengths of the hairs that are shed gives helpful information. If there are a few short hairs, one can’t conclude anything all that much. Everyone loses some short hairs and some long hairs - but mostly it’s long hairs that get shed. But if 20 %, 30 % or 40 % of the hairs that are being shed from the scalp are short less than 3 cm hairs, we need to at least start thinking about a diagnosis of androgenetic alopecia. A modified hair wash test can help quantitate this.

4. Fourth - the types of hairs that are being lost is helpful. We’ve talked about short hairs and long hairs in the section above. But long hairs can be telogen hairs, broken hairs and anagen hairs. If anagen hairs are being lost that look pretty normal anagen hairs, then scarring alopecia needs to be considered. If the anagen hairs are a bit “strange looking” then this may be a dystrophic anagen hair that one is seeing and a diagnosis of alopecia areata or scarring alopecia need to be reviewed. Finally, long hairs can be broken hairs. If broken hairs are what’s coming out of the scalp then alopecia areata, scarring alopecia needs to be considered - as does other entities like trichotillomania and chemotherapy induced loss and over use of heat or chemical styling practices. Of course, one usually knows if chemotherapy induced loss is a possibility because the patient will tell you if they have recently received chemotherapy treatment for cancer or not.

5. Fifth- the patient with shedding needs to figure out if they have hair loss all over or whether it’s occurring form one area more than others. If the patient feels that the back is much much less affected than the front of the scalp, the chances go up that the patient has androgenetic alopecia (AGA) as the cause of at least one of their diagnoses. Of course, they might still have TE and they might even have a scarring alopecia - but if there is a preferential reduction in density from one main area of the scalp that the person can point to with one finger - we need to consider the possibility of AGA.

6. Six - scalp symptoms can occur in any hair loss condition, but if they are profound and disabling and interfere with life then one needs to consider a scarring alopecia as the cause of shedding. Patients with AGA can have a little bit of itching. Patients with TE can have a little bit of itching. But massive 10 out of 10 itching, burning and pain is not a feature of AGA or TE. Conditions that give marked symptoms - that prompt people to put ice bags on their scalps - include scarring alopecias, allergic contact dermatitis, and scalp burns. Others exist too but you can see that AGA and TE are not part of this list.

7. Finally, the loss of other body hair can sometimes give clues. AGA is not associated with loss of eyebrows or eyelashes or body hair. Of course, if a patient says to me “oh, I do have eyebrow loss, come to think of it” this does not mean that they can’t have AGA. Eyebrow loss is common with age and so the simple finding of eyebrow loss does not mean that we have confirmed that the patient can’t have AGA . Not at all. It’s possible the patient has eyebrow loss as part of aging or over styling and now develops AGA too. But rapid loss of eyebrows, eyelashes and body hairs often points to an immune based reaction against hair follicles (with alopecia areata and frontal fibrosing alopecia being most common).

   SUMMARY

   I hope this helps. If you want to explore your shedding more, be sure to review with a hair specialist and pursue it methodically. You can look at the sizes of hairs being lost. You can measure the density on various areas of the scalp to determine if one area is thinner in density than another. You can review your symptoms. Together you can get a sense of whether your shedding is within the realm of normal or whether it is a reflection on an underlying scalp issue like AGA, TE or something else. If you feel that you have the same amount of hair on your head as age 27 and 17, then you are most likely dealing with the normal variations of shedding patterns. That’s really the most important question here.
   
   

Frontal Fibrosing Alopecia: How soon does treatment take effect? How soon for results?

QUESTION

I was just diagnosed with frontal fibrosing alopecia and have just started treatment. How long will it take for me to see changes?

Answer

This is a great question. I answer this question for patients by first asking them if they are actually asking me “How long does it take to know if the new treatment is working?”

Clarifying this question is very important because patients who undertake a successful treatment plan may not notice ANY changes in their hair at all - which actually means the treatment is working. (This may seem obvious once stated but not always beforehand). Sometimes, a successful treatment will help regrow some hair and sometimes a successful treatment will simply help stop further loss (without regrowth). It’s really important that patients understand that both are potentially good signs.

There are two types of positive changes we look for when evaluating the success of treatment - one type is the “immediate” changes and the second is the “longer term” changes.

The immediate changes we look for after starting a treatment include reduction in symptoms (such as reduction in scalp itching, burning or tenderness) as well as reduction in scalp redness or the amount of scale. Some patients with scarring alopecia, especially those with frontal fibrosing alopecia, don’t always have any scalp symptoms to begin with so monitoring symptoms is not useful for this particular subgroup of patients. Even if the patient does not have symptoms, many do have redness or scaling and this parameter can be reevaluated at various intervals after treatment is started.

These so called “immediate changes” can be seen within a few days (ie rapid reduction in symptoms with some treatments) to a few months (ie reduction in scalp redness and scale within a few weeks of starting a treatment).

The ultimate test and most important test of how well treatment is working has nothing to do with symptoms and has nothing to do with what the scalp looks like - it simply has to do with what a photograph shows. However, to actually get a good sense of changes in  actual hair regrowth growth can take 6-12 months depending on how fast the FFA was moving originally before the treatment was started.

A patient who comes in for a 3-4 month visit and says to me “my scalp feels so much better” may or may not be enroute to better controlling their scarring alopecia. I share their enthusiasm but must advise them that we won’t fully know for 6-12 more months if we are truly winning this fight and successfully stopping the scarring alopecia.

Hair loss of the beard: What are the considerations?

Question

I have had beard alopecia areata/alopecia barbae since the age of 21, I am now 33. It began with one small bald patch under the chin and later in this period either simultaneously or after the bald batch grew back (which was within say the first couple of years) developed numerous very small bald patches throughout the entire beard (which on the cheeks appear slightly jagged) however are barely noticeable throughout. One bald patch larger than these very small patches developed on one cheek say 5 years ago and remains to this day. In summary, the condition has never dissipated however has remained static in its behaviour for a number of years to the present day.

My questions are as follows.

1. What is the likelihood of the condition progressing to other hair bearing areas? (I am aware of the study you quote at https://donovanmedical.com/hair-blog/beard-alopecia however this only followed up with patients after 12 months)

2. In the event that the condition did not progress to other hair bearing areas would hair transplantation surgery on the scalp (I have had male pattern hair loss since 2015/2016 and have been advised that it would be not until around age 35 when surgery could sensibly be considered - using FDA approved medications have only slowed down the condition rather than halted, or to any extent, caused its reverse) increase the risk of the condition (alopecia barbae) progressing to other hair bearing areas, especially the scalp?

Answer

The key here is …. what exactly is your diagnosis? It may or may not be alopecia areata and without actually seeing your scalp and beard up close myself, it would be a mistake to assume that it is. There are many mimickers of alopecia areata that need to be ruled out here - especially autoimmune cicatricial alopecia. If the areas are relatively unchanged for an extended period of time, the chances this is alopecia areata goes down.

Of course alopecia areata is on the list (and quite high up on the list of possibilities), but true classic alopecia areata of the beard does not stay unchanged over an extended period of time. You might consider seeing a dermatologist for expert review. A full review of your history and review of your hair loss pattern via dermoscopy is needed. A biopsy might be needed as well.

As far as chances of progression to other areas, it really depends on the precise diagnosis. If the disease has an immune basis, there is most certainly a chance of progression to the scalp. Hair transplantation of the scalp could be associated with an increased risk of the disease developing in the scalp - but it depends entirely on the precise diagnosis. For patients with isolated beard alopecia, my feeling is that there is about a 65-70 % risk over 10 years of alopecia areata being identified in the scalp. This too may be only one patch or may be more severe- but the presence of beard AA sets the stage for scalp AA to develop. Having a transplant is a small risk but only a small one. 2 % of the world will develop alopecia areata and so one generally expects 2 % of hair transplant patients to develop alopecia areata in their lifetimes. In 60-70 % of patients who do develop alopecia areata of the scalp in the years following their hair transplant regrowth happens quite readily with conventional treatments. Some do, however, have a more refractory course.

If the cause of the beard alopecia is actually a variant of immune based primary scarring alopecia (i.e. lichen planopilaris, folliculitis decalvans, lupus) or secondary scarring alopecias (sarcoid, scarring folliculitis etc), a hair transplant carries the risk of actually triggering scarring alopecia on the scalp. The concerns about proceeding with hair transplantation become magnified if the diagnosis actually turns out to be scarring alopecia.

All in all, alopecia areata is still at the top of the list here in the question that has been posed - but there are features of the story that are a bit unusual. You should be absolutely certain before moving on that this is alopecia areata and not something else. There is a risk over the next 10 years of alopecia areata developing on the scalp but in a majority of cases conventional treatments can help maintain the density. It largely comes down to understanding the risks and benefits (so called risk benefit ratio) …. and making an educated decision together with one’s dermatologist and surgeon. Making sure one has as much information as possible before moving forward with surgery is key.

Frontal Hairine Loss in a 48 Year old Black Female

Question.

I'm a black female 48 years old with what I believe is CCCA. I started loosing my hairline in 2014, however in an 18 month period I lost my entire hairline. For the last 14 months I've been treating my scalp with natural oils/home remedies. The hair loss have stopped. I think my condition could be inactive. If the e disease is in fact inactive, without any medical treatment, can my hair grow back on its own or will I need a hair transplant?

Answer

Thanks for the great question. As a physician who sees a lot of women with CCCA, your brief story shouts out to me one main message: this may or may not be CCCA that you have and if it is CCCA, one or more other hair loss conditions might be present too.

Let me begin. Central centrifugal cicatricial alopecia (CCCA) usually starts in the middle of the scalp or in the crown. CCCA does not usually start in the front like you described. However several conditions can affect the frontal hairline just like you described including traction alopecia, cicatricial marginal alopecia and frontal fibrosing alopecia. What’s a bit unexpected from your story is the complete loss of the hairline that you described. That certainly favours a diagnosis of frontal fibrosing alopecia over traction alopecia but of course I would need to see your scalp myself to answer that. An entity called cicatricial marginal alopecia is also on the list.

Your story is not a typical story of CCCA although of course you could have CCCA back in the mid-scalp too. Many black women with hair loss in the frontal hairline also have some degree of CCCA too.

What you really need now is a diagnosis. An expert dermatologist who treats a lot of patients with hair loss might be able to make the diagnosis without a biopsy but if you are thinking of hair transplants down the road a biopsy is going to be helpful to secure the diagnosis and also determine for you (and your doctors) just how active or inactive the disease truly is right now. My advice to anyone with a story like yours would be to consider a sample from the frontal hairline area and also from the crown. Remember that a biopsy always needs to have a hair in it so don’t biopsy any bare area as that is useless.

I’m suspicious about your diagnosis of CCCA but a few things about your story are more definite. First, it’s unlikely you’ll get spontaneous growth if you haven’t had growth since 2014. Depending on the exact and precise diagnosis, you still could get a bit of regrowth with treatment but likely only a bit. Second, you are probably not a candidate for surgery yet. Whether you become a candidate depends somewhat in the diagnosis but also on the activity level of your primary disease. I like to have patients take photos once they feel their disease is quiet... and if there is absolutely no change in hair loss after two years of photography then a hair transplant might be possible. If you feel your scalp has now become quiet, take a picture today and plan to compare that same picture in 2 years. If the two pictures look 100 % identical you might be a candidate for surgery. The longer answer as to whether you are a candidate for surgery actually depends on several factors.

In summary, your story suggests a diagnosis of frontal fibrosing alopecia or traction alopecia much more than it does CCCA. A biopsy could be extremely important for you and your treating physicians right now.

Hair Loss from Relaxers

Question

Can my scalp be treated after severe damage from a hair relaxer?

Answer

Thanks for the great question. This is such an important question and also a very common one. There is a lot to discuss. As you’ll see, the answer to your question is ‘maybe.’ Some patients with hair loss form relaxers will grow back their hair. Some patients do not.

Let’s begin.

When a patient says to me they have hair loss from a relaxer, it’s important to keep in mind that there is not one type of hair loss that they might have. In fact, they might have one or more of many types of hair loss, including hair breakage, inflammatory scarring alopecias, hair loss from chronic inflammation, traction alopecia, telogen effluvium or androgenetic alopecia. Some patients just have one type of hair loss. Others have two or three.

Let’s take a look.

1. Hair breakage (Trichorrhexis nodosa)

Both chemical and heat relaxing of hair can cause breakage of the hair. The hairs simply break off because of the damage to the delicate strand. The heat or chemicals cause “micro tears” in the hair shaft which we call “trichorrhexis nodosa.”

The photo below shows a picture of a hair fibre that has such a tear.

Trichorrhexis nodosa of a hair fiber. This can occur from many agents including heat and chemicals used to relax hair.

If trichorhexis nodosa is the only reason for the hair loss, the hair will grow back. The damaged sections may need to be cut off, but the long term prognosis is good. It may take 6-9 months before hair returns back to the way it once was but it will return. Unfortunately, trichorrhexis nodosa as the ONLY and sole reason for a person’s hair loss from relaxers is not common. Ofter there is another reason present as well, and these are discussed below.

2. Telogen Effluvium

Many patients who come to see me with concern about their hair after using a relaxer also have a a diagnosis of telogen effluvium or “TE.” Telogen effluvium is a type of hair loss that occurs when the body feels some type of shock. This can occur from low iron (low ferritin), thyroid problems, anemias, crash diets, weight loss, stress, medications, and illness. Some of these issues such as anemia and low iron levels may make the hair slightly weaker and slightly more susceptible to hair damage. These issues must be addressed fully. For this reason, I always order blood tests for ferritin, 25 hydroxy-vitamin D, TSH, CBC, ANA in all patients who come to see me with concerns about hair loss from a relaxer. Other causes must be fully evaluated.

3. Traction alopecia.

Traction alopecia is a type of hair loss that occurs from the chronic pulling of hair. Patients who use relaxers may be more susceptible to traction alopecia because their hair is subjected to many pulling forces during relaxers and the hair fibers may be weaker. Traction alopecia can occur anywhere on the scalp. The frontal regions near the temple are often a common site of traction.

Treatment for traction alopecia involves stopping the pulling forces that caused the traction in the first place. If traction alopecia is diagnosed and pulling is stopped immediately (within a few months of the new hair care practice), hair might grow back. However, if traction alopecia has been present many months, the hair may not fully return. Long standing traction alopecia is permanent and may even continue to progress once the hair pulling is stopped.

Traction alopecia of the frontal hairline.

4. Scarring Alopecia and Chronic Inflammation .

It’s a little known fact but chronic use of relaxers, especially chemical relaxers, can create scalp inflammation. It may not be a type of inflammation that can be seen on the surface but rather a type of inflammation that is occurring deep under the scalp. In some people using relaxers (but certainly not all people), this chronic inflammation triggers the body to also create scar tissue beneath the scalp. The exact mechanism is not clear but micro injury to the skin creates microinflammation and chronic microinflamation may induce scar tissue to form.

This pattern of hair loss from relaxers has been most carefully studied in women with afro-textured hair but likely applies to all hair types. Chronic use of relaxers in women with afro-textured hair may be linked to the development of several types of hair loss including traction alopecia and central centrifugal cicatricial alopecia (CCCA). CCCA often affects the central scalp first. The diagnosis must be caught as early as possible to prevent progress and prevent irreversible loss of hair. Too often women with CCCA are told that their hair loss is simply from a relaxer and it will grow back. CCCA is a cause of permanent hair loss. If there is any doubt, a punch biopsy should be considered to properly evaluate for scarring alopecia. Treatment with agents such as topical steroids, steroid injections, and doxycycline can help stop the disease. Hair growth does not usually occur. A photo of a woman with CCCA is shown below.

Central centrifugal cicatricial alopecia (CCCA) in a woman initially misdiagnosed as having temporary hair loss from a relaxer. The correct diagnosis for this patient was CCCA which causes permanent hair loss.

Summary and Conclusion

Thanks again for the great question. Let’s now return to the original question regarding whether or not your scalp can be treated. As we’ve seen above, it really comes down the the exact cause of the hair loss. If the relaxer caused trichorrhexis nodosa, the damaged hair simply needs to be trimmed and hair density will eventually come back. If however, the relaxers have caused traction alopecia, it may or may not come back even if the relaxers are stopped. If the cause is CCCA, the hair is less likely to return and aggressive treatment with various anti-inflammatory medications are needed to stop the inflammation. If there is a telogen effluvium (from low iron for example) that predisposed to some fragility and hair loss, there could be some improvement with iron supplementation and stopping the relaxers as well.

Be sure to see a dermatologists as relaxer related hair loss can be complex sometimes. Blood tests for ferritin, 25 hydroxy-vitamin D, TSH, CBC, ANA might be considered and if any doubt exists, a biopsy might be considered to rule out scarring alopecia.

Seborrheic Dermatitis vs Lichen Planopilaris: Which do I have?

QUESTION

QUESTION:

My doctors can’t decide if I have seborrheic dermatitis or lichen planopilaris. My scalp does feel less itchy and becomes less red with anti dandruff shampoos. However, it also becomes less red and itchy with topical steroids. Overall my shedding has improved after 4 weeks of treatment. Does this information suggest one diagnosis over the other?


ANSWER:

Thanks for the great question. The short answer is that the information provided here does not actually suggest one diagnosis over another. You may have scarring alopecia and you may have seborrheic dermatitis. The key point I would like to make is that you may have both! Up to 50 % of patients with lichen planopilaris have seborrheic dermatitis too. A scalp biopsy can fully answer your question.

Let’s take a closer look at both of these conditions and we’ll see why some patients with lichen planopilaris will benefit from anti-dandruff shampoos and we’ll see why some patients with seborrheic dermatitis benefit from topical steroids (the same ones used to treat lichen planopilaris.)

SEBORRHEIC DERMATITIS
First, seborrheic dermatitis is closely related to dandruff. The exact cause is still being worked out but yeast such as Malassezia may have an important role. Patients with seborrheic dermatitis have many similar (and sometimes identical) symptoms to patients with lichen planopilaris. They have a red, itchy scalp! Seborrheic dermatitis however does not cause scarring for most people and usually only gives minor amounts of hair shedding. (Everything in medicine has exception and seborrheic dermatitis may cause scarring in some cases and may give excessive hair shedding when severe - see previous articles below).

DOES SEBORRHEIC DERMATITIS CAUSE SCARRING?

CAN SEBORRHEIC DERMATITIS TRIGGER SHEDDING?

Seborrheic dermatitis is an inflammatory condition which means there is inflammation in the scalp. Although the standard first line treatment for seborrheic dermatitis is topical anti-dandruff shampoos, treatment with anti-inflammatory agents like topical steroids can help reduce the inflammation which in turn reduces redness and itching. Many patients with seborrheic dermatitis feels better with use of both antidandruff shampoos and topical steroids. In fact, studies have shown that adding topical steroids to a patient’s seborrheic dermatitis treatment plan can greatly help.

To come back to your question for a moment, we would expect seborrheic dermatitis to improve with dandruff shampoos and topical steroids. However, fact that your scalp did improve does not rule out a scarring alopecia as we’ll see next.

LICHEN PLANOPILARIS
Lichen planopilaris is a scarring alopecia that causes patients to experience itching and sometimes burning and tenderness in the scalp. The scalp is typically red. An important difference between lichen planopilaris and seborrheic dermatitis is that lichen planopilaris always associated with scarring. Biopsies of LPP show rings of scar tissue around hair follicles in early stages (called concentric perifollicular fibrosis) and deposits of large bits of scar tissue in the scalp in advanced stages.

Topical steroids are one of many agents used to treat LPP. They help reduce redness and scaling and help the patient feel better too with less itching, burning or pain.

Seborrheic Dermatitis in Patients with LPP: Is is More Common than We Realize?

Seborrheic dermatitis is present in a very large proportion of patients with LPP. In fact, a greater proportion of patients with LPP have seborrheic dermatitis compared to people in the general population. (About 5% of people in the general population have seborrheic dermatitis compared to nearly 50% of patients with LPP). On account of seborrheic dermatitis being so common in LPP, it makes sense that many people with LPP will feel better and gain some relief with use of antidandruff shampoos! The fact that a patient with LPP reports improvement with antidandruff shampoos does not rule out a scarring alopecia. It simply means they may have seborrheic dermatitis too!

Cleveland Clinic 2016 Study of Seborrheic Dermatitis in LPP

In 2016, Berfeld’s group at the Cleveland clinic studied the incidence of seborrheic dermatitis in patients with lichen planopilaris. This study is important to understand and relevant to the above discussion. It was one of the few studies to date which really documented the increased incidence of seborrheic dermatitis in patients with LPP.

The study I am referring to was a retrospective review of 246 patients seen over the period 2004-2015. Interestingly seborrheic dermatitis (SD) was present in 46.2 % of LPP cases. In 27.4 % of cases the SD was found outside the area affected by the LPP. On average the SD was diagnosed 7.8 months prior to the LPP diagnosis. Having SD seemed to delay an actual diagnosis of LPP. Patients with both SD and LPP diagnosis (LPP-SD) received their diagnosis with significantly more delay than patients with LPP who did not have SD (ie LPP). For example, patients with LPP-SD received their diagnose in 7.6 months on average comapred to 2.3 months for LPP alone.

Whether SD actually plays a role in the scarring process as well remains to be determined. It is interesting that there was a greater prevalence of late stage scarring alopecia in ptient with LPP-SD than LPP alone (41.5 % vs 15.7%). Patients with LPP-SD had greater rates of hyperandrogenism compared to patients with LPP alone.

SUMMARY AND CONCLUSION

Thanks again for the great question. One can’t determine if you are more likely to have SD or LPP from the information provided. It would be entirely within the realm of expected for a patient with LPP to improve with topical antidandruff agents since many have seborrheic dermatitis present as well. Likewise, it would be expected that a patient with seborrheic dermatitis would improve with topical steroids because this is an inflammatory disease just like LPP.

A biopsy can help distinguish if lichen planopilaris is truly present or not.

Reference
Ratnaparkhi et al. Association of lichen planopilaris with seborrheic dermatitis l: A retrospective case-control study. Poster 3727. JAAD May 2016.


https://www.aad.org/eposters/view/Meeting.aspx?id=43&c=2

How long does it take to know if scarring alopecia treatments are working?T

QUESTION

QUESTION: I was diagnosed with lichen planopilaris. My dermatologist put me on topical steroids (betamethasone diproprionate) and doxycycline (100 mg daily). How long does this treatment take before I know if I am benefiting?

ANSWER

Thanks for the question. The real answer depends on a few factors as you'll see below. It could be as early as a few days before your get a sense if you are on track or several months. Let me explain. 

As you've probably come to know from your own physicians, lichen planopilaris (LPP) is a type of scarring alopecia that causes permanent hair loss.  We don't typically expect to see hair regrowth to any significant degree (unless treatment is undertaken in the very earliest of stages). The goal of treatment is to stop the disease and prevent it from getting any worse. 

Lichen planopilaris (LPP) is often 'symptomatic', meaning that many patients have itching, burning or pain/tenderness and notice increased amounts of daily shedding.  Some have all four of these of these symptoms and some have two or three. Of course, about one-third or so of patients don't really have much in the way of symptoms and the scalp feels pretty normal to them. They may just notice a bit of increased shedding. 

The reason this concept is important to mention is because patients who do experience scalp symptoms with their LPP will know if a matter of a few days if they are benefiting from topical steroid treatments. Strong steroids like betmethasone dipropionate usually act to relieve symptoms very quickly and can help reduce shedding quite quickly as well. Oral immunomodulating medications like doxycycline take a bit long but also act within a few weeks. So, if a patient with LPP has considerable itching, burning and tenderness and finds that that the betamethasone is helping to relieve symptoms and shedding after a few days - this means the treatment is benefiting.

Now for a bit more involved discussion.

 

Difference between short term vs long term benefits

The "first step" for a patient with LPP who is symptomatic is to reduce their scalp symptoms and shedding. This is what we are watching for. This is what we are hoping for. If a patient has itching that they rate as 7 out of 10, we hope in future apportionments that it reduces to 1 out of 10 or maybe even 0 out of 10.  If they feel they once were losing 100 hairs daily and now feel it's under 50 hairs per day... this too is a good sign. 

What we don't know early on in the course of treatment is whether the reduction in symptoms actually correlates with a cessation of hair loss. In other words, a reduction in symptoms is terrific, but it's really the ability to prove that the hair loss is slowing down or stopping that is the most important thing. This comes with scalp examination and photography. 

Scalp examination and photography prove a treatment is benefiting

If a patient states that his or her itching is greatly improved, but a photograph at the 4-6 month follow up appointment shows that more hair loss has occurred, this means that the treatment is not working at all or not working well enough. If the treatment is not working at all, it needs to be stopped and another treatment started. If the treatment is not working well enough but is still helping to slow the rate of loss down a bit, one might consider continuing that treatment (as it is doing something) and adding a second treatment. Of course, this is a professional judgement, and something we stop treatments that are are only working a bit and bring on board treatments that have potential to stop the disease completely.  

Generally speaking if treatments are not working, a photograph will show more and more loss every 4-6 months. Some patients have very slowly progressing LPP and it will take 1 year to show that further hair loss is occurring. Nevertheless, carefully documented photographs will show whether the disease is progressing or stopping. The importance of photography can't be overemphasized. 

Up close examination of the scalp will also provide helpful signs for patients with LPP and so frequent examination by a dermatologist is important. The presence of redness and scaling in the scalp are all potential signs of disease activity. If the amount of redness or scale improves with treatment, this usually means the treatment is working. While the up close examination is important to judge whether a disease is active or not - the most important of all is the photograph of the scalp.

 

Summary

Thanks again for the great question. I hope this clarifies things.  The real answer is that a patient will truly know in several months if the treatment is truly working by comparing photographs. There are some really helpful things to observe for in the first few weeks and months to give us hints that things are working. This includes a decrease in symptoms and shedding and a decrease in redness and scaling. The most valuable of all is the photograph. 

How often can I have steroid injections?

QUESTION

QUESTION: How often can scalp steroid injections be done? I have alopecia areata and receive injections into the areas of hair loss every 4-6 weeks. Can I get these injections more often? Is my current frequency considered normal or excessive?

ANSWER

Thanks for the question. Let's first review a few things about steroid injections and then circle back to your question.

Steroid injections are used to reduce inflammation and are useful in a variety of hair loss conditions including alopecia areata, lichen planopilaris, frontal fibrosing alopecia, discoid lupus, traction alopecia, central centrifugal cicatricial alopecia and Pseudopelade of Brocq as well as a few others too.

The typical dose injected ranges from 2.5 mg of steroid per mL (ie 2.5 mg triamcinolone acetonide for every 1 mL of saline used) to a maximum of 10 mg per mL. Lower concentrations reduce the chance for “atrophy” (indentations in the scalp) and so many physicians opt for lower concentrations.

Generally speaking, steroid injections are performed as close as every 4 weeks apart. There is no maximum spacing and some patients benefit from injections every 4-6 months and others come into clinic whenever their condition flares.  Injections more often than every 4 weeks are not typical.

 

20 mg every 4 weeks

A limited number of studies suggest that keeping the total dose to no more than 20 mg every 4 weeks has quite a good safety profile. This means a physician can use 8 mL of steroid solution every 4 weeks if they decide to use the 2.5 mg per mL solution. If the physician decides to use a higher concentration such as 5 mg per mL, he or she only has 4 mL available to inject. If one uses 10 mg per mL (which some physicians do), one only has 2 mL.

Some studies have suggested that injecting greater volumes of steroid solution at low concentrations works better than injecting smaller volumes of steroid solution at high concentration. For many patients, I even chose 1.5 or 2 mg per mL solutions and see how it works. Use of a 1.5 mg per mL solutions allows 15 mL of fluid to inject in the scalp (that’s 5 syringes!) ... and this goes alot further than trying to figure out where to inject 2 mL of a 10 mg per mL solution. Clearly, if low concentrations aren’t working, one needs to use higher concentrations at the next visit.

In summary, steroid injections can be performed as close as 4 weeks apart but one is not obligated to continue them at this interval. Limiting the concentration, total dose and frequency of injections helps to reduce side effects. In addition to “atrophy” discussed above, side effects can rarely include fatigue, irregular menstrual cycles in women, blood sugar changes and mood changes. These are not common. Longer term side effects to monitor include osteopenia, cataracts, weight gain and changes in blood pressure. These are quite rare with proper dosing and monitoring.

Reference

Chu TW, et al. Benefit of different concentrations of intralesional triamcinolone acetonide in alopecia areata: An intrasubject pilot study. Randomized controlled trial. J Am Acad Dermatol. 2015.

What causes hair texture changes?

Question

QUESTION: What causes hair texture changes? I used to have very soft and glossy hair. However, now after years of hairless (androgenetic, FFA & LPP) and treatments (injections, topical clobetasol & oral medications) my hair is very dry, dull, almost straw-like. Are these texture changes due to aging, the hair loss conditions or perhaps the treatments? Conditioners do not seem to help. Thank you.

Answer

Thanks for the great question. There are many causes of hair textural changes. In your case specifically, the causes are probably "multi-factorial" rather than a single cause.  Let’s take a look at some of the more common causes of textural changes and how they apply to the question you have raised. 

Consideration 1: Scarring alopecia

Many patients with scarring alopecia notice changes in their hair texture, especially a change to a drier, more brittle and slightly curlier hair texture. As the name suggests, scarring alopecia is associated with the development of scar tissue or ‘fibrosis’ under the scalp. Such fibrosis affects how hairs emerge from the scalp. Hair frequently twist and turn as they emerge from the scalp and sometimes even rotate 180 degrees. We call this twisting and turning ‘pili torti.’ Individuals with pili torti will notice a hair textural change.

Scarring alopecias are universally associated with loss of the oil glands (sebaceous glands) in the scalp. One can not have a scarring alopecia without having a reduction in the oil glands. These oil glands lubricate the hair follicle.  The destruction of sebaceous glands during the process of scarring alopecia contributes in part to the drier texture. 

Scarring alopecia also affects the quality of the hair that is produced. Commonly there is hair breakage on account of the much weaker fibers. 

Consideration 2: Hormonal changes

A variety of hormonal changes can lead to drier, coarser hair.  About 15 % of women are affected by thyroid disease and this a common cause of textural changes. The incidence fo thyroid disease is much more common in the conditions that you mention including lichen planopilaris (LPP) and frontal fibrosing alopecia (FFA) and so thyroid status should always be carefully evaluated in patients with scarring alopecia.

With approaching menopause, the declining estrogen levels and  imbalances in the ratio of androgens to estrogens also results in drier hair. Women who are predisposed to develop androgenetic alopecia may notice that the hair becomes finer and some may notice the texture changes too. About 40 % - 50% of women with frontal fibrosing alopecia (FFA) and lichen planopilaris (LPP) have androgenetic alopecia. 

Consideration 3: Heat and chemicals

A variety of products that are applied to the scalp can lead to the hair becoming drier, and more brittle. Products containing alcohol are frequently a culprit. This includes hairsprays but many other alcohol containing cosmetic products as well. Products such as minoxidil lotion, and topical steroids may contain alcohol-based ingredients which also dry out the hair.

Consideration 4: Inflammatory scalp diseases

A variety of scalp conditions that are associated with inflammation can lead to altered hair texture over time. Conditions such as seborrheic dermatitis and psoriasis can lead to drier duller hair. Many individuals with FFA and LPP have co-existent seborrheic dermatitis and if present, this should be treated. 

Consideration 5: Androgenetic alopecia (AGA)

Androgenetiic alopecia (AGA) is also a cause of hair textural changes. Although we discussed AGA in the context of hormonal changes above (see "Consideration 2"), androgenetic alopecia can also cause textural changes irrespective of any hormonal abnormalities. In fact, 85 % of women with androgenetic alopecia have normal hormone levels. In women, androgenetic alopecia is also known as female pattern hair loss and in men, male pattern balding. 

Women with AGA often notice the hair is finer and some notice the hair becomes curlier. Others notice the hair becomes flatter and less likely to hold it's original shape, curl or wave. 

Consideration 6: Aging

Hair "aging" is a poorly researched area and poorly defined in general.  Age-related changes in hair, independent of the hormonal changes that can occur with age, can also lead to textural changes in the hair. 

Conclusion

There are a variety of reasons for hair textural changes. One can usually determine the cause of the textural changes with a full review of one's story (i.e. the medical history) along with an up close examination of the scalp. Most of the time blood tests are also needed. 

Thanks again for the great question.  

What causes scarring alopecias like FFA and LLP to reactivate?

Question

QUESTION: What causes scarring alopecias like FFA and LLP to reactivate? After a period of approximately 6 months during which my hair loss from FFA & LPP seemed to stabilize and hair density actually improved, the shedding has now significantly increased again. What causes these scarring alopecias to reactivate months, or potentially even years, after a period of being quiet with no measurable hair loss? Thank you.

Answer

Thanks for the question. There are a number of reasons why a scarring alopecia can re-activate after it was once quiet. Here are the top 5 important points of discussion. 

Reason 1: We simply don't know the reason.

Although not the answer one would expect to hear as reason 1, we need to respect that we don't completely understand scarring alopecia in the present day and age. Often, we simply don't know the reason. Scarring alopecias can activate and become quiet for periods on their own. We often attribute the entry into a "quiet (inactive) phase" as proof that some type of treatment we are using is helping but scarring alopecias can become quiet other own. Similarly, we often attribute worsening as an indication that something we are doing is no longer working, or we're doing something 'wrong.' However, scarring alopecias can become active spontaneously for reasons that are not clear.

 

Reason 2: A second hair loss condition has developed.

Whenever there is worsening hair loss, we need to consider that the loss is actually due to another condition, and not the scarring alopecia. Such a condition is often in the form of a 'telogen effluvium," There is an increased incident of iron deficiency, low vitamin D and even thyroid dysfunction among patients with scarring alopecia. For example, a 2014 study from the Cleveland clinic showed that 29 % of patients with LPP develop thyroid dysfunction compared to 9 % of controls. A second study showed that there are also differences in vitamin D status. I've included these references below. 

Levels of vitamin D, TSH, ferritin, zinc should be checked in any patient who experiences a 'flare' following an extended period of quiescences. 

Reason 3: There has been increased life stress.

There's no doubt in my mind that increased life stress can trigger flares in patents with scarring alopecias. It's not clear why and the link seems more relevant for scarring alopecias such as lichen planopilaris (LPP) and frontal fibrosing alopecia (FFA) than many of the other scarring alopecias. Stress can increase a variety of neuromediators and nerve-related hormones in the scalp which impact inflammation.  

Reason 4: There has been injury to the scalp.

It continues to be an area of limited study, by injury can trigger a worsening or 'flare' of a scarring alopecia.  The medical literature documents injuries such as facelifts and hair transplants as triggering scarring alopecias to worsen. However, many types of injuries can cause the disease to reactivate. 

Reason 5: Medications have recently been started or stopped

A scarring alopecia can become active again on account of a) stopping a mediation that was helping, b) starting a medication that was not used before and c) rarely, changing the brand name of a medication that was helping .

If one has recently tapered or reduced a medication within the last one year and is now noticing a worsening of hair loss, they need to consider that the cessation  or reduction of medication could be responsible for the 'flare'. We see that with slow acting medications like hydroxychloroquine. 

Starting a new medication can sometimes trigger shedding. For example, the addition of minoxidil to the scalp in a patient who otherwise had stable disease, can trigger some shedding. Also some medications such as hydroxychoroquine can trigger shedding in some patients. 

Finally, we rarely encounter a situation where a pharmacy changes the brand of the mediation given to the patient. Instead of getting tablets form company X, they are dispensed tablets from company Y. It appears to be the same medication but for some reason a flare occurs. Even more rarely the wrong dose has been prescribed to the patient and they end up receiving less than intended. This of course can cause a flare.

Reason 6: The scarring alopecia has done from "very slightly active" to "slightly active"

To be truly confident a scarring alopecia is inactive, one needs to observe it for two years. After a period of 6 months of observation with a scarring it being "quiet", we can't actually conclude that it was truly inactive.

I often given an analogy of a car moving down the street as an analogy to understand the speed of hair loss. Suppose one's hair loss is moving forward at 6 miles per hour. For the sake of argument, let's say that particular speed is fast enough to see a change in hair density every 6 months. Now let's say the hair loss slows down to a rate of 2 miles per hour. That's really slow. It's not enough to see a change every 6 months but it is just enough to detect a change in density every 1-2 years. If a patient has hair loss moving forward a 2 mies per hour, and they don't see a change after 6 months, they can not conclude it is inactive. Rather there are two possibilities in such a case: either the scarring alopecia is inactive or it is still very slightly active. A clinical examination of the scalp by a dermatologist or time will declare which is correct.  

CONCLUSION

Thanks once again for the great question. When I teach doctors about the reasons for flares in an otherwise stable patient, I frequently use the memory tool "IM WORSE" to help remember the reasons for a flare. This is summarized below. I've also written about the topic in the attached link:

WHY IS MY SCARRING ALOPECIA FLARING AGAIN?

REFERENCE

Atanaskova Mesinkovska N, et al. Association of lichen planopilaris with thyroid disease: a retrospective case-control study. J Am Acad Dermatol. 2014.

Conic RRZ, et al. Vitamin D Status in Scarring and Non-Scarring Alopecia. J Am Acad Dermatol. 2018.

Do I need a scalp biopsy if I have scarring alopecia?

Question:

I have been diagnosed with frontal fibrosing alopecia, which I understand to be a type of scarring alopecia. My dermatologist wants to start me on treatment right away. Do I need a biopsy first?

Answer

Dermatologists have many different views as to whether every patient with potential scarring alopecia needs a scalp biopsy or not. These views fall in three main categories:

1) There are some dermatologists who believe that every single patient with hair loss (scarring or non-scarring) gets a biopsy.  

2) There are some dermatologists who conduct a scalp biopsy in every single patient with scarring alopecia. 

3) There are some dermatologists who perform a biopsy if the diagnosis is not certain and there is even the slightest ambiguity in the diagnosis.

I fall in the third category. My decision on whether a patient needs a biopsy comes during the final steps of a typical patient evaluation. First (step 1), I listen to the patient’s story about their hair loss (we call this a history). Second (step 2), I examine the scalp using a dermatoscope. Third (step 3) I review blood tests. Fourth, I decide whether a biopsy is needed given all the information I have collected during steps 1-3. If the diagnosis is clear and there simply can’t be another diagnosis possible, I don’t do a biopsy.

Here’s an example. Suppose a 56 year old female patient comes to see me. She started losing her eyebrows at age 51. At age 54 she started losing hair along her frontal hairline and it’s receded now about 1⁄2 inch. She’s lost her arm hair, pubic hair and leg hair. Examination shows a scarring alopecia along the frontal hairline. Her blood tests are normal. Based on steps 1-3 I’m confident in the diagnosis of a condition known as frontal fibrosing alopecia.

Will I do a biopsy? No. I will not recommend doing a biopsy in this situation. If the biopsy returns showing scarring alopecia, it’s true that I will have confirmed the diagnosis. Not a bad thing of course. But I will have caused the patient an unnecessary scar. Also, there is always the potential that biopsies (or any trauma) can further activate scarring alopecias, so I’d like to stay away from that.

But suppose the biopsy returns showing something else – such as androgenetic alopecia or alopecia areata. Biopsies are not 100 % accurate so once in a while a scenario like this does occur. In a situation like this, I won’t believe the biopsy results. I’ll simply put the biopsy results aside and move on with discussing treatment. In other words, I’d simply have to explain to the patient that biopsies are not perfect. The reality is that I have caused an unnecessary scar. There may also have been unnecessary expense for getting the biopsy done. There may have even been some pain and discomfort for a few days.

Suppose in the above example, we change things a bit. Suppose the patient is a 56 year old female patient like in the above example. She started losing her eyebrows at age 51. At age 54 she started losing hair along her frontal hairline and it’s receded now about 1⁄2 inch. She’s lost her arm hair, pubic hair and leg hair. She has joint pain in her wrists and ankles, unusual rashes, extreme fatigue and prominent lymph nodes enlarged in her neck. She is troubled by headaches and has had 2 seizures this year that nobody can figure out why. She has dry mouth and dry eyes. Examination shows a scarring alopecia along the frontal hairline. Her blood tests are abnormal with low white cells, abnormal kidney function tests, as elevated liver enzymes. Her ANA is borderline positive at 1:160. When I examine her scalp, I have the impression this is a scarring alopecia – resembling very close frontal fibrosing alopecia.

Here’s a good example of where I will do a scalp biopsy. Even though it seems the patient has frontal fibrosing alopecia, I want to rule out other conditions such as cutaneous lupus, discoid lupus, lymphomas, various infiltrative conditions, including some rare cancers.

You may wish to review these helpful articles (below) I've written in the past. Thanks again for the question. 

Top 25 Frequently Asked Questions about Scarring Alopecia

What topical steroids are safe to use in FFA?

Question:

I was diagnosed with frontal fibrosing alopecia and prescribed a topical steroid by my dermatologist. I've been using it for 5 months. I am wondering if it's too strong because my skin seems thin in the area of the hair loss. What topical steroids are best to use for FFA?

Answer:

Topical steroids can be mildly helpful for some patients with FFA. Generally speaking they are not as effective as steroid injections, and oral medications such as finasteride, doxycycline or hydroxychloroquine. Nevertheless, topical steroids do have a role in the treatment of FFA.

There are many classes of topical steroids and they range from class I to class VII. Class I steroids are the strongest and include agents like clobetsol. Class VII steroids include weak steroids like hydrocortisone.  Clobetasol is up to 600 times strong than  hydrocortisone and so has much more potent anti-inflammatory effects.  There's no doubt about it that stronger steroids suppress inflammation better- but that does not mean that stronger steroids are better, especially for FFA. In FFA, we need to consider side effects  - in particular the thinning of the skin that both the steroids and the disease itself can cause. 

Clobetasol, however, carries a greater risk of side effects including thinning of the skin. Patients with FFA already have thin skin to begin with (on account of their disease). So, one needs to be careful when treating FFA not to thin the skin further. Monitoring is needed and photographs are essential in this regard. 

Generally speaking, when someone with FFA notices thinner skin and blue veins appearing it's typically the disease itself that caused this - not the topical steroid. Nevertheless, to limit the side effects of topical steroids, dermatologists frequently prescribe weaker steroids to use on the frontal hairline for those with FFA. Instead of using clboetasol, steroids like fluocinonide or betamethasone are often used. Rather than using daily, these are frequently used every other day to limit side effects.  In addition, a non-steroid medication like pimecrolimus might be used as well. Pimecrolimus does not cause thinning of the skin but the trade off is they are not quite as consistently effective as the topical steroids. 

If clobetasol is going to be used, that is a decision that the dermatologist and the patient must both review together and be comfortable with. Daily use of clobetasol on the frontal hairline for a prolonged period is probably not a good idea when treating FFA. Some physicians might use it a few times per week or daily for a very short period of time. However, daily use of a strong steroid increases the risk of the patient experiencing further thinning of the skin.  

You may wish to review these helpful articles (below) I've written in the past. Thanks again for the question. 

Topical steroids and FFA

General articles on frontal fibrosing alopecia