Chronic shedding after Stopping Oral Minxoidil

Alopecia Areata Incognita, Androgenetic Alopecia and Chronic Shedding

I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in the the diagnosis and treatment of chronic shedding in the context of androgenetic alopecia.

QUESTION

Good evening Dr. Donovan, I am in my late 30s, female, and have been suffering from androgenetic alopecia since 2009.

Since 2014, following a biopsy, I have also been diagnosed with alopecia areata incognita. I would like to ask you about a question that my dermatologists have not been able to explain to me.

I was treated the first few years with 2% minoxidil and later 5%. Over the years also courses of cortisone, oral, local and intramuscular, in order to control the alopecia areata.

In 2019, in addition to the topical minoxidil that I’ve never stopped, I was prescribed oral minoxidil, gradually increasing to 2.5 mg. After 6-7 months I had severe insomnia and had to stop it.

In the years that followed, until last October, I made other attempts with oral minoxidil both by lowering the dose and by changing different pharmacies (in Italy it's only galenic). I always had to stop after a few months, I experienced several side effects (tingling in the limbs, tachycardia).

I never had problems with the topical version, but the oral one is not for me.

Since I was diagnosed with alopecia I have always had a strong hair fall, but during the 6 months of oral minoxidil the fall had disappeared almost completely! I was happy!

Already in the last few weeks I began to notice the loss of several short and fine hairs, which got enormously worse after the abrupt interruption due to insomnia. I have been losing 100/200 hairs every day and 300/400 when I wash them for more than 3 years.

70% of the hair that falls out nowadays is less than 2 cm or vellus.

I still have strong regrowth but they fall off quickly.

As you can imagine, in 3 years the volume of my hair has halved, especially at the top. At the moment I use topical minoxidil 5% and also finasteride 2.5 mg since 2022.

I'm afraid attempts at oral minoxidil have permanently messed up my hair cycle. Is it possible? Could it have triggered a chronic telogen effluvium? It will never have an end? Thanks for your attention and thanks if you want to answer me.

ANSWER

 Thanks for the question. This is a challenging question. Thanks for describing things so carefully – you really understand these issues very well and I can tell you’ve given a lot of thought to all this!

It could be that there are three potential issues here:

a) the androgenetic alopecia has accelerated after the oral minoxidil was stopped

b) the alopecia areata incognita is active

c) there is a telogen effluvium present here.

It would seem that with these short hairs you describe (70% less than 2cm) that we are dealing with some kind of advancing androgenetic alopecia. The presentation of androgenetic alopecia in the context of alopecia areata incognita can certainly be complex.

The first issue that will need to be addressed is the diagnosis and then treatment can be discussed.

It would be less likely that a true CTE is present here. The main issue here is an accumulation of short hairs.

So what is the diagnosis?

The main question is what is the MAIN diagnosis now. Is it mostly androgenetic alopecia ? Is the alopecia areata incognita contributing a significant role right now (or is it quiet)?

Trichoscopy and possibly repeat biopsy could be helpful.

It is important to know what is the main diagnosis as that influences which treatment to consider.

It would seem that the most likely is that there has been an acceleration of androgenetic alopecia and this is the most relevant issue right now.  However, trichoscopy and biopsy can guide things.

I’m also a big fan of hair collections in these complex situations. This is known as the “5 day modified hair wash test”. Hair collections allow us to see how many short hairs there are (like you have said) but also allow us to see how many ‘dystrophic’ hairs there are. These include abnormally shaped and broken hairs. If there are a lot of dystrophic hairs, then I am a little more likely to feel that a 1-2 month course of oral steroids is worthwhile to see if the shedding can be shut off.  That in and of itself is a therapeutic trial and gives valuable information – if the shedding shuts off dramatically with a course of steroids, we know this is not all due to androgenetic alopecia.

Finally, in these sorts of situations, I often will order some blood tests. The exact tests I like to order depends on the patient’s full story. I don’t have your full story so it’s not possible to say all the tests that are needed.  Tests for LH, FSH, estradiol are helpful as rarely the acceleration of AGA and poor sleep have been seen in some of our patients in the context of premature transition to menopause. A day 3-5 FSH that is within normal range is reassuring. In general, if menstrual cycles are regular, that is also reassuring that there is not likely a concerning hormonal issue.

I can only imagine that you have had many tests for TSH, ferritin. You probably don’t need those repeated.  

What needs to be excluded here as well is that there is any sort of autoimmune issue arising or any sort of COVID related issue (longCOVID) that is present. Of course, that can only be ascertained by history.  There are a variety of complex shedding issues that can occur and a full history to exclude autoimmune or hormonal issues is really important and necessary. I would not say that all patients with chronic shedding like this need an ‘autoimmune work up’ but certainly if there is abnormal fatigue, joint pains, Reynaud’s, photosensitivity, it does now become important.

Finally, I’m not 100% convinced that COVID shedding always shuts off perfectly so if a patient had COVID 19 in the past, this needs to be addressed.

But assuming the hair loss is androgenetic alopecia, I believe there are a few options to consider:

1. slowly increasing topical minoxidil 50% -100% above current levels.

2. adding oral minoxidil back to the plan at 0.25 mg once daily and very slowly moving to 0.5 mg

3. adding oral spironolactone 50 mg with the finasteride.

4. using topical minoxidil compounded with cetirizine 1 % or topical minoxidil compounded with latanoprost 0.1 % or retinoic acid

5. Considering PRP therapies or low level laser therapies

6. Considering topical minoxidil compounded with latanoprost 0.1 %

Option 1: Slowly increasing topical minoxidil 50% -100% above current levels.

It does seem that oral minoxidil helped you. The goal then is to attempt to use more without using so much that it affects your sleep or causes cardiovascular complications. It might not be possible but it is worth considering.

The first step may be to use more topical (local) minoxidil. I’m not sure how much you use but it may be worthwhile in these situations to increase to twice daily or simply use more.

I can’t comment specifically in your situation but some of my own patients will use 5 % Rogaine foam a full cap (or more) under appropriate supervision.

 Using more may make sense.

These agents may also help any alopecia areata incognita component if it is present.

Option 2: Adding oral minoxidil back to the plan at 0.25 mg once daily and very slowly moving to 0.5 mg.

I have had patients with sleep problems with 1.25 mg and higher doses but some patients have noted significant improvement in sleep with 0.25 mg or 0.5 mg taken in the morning. Not all patients find the lower doses improve sleep, and in fact, studies by Sanabria and colleagues did not find that there was a clear trend towards lower doses being associated with lower chances of sleep problems. These small doses may help some patients (especially when combined with other treatments like those discussed in option 1, 3, 4, 5, 6).

These agents may also help any alopecia areata incognita component if it is present.

Option 3: Adding oral spironolactone 50 mg with the finasteride.

If the cause of the acceleration of hair loss is truly the androgenetic alopecia, then more aggressive treatment of the AGA makes sense. This includes more minoxidil or more antiandrogens, or PRP or laser.
Spironolactone and finasteride have different mechanisms of action and some patients can combine them. You and your doctors can review if this makes sense or not but it could add further benefit for some patients.

Option 4:  using topical minoxidil compounded with cetirizine 1 % or considering topical minoxidil compounded with latanoprost 0.1 %

There are options to add additional ingredients to the topical minoxidil. For some patients, adding more retinoic acid helps. For others adding cetirizine or latanoprost could help. 

These agents may also help any alopecia areata incognita component if it is present.

Option 5: Considering PRP therapies or low level laser.

There are options to add PRP or laser for some patients. Both of these may (theoretically) help alopecia areata incognita and androgenetic alopecia.  These are probably less effective than the options outlined in 1-4.

Final Comments

Thank you again for the question. I do think it’s likely that the AGA has accelerated after stopping the oral minoxidil. In situations like this, I do find that use of hair collections really helps me (as I can find dystrophic hairs and get a good count of telogen vellus hairs). Sometimes a hair collection helps me identify rare situations too – like a late onset loose anagen hair syndrome,  for example.

You are very knowledgeable about your hair and I would encourage you to discuss a variety of these options with your doctors and take each treatment step by step if it is decided that a treatment does make sense to start.

It may be that you never want to return to oral minoxidil again, but it may be that you wish to consider very small doses.

Photos will be important to document progress and so will hair collections (whether formal ones or informal ones).

I thank you very much for sending your question our way and hope this was helpful.   

REFERENCE

Sanabria B, Vanzela TN, Miot HA, Müller Ramos P.Adverse effects of low-dose oral minoxidil for androgenetic alopecia in 435 patients. J Am Acad Dermatol. 2021 Apr;84

Perifollicular Scaling and Possible Diagnoses

Does perifollicular scaling mean lichen planopilaris is my diagnosis?

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

Question

I have a challenging case. One doc thinks I have lichen planopilaris (LPP) and one does not. The first doc saw scaling and did a biopsy and thinks I have LPP. The second doctor does not think I have LPP and feels a biopys is not needed at all.

Is the perifollcilar scale enough to make you want to do a second biopsy?

Answer

Thanks for the question. In general, the answer to your question is no - perifollicular scale in and of itself does not necessarily mean the diagnosis is LPP. Perifollicular scaling is non-specific and seen in many conditions. I would do a biopsy if I am not 100 % sure this is LPP or I am not 100 % sure this is not LPP.

Generally, a really good history and really good trichoscopic examination gets one to the diagnosis and a biopsy is not even needed.

Now that you have one biopsy the key is to make sure all the information is extracted from that tiny biopsy before punching more holes in the scalp. If there is loss of sebaceous glands and clear lichenoid change or necrotic keratinocytes on biopsy AND an experienced doc thinks it’s LPP, then it’s probably LPP. No more biopsies needed. End of story.

Now if there is no loss of sebaceous glands and no real findings in the biopsy of LPP AND an experienced doc thinks it’s really and truly LPP, then a second biopsy is probably going to be needed.

Perifollicular scale is seen in LPP but it’s also seen in a zillion conditions including LPP, FFA, dandruff, seborrheic dermatitis, psoriasis, fungal infections, discoid lupus, dermatomyositis, contact dermatitis …. and more! Perifollicular scale with destruction of the normal nice architecture of the scalp hair follicle design is suggestive of LPP especially when patches of scarring are seen and there is itching and burning and redness. But random scaling does not mean much.

In the image below, I’ll show two examples of scaling. One in a patient with LPP and one in a patient with dandruff. Both have perifollicular scaling.

Two examples of hairs with perifollicular scaling. In the image on the left, mostly single hairs are seen and the process of hair loss here is destructive in nature. In the image on the right, a range of thick and thin hairs are seen and the scalp is not red. There is a single hair with scale here and it represents dandruff or non specific scaling in a patient with androgenetic alopecia.

Also - in the early stages of LPP you sure don’t see scarring. That’s under the scalp and the whole reason we jump on treating LPP as early as possible is to limit the hair loss and limit the amount of scarring that ever gets seen.

Is a biopsy from the side of my scalp a good idea?

Sites of a Scalp biopsy

I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in biopsies for male androgenetic alopecia.

Question

Hi Dr. Donovan. I am a 28 year old male. I had a biopsy from side of my scalp and doctor said my diagnosis is androgenetic alopecia Is this a good place to take the biopsy? I have zero thinning from the crown!!

Answer

Well, I would need to see the scalp and know more about your story. If your doctors are really concerned about diffuse unpatterned alopecia (or DUPA - a rare form of AGA) then sure it could make sense to take it there as DUPA causes hair loss from the sides of the sclap But if none of your clinicians are really thinking about DUPA, then no, that is not a typical location.

I regret I can not offer more general information without obtaining a lot more information. If there is no thinning (or at minimum no trichoscopic evidence of miniaturization) on the crown and no thinning at all in the mid scalp or temples, then a diagnosis of AGA becomes increasingly unlikely. Not impossible, but statistically unlikely.

Biopsies of the sides of the scalp are still helpful sometimes to exclude other diseases (like scarring alopecia, diffuse alopecia areata, psoriatic alopecia, etc) but are rarely a great place to confirm AGA.

If AGA is really on the list and someone feels a biopsy is necessary, it is preferable that it be done somewhere in the area marked in black color below (for males). Temples are a bit more unreliable.

Pilar Cysts: What are my options?

Pilar Cysts vs Alopecia Areata

I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in the diagnosis and treatment of pilar cysts also known as trichilemmal cysts and formerly sebaceous cysts.

Question

Do I have Alopecia Areata or do I have Alopecia Areata from pilar cysts? I have attached some photos and provided a full background story.

I have always had Pilar cysts growing up. I had one on my left front scalp back in 2021. I started noticing it getting very inflamed. I went to the doctor in January 2021 and they injected me with triamcinolone to reduce the inflammation (10 mg/cc x 1.0 cc injected total across 1 lesions) the cyst went flat.

Once they did that and I noticed complete hair loss in the area. After two weeks, the cyst got inflamed again so I went back to the doctor in February 2021 and he decided to make an incision and drain the cyst out for me (it was not surgically removed). Once he drained it out, after about two weeks or three weeks I started noticing hair regrowth in the area and the cyst never came back and my hair grew fine.

Fast forward, it is now 2023 RECENTLY I noticed in the same. area where that cyst occurred and the shot of triamcinolone was given to me, a small piece of hair loss in that same area has re-occured. My dermatologist went ahead and injected me with 5 mg/cc, Total volume used was 0.1cc.

Questions on this procedure done above:

1. did the hair grow back the first time because the cyst was drained (I am aware that cysts that cause hair follicles to be blocked so maybe the fact it was drained made a difference for hair to grow back?) or was it due to the steroid shot that was given about a month or so prior to reduce inflammation?

2. is the cyst (no longer palpable and my dermatologist can no longer "feel it") causing this hair loss and the re-occurence of alopecia areata in the area?

Current Situation: Fast forward, it is December of 2022 and I noticed another one of my Pilar cysts, a new one develops in a different area (middle of the top of my scalp this time) starts to get inflamed, I start to notice hair loss again as it gets inflamed and then all of a sudden about a week or two later the cyst goes back down on its own and becomes completely flat with complete hair loss in the region where the cyst is. I went to a dermatologist in the US and she said since the cyst went back down on its own, I shouldn't remove it surgically because even when she touches the area she doesn't feel anything except a bald spot, she claims she feels no cyst anymore, so instead she suggested I should just take a shot of kenalog for hair regrowth. she injected me with (Kenalog 5mg/cc 0.2ccs was injected into the lesion.) this was done in December 2022. it is now January 18th, 2023 and I have seen very little hair regrowth ( and I had her use a dermascope to look at it and her words were "I see some hairs regrowing, nothing overwhelming but there is some growth and I am hopeful for the future".

Questions + Concerns: 1. It has been over a month at this point when I got the steroid shot, should I go back and get more? if so, at what dose? or should I wait even longer to see if hair continues to grow? WHAT DO I DO NEXT? 2. Is the hair loss caused by the cyst? 3. should I get a biopsy of the area to see if the cyst causes the hair loss? (because I went to a dermatologist in US and she said the hair loss and cyst is not related but that doesnt make sense to me because everytime my cysts get inflamed that is when I get hair loss in the region of where the cyst is.) 4. will the shot of kenalog she gave me work for hair growth even though I didn't remove the cyst (since cysts cause hair follicles to be blocked?) She says that she can no longer feel a cyst on the head when she touches the bald spot, therefore she is skeptical to even open up the area and cause any scarring incase she doesn't find anything when she does this?)

original appearance of pilar cyst.

original appearance of pilar cyst.

appearance of pilar cyst after steroid injection

Answer

Thanks for the question. These are pilar cysts and there is no evidence in what you have written or shown for alopecia areata so I won’t discuss that further. Alopecia areata does not appear to even be in this discussion. If there are features of alopecia areata you see in other areas, be sure to review with your doctors. I don’t see evidence for alopecai areata in what has been presented here. Yes, they can look similar. But there are 10 different things that cause circular areas of hair loss like this.

So, we’re dealing with pilar cysts, also called trichilemmal cysts. About 5 % of the population has them and they an often be multiple. Often there is a family history in mom or dad too - but there does not have to be. Some just crop up sporadically with no such family history. They are more common in females than males but both get them. Young females are particularly a common group.

The key on what to ‘do next’ for anyone depends on a few things:

a) does the cyst come back (reform) after injections?

b) do they come back with one drainage?

c) are they causing hair loss when they occur? and is it permanent or temporary

d) are they causing pain?

e) how inflamed do they get?

f) how much trouble to they cause?

The reality is that once someone has a cyst, there is a good chance it is not going away unless the entire cyst is removed from the scalp. I’m not talking about being drained - but actually removed. Removal (when inflammation is low) is often the best plan for a lot of people. Not everyone needs them removed- but many prefer to. Now, if the cyst is small and not causing hair loss and not causing pain or irritation it’s fine to leave it. But it’s unlikely to go away. Many people live with tiny bumps and domes in the scalp and they are hidden away. They don’t cause problems in most cases.

So for many people, pilar cysts are just left alone if they don’t are not causing problems. If they get inflamed and puffs up, one can try a steroid injection like you did, to see if they settle down again and return to a quiet state. But if they don’t settle or just keep getting inflamed (or infected), surgery may be the best plan. You’ll know over time how much trouble a given pilar cyst causes - and the best plan. Your doctors can help with that.

Your story really should be reviewed with a dermatologic surgeon. You have new cysts forming and you have recurrent cysts in prior areas that were drained. It’s not surprising that prior areas are getting the cyst again - because unless the entire “wall” of the cyst is removed, it can just fill up again and possibly even rupture. We really want to prevent that because sometimes repeated rupture can lead to scarring in the scalp. If cysts are repeatedly getting inflamed, it’s often sign that serious discussion about removal should take place

Surgery can be helpful once the inflammation has settled. Generally speaking, the best time to remove a pilar cyst is when it’s not inflamed. With surgery, the chance is around 2 % that the cyst will come back again in that same spot. That’s assuming the entire capsule of the cyst was removed. If the entire wall was not removed, there is a 25-50% chance this will keep coming back. So with drainage of the cyst, the wall does not get removed at all, and so there’s a very high chance it will just reform again in the future. For an occasional patient, drainage along (rather than surgery) does solve the problem and gives long term relief. But for many, the cyst just comes back with things like drainage or steroid injections. The purpose of a trial of drainage is to give relief of the pain, stop inflammation and settle things down. The purpose of the steroids is to chase away inflammation that contributes to redness and pain and swelling. But drainage does not cure these cysts - nor do injections. They just help settle things down.

You have asked which of the two helped the hair come back. It’s likely both.

It makes sense at this point to have a plan in place for what to do for the current cysts and any future cysts that form. It’s likely there could be another cyst in your lifetime. This is something you are your doctors can decide. Often, if they don’t bother a person, they are left or removed immediately when not inflamed (before the cycles of inflammation and rupture start). You’ll know over time what feels right for you but the key is to remove them when they are quiet (if one decides to remove them).

As for the present ones, it is a combination of pressure and inflammation that is causing the hair loss. Hairs don’t grow well when all this inflammation is around and don’t grow well when under pressure. If there has been any infection of the cyst over time, that’s going to affect things too.

I usually advise my patients to watch carefully over time what their cysts tend to do. If they remain small and stay quiet, then watchful waiting is a good idea. If a person’s cyst tends to grow and rupture or grow and become inflamed or grow and cause hair loss, then removal of new cysts rather soon in their evolution may be a good idea.

As for the cysts that are present, it would appear that the newest one has settled nicely. It has a high chance to return again at some point but also currently has a high chance to regrow hair. For many of my own patients, I inject again in 2 months (often with 2.5 to 5 mg per mL) and have the patient use topical minoxidil over the area for 4 months (if there are no ‘contraindications’ or reasons not to). This second cyst area has a high chance of hair regrowth but it has a high chance of coming back in the future. You’ll need to decide with your doctor if you want to just wait and see what happens in the future and excise it if it does come back.

As fas as the first area goes, this is behaving exactly as we expect. The area settles and then slowly fills up again and comes back. Periodic steroid injections are an option but if you find it happens too often or you find the hair is not growing back completely, then removal may need to be considered.

A word about steroid injections before we leave this topic. For some patients, 10 mg per mL is a good dose and for others 5 mg per mL is a better dose and less likely to trigger hair loss. This is something you and your doctors can review. All in all it would appear you have been getting very little in the way of steroid so I don’t think the dose is likely much of an issue for you.

In summary, it’s a combination of inflammation and pressure that is causing the hair loss - with the bigger contribution generally being the inflammation at this point for you. Steroid injections settle both. Incision and drainage relieves the pressure.

You are your doctors can decide if periodic steroid injections and drainage is the right plan for you or whether surgical removal is the best plan. If the areas are filling up too quickly or are causing hair loss or too much days of pain or tenderness or there is a worry about any kind of permanent hair loss (from repeated inflammation), then excision often becomes the right plan.

if this always grows back fine and it’s once every 10 years that you are dealing with inflamed cyst issues, then a conservative approach may be best. If it’s every 3-6 months that you’re dealing with cyst issues and it’s affecting how you feel and look, then a more aggressive approach may be right to you.

All this takes some good discussion with a knowledgable physician.

There is no right or wrong answer for pilar cysts. Some patients live with them if they don’t cause issue. Others get them removed if they are tending to become inflamed or infected or carry a risk of temporary or permanent hair loss. Some get them removed quickly when the pop up and others get them removed after many years. You’ll know what feels right for you.

The goal now is for you to develop a plan that suits you the best. Some patients will say “I’m going to inject this now and if it comes back ever again I’m going to have it removed” Other patients will say, “unless it causes hair loss or becomes inflamed I’m just going to leave it alone. If it does’t bother me then I’m not going to bother it.”

it would appear that your cysts are teaching you and your doctors that they tend to return and carry a risk of temporary hair loss when they do occur. This makes discussions about removal in the future all the more important. But these are really important discussions that you and your doctors will want to have. It’s great that regrowth is ocurring. It can take 3-5 months for regrowth to occur. - assuming inflammation has settled.

Is endometriosis causing my hair loss?

Endometriosis

I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in endometrosis and hair loss.

Question

Does endometriosis cause hair loss? I’ve had endometriosis for a few years now and lately I’m noticing that I’m losing hair.

Answer

There not often a super close relationship between the two. Endometriosis is common (10 % of women) and hair loss of various kinds is also common in women. Because both issues are common many women with endometriosis will also mention hair loss. But they are generally separate issues. In some cases, medications used to treat endometriosis can cause hair loss. Oral contraceptives, GnRH analogues, Danazol and aromatase inhibitors all have a slight chance to trigger a form of hair loss called telogen effluvium and some medications like Danazol and aromatase inhibitors used for endometriosis can worsen androgenetic alopecia in some women.

In addition, the pain and stress from endometriosis have been noted to worsen hair shedding in some of our patients. That’s due to the stress rather than the underlying mechanisms governing endometriosis.

Overall although endometriosis is a cause of mentrual irregularities for some women it is not commonly a direct cause of hair loss.

Hydroxychloroquine for Lichen Planopilaris (LPP): Should I change?

Hydroxychloroquine for Lichen Planopilaris.

I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in the use of hydroxychloroquine for scarring alopecia.

Question

I have been on hydroxychloroquine for three months and it’s not working. Is this long enough? Should I change to methotrexate? My scalp is still red!

Answer

Well, to offer some solid thoughts I would need to ideally review your entire story and examine your scalp. But let’s review a couple of key points here.

I’m not so worried if your scalp is red. What I’m more concerned about is whether your scarring alopecia is active (Of course, I’m always concerned whether or not scarring alopecia is the correct diagnosis but I will assume it is for the sake of the question).

If your redness is from allergic contact dermatitis rather than LPP, then no MTX sure is not the ideal plan. The goal in that case is to stop allergens! If redness is from seborrheic dermatitis and not LPP, then the plan would be to bring on board some dandruff shampoos! If the redness is from overuse of topical steroids (like in the photo below), the goal is to get off the steroids ASAP.

Dilated blood vessels (steroid telangiectasias) in a patient using excessive amounts of the topical steroids clobetasol.

But let’s return to assuming the redness is from the scarring alopecia. Hydroxychloroquine can take 6-9 months to figure out if it’s working so you’ll want to be closely followed by your doctor. One month on a new dose means little. We need to give it longer. I don’t know your full story but I’d be hesitant to switch to MTX yet. Be sure to check the dosing as too many people are on the wrong dose. Steroid injections, cetirizine, doxycycline, low dose naltrexone, clobetasol, doxycycline, tacrolimus may be options before starting MTX but again I don’t know enough about your story. Be sure to get an expert review!

Here is my general treatment approach to lichen planopilaris (first-line options, second-line options and third line options).

Hypothalamic amenorrhea

Hypothalamic amenorrhrea: Will my hair return?

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

Question

I have hypothalamic amenorrhea (HA) and hair loss. Will the hair loss stop once the HA resolves?

Answer

Hypothalamic amennorrhea (HA) occurs when reduced stimulatory hormones from the hypothalamus leads to reduced estrogen production by the ovaries. The results is a cessation of normal menstrual cycles. It estimated that HA effects about 1.62 million women between the ages of 18 and 44 years in the United States and about 20 million women around the world. Three main types of functional HA are psychological stress, intense exercise, and eating disorders.

So now to the question at hand - does resolution of HA lead to return of hair density?
The answer is complex as it really depends if the hypoestrogenic state and other other changes associated with reduce hypothalamic function lead to an acceleration of underlying androgenetic alopecia or not. This really requires a proper up close examination.

If there is zero evidence of AGA and the diagnosis of the hair loss is truly a ‘telogen effluvium’, then it may return. Often there is evolving AGA in these situations. Be sure to review with an expert if there is any component of androgenetic alopecia present

Baricitinib (Olumiant) vs Tofacitinib (Xeljanz) for Alopecia Areata : Should I switch?

Baricitinib (Olumiant) vs Tofacitinib (Xeljanz) : No Comparative Data yet!

I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in the use of JAK inhibitors for alopecia areata

Question

I am on tofacitinib for alopecia areata and doing really well. I once had 90 % hair loss and it grew back with tofacitinib. I heard that baricitinib is now FDA approved and I’m wondering if I should switch to baricitinib.

What are your thoughts about this topic?

Answer

Thanks for the question. Let’s jump in and look at many issues here.

Baricitinib made headlines on June 13, 2022. It was the first FDA approved treatment for alopecia areata. Since that time, many patients and physicians have asked me if I would consider switching a patient on tofacitinib to baricitinib.

That answer is sometimes a resounding yes, but sometimes a definite no.

FDA Approval is a Medal - Not necessarily a Gold Medal

FDA approval tells us that a medication is at least reasonably safe and at least reasonably effective for the population of the United States to now proceed to think about using this medication. FDA approval does not mean a drug is entirely safe and FDA approval does not mean a drug even works all that well. FDA approval means that a drug has the green light for the company to start making the drug and doing what they want to try to get it to patients.

For baricitinib, FDA approval means the drug is viewed by the FDA as okay to use in patients with advanced alopecia areata provided patients are aware of side effects and have considered the alternatives. Baricitinib helps about 25 % of patients with advanced alopecia areata a great amount and about 1/3 of patients a pretty significant amount. 60-70 % of patients with advanced alopecia areata won’t be helped as much as they hoped for with use of baricitinib. As far as safety, issues such as infections, nausea, vomiting, blood clots, heart disease, cancer, blood test abnormalities, GI perforation, at least need to be discussed with patients. Fortunately, it seems this issues are quite uncommon in healthy patients with alopecia areata and may in fact be more common in other patient groups that use this drug (like rheumatoid arthritis patients).

Should a patient switch from tofacitinib to baricitinib?

I’m often asked if a patient who is currently using tofacitinib should switch to baricitinib. Sometimes, the answer is yes … and sometimes it’s no.

There could be reasons why switching makes sense. The main reason is drug coverage. Many insurance companies now recognize baricitinib as an FDA approved treatment and will pay for the drug. Many companies realize that tofacitinib is not FDA approved and is therefore off label. If a patient can obtained baricitinib with low cost (or not cost) but needs to pay 20,000-30000 USD out of pocket for tofacitinib, I’d say go for the low cost option.

However, one should not switch if they are hoping to switch simply with the mindset that baricitinib is better than tofacitinib.

We don’t know that. The only thing we know is that one (baricitinib) is stamped with FDA approval and has undergone fairly rigorous scrutiny. That other (tofacitinib) is not stamped with FDA approval.

We do not know if oral tofacitinib is more effective than oral baricitinib for treating alopecia areata. Similarly, we don’t know if oral tofacitinib is of similar effectiveness to baricitinib or less effective than baricitinib. Those could comparative studies just have not been done. Anywhere. Therefore I would strongly recommend that oral tofacitinib be continued if one is using it now and financial issues are not entering into the decision process.

All that we do know in 2023 is that the company that makes baricitinib has gone to the efforts to have the medication processed through the FDA for approval. It does not say anything about how effective it is compared to tofacitinib. It could be that baricitinib is more effective than tofacitinib. It could be that baricitinib is less effective than tofacitinib. It could be that someday we prove they are similarly effective. It could be that baricitinib is more effective than tofacitinib but has certain side effects which are not as good as tofacitinib. Conversely, it could be that baricitinib is less effective than tofacitinib but has certain side effects that make it a better choice compared to tofacitinib. We just don’t know.

In many counties, baracitinib and tofacitinib are not formally approved so they are all off label. That means bottles of tofacitinib and bottles of baricitinib are sitting in the pharmacy. It’s up to the physician to review what he or she feels about safety, affordability, feasability and effectiveness (the SAFE principle) in order to come up with recommendations for the patient in front of them.

Consider 3 patients with advanced alopecia areata living in countries, X, Y and Q.

In hypothetical country X, if baricitinib is $ 18,000 per year and tofacitinib is $ 9,000 per year, I’d say go with tofacitinib. There’s no reason to believe one is better than another and there is no reason to believe safety is all that different. They are just as easy to use. The SAFE principle highlights that cost is that difference.

In hypothetical country Z, if baricitinib is $ 8,000 per year and tofacitinib is $ 19,000 per year, I’d say go with baricitinib. There’s no reason to believe one is better than another and there is no reason to believe safety is all that different. They are just as easy to use. The SAFE principle highlights that cost is that difference.

In hypothetical country Q, if baricitinib is $ 18,000 per year and covered by insurance and tofacitinib is $ 9,000 per year and not covered by insurance, I’d say go with baricitinib. There’s no reason to believe one is better than another and there is no reason to believe safety is all that different. They are just as easy to use. The SAFE principle highlights that cost is that difference.

Conclusion

These are the early days of JAK inhibitors for alopecia areata. They are great options for patients with advanced forms. They do not help everyone and they are not without some risk. Fortunately, risk is relatively low and may even be lower for those who use JAK inhibitors to treat aloepcia areata compared to those who use JAK inhibitors to treat rheumatoid arthritis.

There could be a number of reasons why someone using tofacitinib might switch to baricitinib. However, switching simply with the view that baricitinib might be more effective than tofacitinib is without evidence and not backed up by any good studies that have been done to date. Similarly, switching simply with the view that baricitinib might be safer than tofacitinib is without evidence and not backed up by any good studies that have been done to date.

Cost prevails in decision making so far.

Spironolactone and decreased libido

Does spironolactone affects libido (sex drive)?

 
I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in the effects of spironolactone on sex drive

Question

I am a 33 woman and have been taking spironolactone 100 mg for my androgenetic hair loss for about 6 months. It’s helping my hair but I feel that it might be lowering my sex drive. I know there are many factors that affect this aspect of health (stress, medications, etc) but I’d like to get more of an understanding.

Answer

Thanks for the important question. I’d recommend you consider reviewing a prior article I wrote last year on the topic. There is a lot of good information in there:

Article: Does use of oral Spironolactone Affect Libido?

Spironolactone can certainly affect many aspects of sexual health. A number of studies have addressed sexual type side effects but clear estimates of the frequency of these issues are not available. I would estimate the following proportion of women who use spironolactone experience these side effects

a) decreased libido (sex drive) - about 10-15 % of users
b) vaginal dryness or changes in lubrication - 15-25% of users
c) reduced ability to achieve an orgasm - 1-2 %

d) vulvar (vestibular) irritation and pain - risk unclear

e) vulvar atrophy - risk unclear

f) dyspareunia (painful intercourse) - risk unclear

We really do need better studies to understand these proportions better.

Sexual Side Effects are Often Dependent on the Spironolactone Dose Chosen

These changes is sexual health are often dose dependent. In other words, some women will notice fewer side effects on 50 mg than 100 mg and fewer on 100 mg than 200 mg. (The optimal dose for hair loss is not clear but 100-200 mg doses may be slightly better for some than 50-100 mg doses).

What to do with spironolactone associated sexual dysfunction?

Sexual health has many components and I often recommend patients speak with their primary care physician or gynecologist to ensure a proper evaluation can be done. There are several options that can be considered if spironolactone is implicated in the changes in sexual function:

1) The spironolactone dose can be reduced.

As mentioned above, many female patients find they have fewer side effects on lower doses of spironoactone. A patient on 150 mg may find improvements in various aspects of sexual health by reducing to 100 mg or 50 mg. There is a risk of hair loss by doing this but the risk is low and some women will choose to introduce another hair loss treatment (like topical or oral minoxidil) with the hopes to compensate for the reduced spironolactone.

Changes in sexual function, such as a return to prior levels of libido can occur in 2 weeks to 4 months. It does vary from patient to patient. In some, it is quite rapid, in others it takes many months.

2) Spironolactone can be stopped for 2 weeks and reintroduced at a lower dose.

I generally recommend that medications that give side effects be stopped until side effects clear and then reintroduce if that is an option. Stopping spironolactone for 2 weeks will not be an issue for hair loss for most patients (2 weeks is very short) but can give time for the medication to clear from the body and side effects to resolve (or at least improve somewhat).

There is an option to stop completely until side effects are gone as well. That carries the highest risk of causing hair loss but it is an option too.

3) The medication can be stopped and alternative treatments discussed.

The option also exists to stop spironolactone and review other options for treating female pattern hair loss. These would include topical minoxidil, oral minoxidil, topical spironolactone, PRP, laser and hair transplantation.

4) In the case of vulvar pain and dyspareunia (painful intercourse), Spironolactone can be stopped and estradiol 0.01% /testosterone 0.1 % gel can be used twice daily.

This is the protocol reported by Mitchell and colleagues as we reviewed together last year.

Summary

Thank you again for this question. It’s such an important question as there are many women who use spironolactone without a clear understanding of side effects on sexual health. Reduced libido does occur in a proportion of spironolactone users and not everyone is aware of the link back to the medication they are using. For some women, it can taken months or years before a link back to the drug is questioned. An improvement in libido and other aspects of sexual health (lubrication, orgasm) can occur within a few weeks to up to 3-4 months of reducing or stopping spironolactone. Although the effects on sexual health can be troublesome, there is reason to be hopeful as changes can occur very quickly in some patients. A return to normal levels of sex drive and prior abilities to achieve orgasm can often occur in a matter of 1-2 weeks.

Patients should be sure to speak to their practitioners as reducing the dose of spironolactone does carry the risk of causing hair loss in those patients using it for treating androgenetic hair loss.

The key here is to have a good plan in place to address these issues and monitor improvement.

Does low copper levels really cause hair loss?

Low Copper and Hair Loss

 
I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in copper levels and hair loss.

Question

I have read that copper deficiency can cause hair loss and people with a condition called Menkes syndrome have low copper and hair loss. So, I’d like to know - can copper deficiency cause hair loss?

Answer

Thanks for the question!

Sure it’s possible. However, if a person has a copper deficiency that is truly sufficient to cause hair loss, most patients would be at least somewhat ill (or have other medical issues of note). Individuals with Menkes syndrome in particular have a number of systemic issues. In addition to sparse hair, children with Menkes syndrome are often very unwell. Children with Menkes syndrome don’t gain weight properly, have several neurological issues including seizures and poor muscle tone and many die in early childhood.

Adults with copper deficiency should not compare themselves to children with Menkes as the two are very different. Generally speaking, most minor degrees of copper deficiency in adults is not sufficient to cause hair loss. However, if you are worried, you should, of course see your physician for a full physical examination and exploration of further blood tests. Total copper levels are generally in the range 10-22 μmol/L or 63.7-140.12 μg/dL. Copper levels just below this cut off usually have little consequence but your doctors can look into this in greater detail. Isolated copper deficiency that is to sufficient magnitude to cause hair loss is not common. Minor amounts of copper deficiency can occur but that’s a different situation than major copper deficiency.

Other mineral abnormalities often go along with copper abnormalities in most adult patients and deficiencies of copper and deficiencies/excesses of other minerals should be given proper medical attention and a full medical evaluation is needed. One of the most common causes of minor degrees of copper deficiency amongst hair loss patients is excessive use of zinc supplements. Zinc intake dramatically lowers the levels of copper in the blood. Please see your doctors if concerned so that a proper evaluation can be done. In 99.9 % of patients I see with minor copper deficiency, the deficiency is unrelated to the hair loss issue.

Why isn't Rogaine helping?

Rogaine: Does it help everyrone ?

 
I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in the use of Rogaine to treat hair loss

Question

My hair is not growing longer despite the religious use of Rogaine. Is this not a surprise? What should be done?

Answer

Thanks for the question. Perhaps you are assuming minoxidil helps everyone who uses it? It does not. I think that’s really important to understand first. In fact there is no treatment that helps everyone.

I don’t know why your hair is growing slowly. That would require me to see your scalp and review your entire story with you. A few things to keep in mind though:

If there is any seborrheic dermatitis or psoriasis on your scalp, hair might not grow as robustly as one would hope until the psoriasis or seborrhea is treated.

If there is any significant component of telogen effluvium it might not grow as robustly as one would hope until the telogen effluvium is treated.

If there is any significant component of lichen planopilaris, folliculitis decalvans or other scarring alopecia it might not grow as robustly as one would hope until the scarring alopecia is treated.

If there is any significant component of hair breakage it might not grow as robustly as one would hope until the hair breakage is treated.

Summary

Minoxidil does not help everyone. Be sure to keep close follow up with your practitioner so that a proper examination can be done. The key question here for you is “what type of hair loss do you have?” and is minoxidil even a good option for that type of hair loss.

Hair Loss and Red Scalp and TNF Inhibitors

TNF inhibitor induced psoriasis: An Important Consideration in Patients with Refractory Red Scalp Issues Following TNF Inhibitors

 
I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in TNF inhibitor triggered psoriasis.

Question

I am 19 and have been battling a red scalp and hair loss since starting a TNF inhibitor for my Crohn’s disease. No one can figure out what’s going on and I’ve been diagnosed with psoriasis, seborrheic dermatitis, allergy and telogen effluvium and genetic hair loss.

Do you think it’s related to my hair loss is related to this drug? Do I need to stop this drug?

Answer

Thank you so much for reaching out!

I am concerned in this case that what we might be dealing with is TNF inhibitor induced psoriasis. She could have AGA as well …..but until we aggressively treat the psoriasis, I’m not sure we can say just how much AGA she actually has.  Of course, we’d want to make sure there is no telogen effluvium here so blood tests for ferritin, TSH are important.

The ability of TNF inhibitors to cause psoriasis rather than be used to treat psoriasis is called “paradoxical psoriasis”. The terms TNF inhibitor induced Psoriasis and paradoxical psoriasis can be used interchangeably. The prevalence of anti-TNF-induced psoriasis ranges from 1-7 %.  In the pediatric literature, Cyrenne et al identified 210 patients with TNF induced psoriasis out of 4564 pediatric patients treated with these drugs. That put the frequency of the condition at 4.6 %.

Many authors have shown that females comprised a greater number of cases. It ranges from just a slightly greater proportion of females than males to upwards of 70 % females affected by the phenomenon. The time from initiation of treatment to onset of lesions is around 8-11 months on average. Most cases therefore develop within the first year of treatment.

You might consider if this timing is related. Of course some cases of TNF inhibitor induced psoriasis are also a worsening of existing psoriasis so even if she had psoriasis before the question is really whether it got worse.

Patients with paradoxical psoriasis can have many underlying conditions. However, rheumatoid arthritis, ankylosing spondylitis, and Crohn's disease account for the vast majority of background disease states in patients who develop TNF Inhibitor Induced Psoriasis.

Most cases of TNF Inhibitor-induced psoriasis are linked to infliximab, with fewer cases described with adalimumab, certolizumab, and etanercept. In 2009, Ko et al evaluated 127 cases of TNF Inhibitor-induced psoriasis. Inflixmimab topped the list of TNF inhibitors implicated. There were 70 in patients on infliximab (55.1%), 35 using etanercept (27.6%), and 22 with adalimumab (17.3%). Infliximab also stands out in the pediatric literature as also being the number one cause of paradoxical psoriasis from TNF inhibitor use. In 2021, Cyrenne et al showed that infliximab was the drug most likely to induce psoriasis in pediatric patients followed by adalimumab.

In pediatric patients, Cyrenne et al found that the scalp was the most commonly affected area in TNF Inhibitor induced psoriasis (47.5%), followed by the ears (30.8%).

How should this be treated?

The options for treating of this patient is to aim to eradicate the psoriasis and then see how much hair loss is left over. That would then guide how aggressively to treat the AGA.

There are three options for treatment of TNF inhibitor induced psoriasis. Option 1 is to “treat through” the TNF inhibitor - in other words, one has the option to continue the TNF inhibitor and try to aggressively treat the psoriasis. Option 2 involves switching to a different TNF inhibitor and option 3 is to completely abandon the TNF inhibitor therapy altogether.

Option 1: Continuing the Same TNF I and Treating the Psoriasis (Treating through)

Continuing the TNF inhibitor and trying to aggressively treat the skin disease is among the top option. This is often worth trying first as some patients with TNF inhibitor induced psoriasis respond well to basic psoriasis treatments.

That might be the preference here although I don’t know how well the patient is responding to IBD treatments with adalimumab. I would recommend starting a topical steroid and aggressive shampooing regimen with tar, salicylic acid and anti-dandruff ingredients. She may tolerate some low concentration steroid injections such as triamcinolone acetonide 2 mg per mL at 3-4 cc every 3 months. Sometimes, steroid injections just ‘melt’ psoriasis as the expression goes

In 2022, Lian et al described 10 patients who developed paradoxical psoriasis on TNF inhibitors. 8 of the 10 patients regained control of their skin disease despite continuing the TNF Inhibitor. In other words, 80 % of patients did well using option 1.

A 2020 study by Mazloom et al showed that topical medications alone improved or resolved TNFI-induced psoriasis in 63.5% of adult patients. Cyclosporine and methotrexate (>10 mg weekly) were often effective if topicals failed.

In a systematic review of pediatric patients by Cyrenne et al, it was found that the majority of patients continued the TNF inhibitor and treated the psoriasis they had with psoriasis-directed therapies.

Option 2: Switching to a New TNF Inhibitor

Changing to another TNF inhibitor is rarely a good option as it often does not clear psoriasis lesions. Nevertheless, it is an option.

in 2009, Ko et al showed that switching to a different anti-TNF agent led to resolution in only 15.4% of cases.

Among pediatric patients, a 2021 study by Cyrenne et al found in a systematic review that only 32.0% of those who switched to a new TNF inhibitor had complete clearance of their skin lesions.

Option 3: Stopping TNF Inhibitor Therapy

Stopping the TNF inhibitor group of drugs altogether is probably the option with the best chance of helping. Of course, that may not be the first step but it is one with a good chance of helping. In fact, many researchers have the view that TNF inhibitor psoriasis is different from regular psoriasis in that psoriasis caused by TNF inhibitors is not really a de novo type of psoriasis but simply a type of psoriasis that is maintained by blocking TNF signalling. For this reason, stopping TNF inhibitor therapy often proves extremely helpful in challenging cases of paradoxical psoriasis.

This is by no means a guarantee and in mild cases one may still consider option 1 (treating through). Ko et al suggested that cessation of anti-TNF therapy with systemic therapy led to resolution in 64.3% of cases. A 2020 study by showed that discontinuation of the TNFI with or without other interventions improved or resolved TNFI-induced psoriasis in 67% of refractory cases.

In a series of 125 patients by Guerra et al, 37 % of patients with TNF Inhibitor Induced Psoriasis ultimately needed to stop their TNF inhibitors.

In the pediatric age group, stopping TNF inhibitors frequently helps a great deal as well. For example, Cyrenne et al found that among patients who were switched to another drug rather than a TNF inhibitor, 81% had complete clearance of their paradoxical psoriasis.

Final Comment

It’s possible here that Adalimumab is involved – especially if it developed (or worsened) within a year or so of starting.

In my view, the red scalp issues warrant aggressive treatment before deciding on how much AGA to treat. Certainly spironolactone or topical minoxidil or oral minoxidil are good options but I’d really like to see the psoriasis gone before aggressively treating the AGA (if indeed there is much AGA).

Thinning” of this kind can trick you into thinking there is more AGA than there is

For my typical patient with similar situation I might

1.    Start a salicylic acid – tar shampoo twice weekly.

2.    Start fluocinolone acetonide oil once weekly and night followed by shampooing out the next morning with zinc pyrithione or ketoconazole shampoo. Once things improve, we can get rid of the fluocinolone acetonide oil. It’s not so elegant but it can work great to lift scales

3.    Steroid injections every 3 months and low doses (2 mg per mL) not 5 and not 10 mg per mL

4.    Add 2.5 to 5 mg of methotrexate once weekly if we need to (if the psoriasis does not disappear)

5.    Stop adalimumab if it seems we are not really winning here.

6.    Starting 0.625 mg of oral minoxidil (after counseling) and then increasing to 1.25 mg after 3 months is well tolerated.  50 to 100 mg of oral spironolactone can be added after 9 months if the response is not as good as hoped.. In situations like this I often avoid topical minoxidil but there is nothing wrong per se in starting topical minoxidil. I just find it sometimes irritates.

References

Alessia Nidegger et al. [Paradoxical psoriasis induced by anti-TNF - a clinical challenge]. Rev Med Suisse. 2019 Mar 27;15(644):668-671.

Boggs J et al. Paradoxical psoriasis caused by tumour necrosis factor inhibitor therapy. Clin Exp Dermatol. 2021 Apr;46(3):580-582.

Brown G, Wang E, Leon A, et al. Tumor necrosis factor-alpha inhibitor-induced psoriasis: systematic review of clinical features, histopathological findings, and management experience. J Am Acad Dermatol. 2017;76(2):334–341.

Cyrenne et al. Paradoxical psoriasis in pediatric patients: A systematic review. Pediatr Dermatol . 2021 Sep;38(5):1086-1093.

Guerra I, Perez-Jeldres T, Iborra M, et al. Incidence, clinical characteristics, and management of psoriasis induced by anti-TNF therapy in patients with inflammatory bowel disease: a nationwide cohort study. Inflamm Bowel Dis. 2016;22(4):894–901.

Ko J et al. Induction and exacerbation of psoriasis with TNF-blockade therapy: a review and analysis of 127 cases. J Dermatolog Treat . 2009;20(2):100-8.

Lian N et al. Tumor necrosis factors-α inhibition-induced paradoxical psoriasis: A case series and literature review. Dermatol Ther . 2020 Nov;33(6):e14225.

Jun et al Antitumor necrosis factor treatment in patients with inflammatory bowel disease does not promote psoriasis development: A meta-analysis. Medicine (Baltimore). 2022 Jul 8;101(27):e29872.

Mazloom et al. TNF-α inhibitor-induced psoriasis: A decade of experience at the Cleveland Clinic. J Am Acad Dermatol . 2020 Dec;83(6):1590-1598.

Olteanu R, Zota A. Paradoxical reactions induced by tumor necrosis factor-alpha antagonists: a literature review based on 46 cases. Indian J Dermatol Venereol Leprol. 2016;82(1):7–12.

Pugliese D, Guidi L, Ferraro PM, et al. Paradoxical psoriasis in a large cohort of patients with inflammatory bowel disease receiving treatment with anti-TNF alpha: 5-year follow-up study. Aliment Pharmacol Ther. 2015;42(7):880–888.

Ya et al. Family history of psoriasis, psychological stressors, and tobacco use are associated with the development of tumor necrosis factor-α inhibitor-induced psoriasis: A case-control study. J Am Acad Dermatol . 2020 Dec;83(6):1599-1605.

Thank you again
 

Is Keratosis Pilaris associated with Lichen Planopilaris?

Is keratosis pilaris associated with lichen planopilaris?

 
I’ve selected this question below for this week’s question of the week. It allows us to review the link (or lack of a link) between lichen planopilaris and keratosis pilaris

Question

I would like to know if there is a link between keratosis pilaris and lichen planopilaris (LPP). I have both and wondered if it’s coincidental or a true link?

Answer

Thanks for the question! The answer is - maybe and maybe not!

40 % of adults in the general population have keratosis pilaris. That means 40 % of your neighbors have keratosis pilaris and 40 % of your friends do too.

But 40 % of adults don’t have lichen planopilaris. In fact, about 1:1500 to 1:2500 adults have lichen planopilaris.

That means that there are lots and lots of people with keratosis pilaris who don’t have LPP and never will develop this condition.

In fact, about 99.93 % of people with keratosis pilaris will never develop lichen planopilaris.

So what is the relationship of keratosis pilaris and LPP then?

Well, a very very small proportion of patients with keratosis pilaris have a more extensive form of the condition which is associated with keratosis pilaris like papules affecting the abdomen, and other parts of the body sometimes too along with a clinically non-scarring hair loss condition affecting the pubic area and underarms (called the axillae) and sometimes the eyebrows too. This is called the Graham Little-Piccardi-Lassueur syndrome.

Summary

In summary, keratosis pilaris is sometimes linked to LPP but usually not. Almost half of the world has keratosis pilaris and not surprisingly a great proportion of patients with LPP have keratosis pilaris too. However, the more and more that the patient’s keratosis pilaris affects the abdominal skin and eyebrows as opposed to just the back of the arms, the more likely it is that there is a link between the two conditions. The same is true for those with loss of hair in the underarm and pubic region. 

Keratosis pilaris plus lichen planopilaris does not automatically equal Graham Little-Piccardi-Lassueur syndrome. However, keratosis pilaris associated with hair loss in the underarm area and pubic area, eyebrows and keratosis pilaris type papules on the abdomen together with LPP does.

Elevated AST in Lichen Planopilaris (LPP): Is their a connection?

Elevated AST Liver Enzymes in Patients with Lichen Planopilaris

I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in elevated liver enzymes in patients with autoimmune diseases.

Question

Has there been a correlation found between LPP and high AST levels before any medications? I was diagnosed with LPP a year ago and my doctor. I was prescribed hydroxychloroquine and ordered blood tests to monitor my reaction to the hydroxy and my AST was elevated to 151. The AST levels were the only elevated levels on the panel. Almost a year later my levels have increased to 210 and I have not been on any medications at all. They have run multiple liver tests and so far can find no reason for the elevated AST levels. I'm trying to find out if there has ever been any studies done linking high AST to LPP.

Thank you for your time.

Answer

Thanks for submitting this interesting question. There’s no clear or well defined relationship between elevated AST and LPP that we understand yet. However, there are a few important things to mention here. There’s little doubt in my mind that you’ll want to make sure you’ve had three things completed to figure out why your AST is elevated. Perhaps you’ve already had some of these three things done:

1) you’ll want to have a full panel of liver tests, including assessment of macro AST (see below)

2) you’ll want to have a liver ultrasound and

3) you’ll want to visit with a gastroenterologist or gastroenterologist specializing in liver issues (called a hepatologist.

Let’s go through the points that are relevant here. I’ll assume that your AST elevations are not due to hydroxychloroquine.

First, it’s important to note that there are many causes of elevated liver enzymes including medications, alcohol, viral infections, autoimmune diseases and malignancies.

The most common causes of elevated liver enzymes are nonalcoholic fatty liver disease (NAFLD) and alcoholic liver disease. Other causes that need to be considered in anyone with elevated liver enzymes medication-induced liver injury (drug induced liver injury), hepatitis B and C, hereditary hemochromatosis, alpha1-antitrypsin deficiency, autoimmune hepatitis, biliary diseases, and Wilson disease. Other diseases due to diseases outside the liver (called extrahepatic sources) include thyroid disorders, celiac disease, renal disease, muscle disorders (cardiac and skeletal), and hemolysis.

As you can see from the above list, it’s critically important for you and your doctors to realize that elevated liver enzymes don’t necessarily mean there’s an issue with just the liver itself. Elevations of the AST level may be seen in acute injury to cardiac or skeletal muscle. Elevated ALT can be seen with obesity, diseases of the biliary tract, anorexia, muscle diseases, heart diseases, and hypothyroidism.

The key point with your story is to confirm that your AST is elevated all on its own and everything else is perfectly. Elevated AST (with normal ALT levels) is not a common phenomenon. If any other tests are abnormal like ALT, ALP or bilirubin it changes the list of possibilities quite dramatically. So I’ll assume here that largely your AST is high and everything else is normal.

Do patients with LPP have an increased risk of Liver disease?

Liver disease is not that uncommon in the population. According to the CDC, at least 2 % of the US population has some kind of liver disease. It has been estimated that 1 in 10 people in the US have elevated liver enzymes. So it’s not that uncommon that someone comes into the hair clinic with abnormal liver enzymes. About 5 % of those with elevated liver enzymes will have some sort of underlying serious disease. Most do not.

Patients with LPP don’t seem to be at all that much of an increased risk of developing liver disease - at least how we understand it now. it would seem that 1 in 10 patient with LPP should have elevated liver enzymes just like the risk in the general population.

Whether patient with LPP truly are at increased risk of non alcoholic fatty liver disease (NAFLD) is not clear, but it’s something that needs more research study. We know that patients with LPP are at increased risk for metabolic syndrome (see prior article) and patients with metabolic syndrome are at increased risk for NAFLD. Therefore, it’s at least conceivable that patients with LPP are at increased with for NAFLD. NAFLD is commonly seen in those with metabolic syndrome.

However, non alcoholic fatty liver disease does not typically give an elevated AST and a completely normal ALT. Rather, the typical findings in NAFLD are raised ALT and AST. The levels are not elevated equally - and the ALT is generally elevated more than AST with an ALT: AST ratio of around 1.5. Patients with NAFLD may have a raised gamma glutamyl transferase (GGT) and, occasionally, raised alkaline phosphatase (ALP). During progression of NAFLD to cirrhosis this ratio of AST:ALT can change.

We don’t have any reason to suspect that patients with LPP are at increased risk to be diagnosed with underlying hepatitis C. This has been described in some countries with lichen planus - but not with lichen planopilaris. Still, as you’ll see below, most physicians will screen for hepatitis C in someone with LPP and elevated liver enzymes.

Blood tests for those with Elevated Liver Enzymes

There are a series of liver and non-liver related tests that your doctor will consider. The exact tests you’ll need will depend on your complete story since birth and what is found on physical examination so I can’t say for sure which tests you should have (because I don’t know your full story and haven’t examined you).

The following blood tests, however, should at least be considered in anyone with your story:

CBC, reticulocyte count, urinalysis, AST, ALT, GGT, CK, LDH, amylase, albumin, PTT, INR, ferritin, total protein, bilirubin, ALP, TSH, anti-tissue transglutaminase, serum zinc and copper. Fasting cholesterol, HDL, LDL, triglycerides, glucose and hemoglobin A1C are generally ordered. Hepatitis C screening (anti HCV), hepatitis B screening (anti - HBSAb, anti HBSAg), CMV and EBV. ANA is often appropriate in these cases to order as well. I generally order a serum protein electrophoresis - especially in those with elevated AST.

The above tests are the tests I typically order myself in patients with liver enzyme issues. There are more tests yet that can be ordered- but I typically leave these for the gastroenterologist (or liver specialist) to order or advise me on ordering.

For example, your gastroenterologist or liver doctors will decide whether any of the autoimmune hepatitis panels are appropriate but generally those should be left for the internists or liver doctors. These include the anti-liver-kidney microsomal antibodies (so called anti LMK test ) and anti smooth muscle (anti SMA) antibody. I also generally leave screening for Wilson’s disease to the liver doctor (these are tests called ceruloplasmin, copper). Tests for alpha-1-antitrypsin deficiency are also best left for the liver doctor.

Blood tests for those with Elevated AST

ALT is said to be a more liver ‘specific’ enzyme. AST can be elevated in many conditions including thyroid disorders, muscle disorder, celiac disease and blood problems causing hemolysis. Alcohol consumption can injure the liver and raise AST. Generally the ratio of AST to ALT is above 2:1 in alcoholic liver disease (often 3:1 or more) It’s not common for AST to be elevated and ALT to be normal in alcoholic liver disease.

AST is rich in heart tissue, liver, muscle, kidney, pancreas, brain and red blood cells. You can quickly see that elevated AST can come from many sources - not only the liver. For this reason, it is often said that ALT is more specific test for liver injury. A work up by a liver doctor is reasonable to help sort all this out (see below).

If AST is the only test that’s really elevated (and ALT, bilirubin and the other tests are normal), you’ll want to consider the possibility of something known as “macro‐AST” as a possible cause for this increase in AST. Using a special lab test involving precipitation with polyethylene glycol (PEG), ultracentrifugation and gel filtration chromatography (GFC) the lab can determine a person’s true AST level.

Macro AST is generally thought to be increased in those with various autoimmune issues and tends to occur when AST forms complexes each other or with immunoglobulins (like IgG and IgA) in the blood stream. Because these complexes are so big, they can’t be cleared by the kidneys very easily so they just accumulate in the blood.

In 2011, Lee and colleagues suggested that about 13% to 60 % of those being evaluated for elevated AST levels had macro AST.

It’s difficult sometimes to find a lab that knows how to deal with macro AST testing and perform the necessarily testing to evaluate true AST from macro AST levels. However, a liver doctor will know how to access these tests.

The AST and ALT Ratio: DeRetis Ratio

A lot of attention is often paid to the ratio of AST and ALT in liver disease. It’s not very specific. But AST to ALT levels well above 3:1 are often seen in alcoholic liver disease. As mentioned above, one needs to consider macro AST when there is no good history of alcohol use and the rest of the blood tests come back normal.

AST to ALT level are often above 2:1 in alcoholic hepatitis, non alcoholic steatohepatitis, myocardial infarction, drug, and some viral hepatitis infections. Liver cirrhosis and liver metastases often have AST to ALT above 2:1

Levels of AST to ALT are less than 1 (ie ALT is the bigger number) with various liver toxins, hepatocellular injury, viruses (viral hepatitis), and intrahepatitic cholestasis and extrahepatic biliary obstruction

Liver Ultrasound

You’ll want to discuss with your doctors the possibility of having a liver ultrasound scan to further evaluation for any liver issues. This can be a very useful test to evaluate for possible liver disease or disease in the biliary tree.

Referral to a Gastroenterologist or Subspecialty Liver Doctor

Referral to a liver doctor may be advised in some cases. Generally speaking, levels of AST or ALT above 5 time the upper limit of normal make if all the more important to consider referral. With levels of 210, referral to a liver doctor makes good sense. The liver doctor will review the story, perform an examination and review the blood tests (see above) and liver ultrasound findings. The liver doctor will determine if any other tests are needed (liver MRI) and whether a liver biopsy is likely to help.

Certainly a liver doctor will know how to access tests to evaluate for macro AST.

The liver doctor will help formulate the exact reason for the elevated AST and can always refer to other specialists (rheumatologist etc) if this is thought to be helpful. Referral to a rheumatologist is helpful if there is any joint stiffness, fevers or unusual fatigue (and if any of the tests for ANA or autoimmune panels come back positive).

Conclusion and Summary

Thanks for submitting this question. I think it’s important to make sure you’ve had a proper work up and evaluation via all the blood tests. An internist or general practitioner can help get these ordered and can perform a good history and good head to toe examination looking for any concerns. Some of the more autoimmune based tests (ANA, anti SMA, anti LMK) are relevant to anyone with autoimmune disease like LPP but these are often left to the liver doctor to decide how best to order.

A liver ultrasound may be needed to rule out any pathology.

In the setting of completely normal tests, and good health, it may be really important to consider the MACRO-AST phenomenon. Your liver doctor can help you with that.

REFERENCE

Lee M, Vajro P, Keeffe EB. Isolated aspartate aminotransferase elevation: think macro-AST. Dig Dis Sci. 2011;56:311-313.

Giannini EG, Testa R, Savarino V. Liver enzyme alteration: a guide for clinicians.CMAJ. 2005 Feb 1;172(3):367-79. doi: 10.1503/cmaj.1040752

Oh RC et al. Mildly Elevated Liver Transaminase Levels: Causes and Evaluation., Hustead TR, Ali SM, Pantsari MW.Am Fam Physician. 2017 Dec 1;96(11):709-715.

Does finasteride cause beard hair loss?

Does finasteride cause beard hair loss ?

 
I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in beard hair growth patterns among finasteride users.

Question

Dear Dr. Donovan,

I am about to start finasteride 1.25 mg per day. I have a thick beard and my beard is very important to me and my culture. I do not want to lose my beard. I have heard conflicting reports if finasteride can affect my beard or not. What is your opinion? Thank you for your time, sir!

Answer

There are really no great published medical studies which attempt to address this question with any clear scientific rigor. The topic is certainly quite emotion-driven and everyone has an opinion on the answer. Not a week goes by that someone doesn’t ask me about the question.

Most beard growth is governed by genetics. If you have the right genetics, you are more likely to be able to grow a beard. If 50 % of the males in the family reunion are sporting beards, there is a good chance you’ll sport one too. Patients of more Northern European ancestry are generally less able to grow thick beards compared to males from other parts of the world. These are generalizations not rules.

Having treated large number of patients over the years, I absolutely do feel finasteride can affect beard hair growth. Fortunately, it seems fairly uncommon. That’s the key message not to be missed here.

DHT stimulates terminal hair growth of the beard hair as well as hair growth in other areas like the trunk and limbs, external ears and nostrils. It’s clear that 5 alpha reductase is expressed in beard hair follicles dermal papilla cells quite significantly. It would seem that finasteride should affect beard hair more than it does - but it doesn’t.

Responses to finasteride in males are extremely varied - actually they are extremely extremely varied. This is not surprising given that levels of DHT and activity of the 5 alpha reductase enzymes are so different among males in general and in different body sites.

Did I mention yet that responses to finasteride are so varied?

Patterns of beard changes with finasteride

There are several effects on the beard that I have seen over the years. I’ll put my best estimates beside it to give some perspective.

1. Finasteride did not affect my beard hair in any way (95 - 98 % of male users)

2. Finasteride did affect my beard by causing it to grow more slowly but I could still maintain a pretty good beard (2-4% of male users).

3. Finasteride did not affect my beard in any way but did thin my chest hair (1 in 300 male users)

4. Finasteride did affect my beard hair causing it to be thinner and feel less thick. (1 in 200 male users).

5. Finasteride actually seemed to improve my beard (1 in 500 male users).

We really need better studies pertaining to the effects of finasteride and dutasteride on the beard. These are my experiences treating males with hair loss who have beards. I’ve seen pretty convincing evidence that finasteride can effect beard growth but fortunately I’m equally convinced it’s not common.  I think most of what I’ve learned about finasteride and beard growth has come in the last 5 years where males are increasingly likely in North America to grow beards.

I would even say that dutasteride is a bit more likely to cause beard thinning than finasteride but I certainly don’t have near the number of bearded patients on dutasteride to make any reasonable comment. But it seems to point that way. Still, it’s rare.

So what is convincing evidence anyways? Well, convincing evidence means that one notes hair loss or thinning or the beard after starting finasteride or dutasteride and one notes improvement when doses are reduced or stopped and then further thinning again when doses are resumed or increased. This kind of meticulous observation is really what has convinced me over the years that there is in fact a link. Again, it’s rare.

If one needs a thick beard and is not willing to take any chance that their beard will be affected in any way, I would say don’t use oral finasteride. However, if one is willing to accept the extremely small risk that it could have a pretty minor effect on how fast the beard grows then it’s not an issue.

In summary, males using finasteride and dutasteride who have a beard usually don’t notice any changes in their beard. A very small proportion note that it grows slower and a smaller proportion yet notice that it’s thinner than it once was.

I hope this helps and thanks again for the question.

Shedding from Oral Minoxidil: Is there a dread shed?

Does oral minoxidil cause a dread shed?

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

Question

Hi Dr. Donovan!

I am a 23 yr old female who has never had hair loss in my life until I had Covid in March of 2020. Since then, for two years I have had diffuse excessive shedding. It was originally considered a viral acute TE but after a biopsy my dermatologist is considering it chronic TE with possible mild AGA even though I have no history. I have tried supplements, and get blood work done every few months to check hair loss values and nothing is ever abnormal with no other obvious triggers. She put me on oral minoxidil 0.25mg I have been on it for 2 months (went up to 0.625mg on my 6th week of medications). I am still seeing consistent diffuse shedding which feels like it has increased specifically when i shower in the past few weeks.

My dermatologist is saying that oral minoxidil shedding is not common in patients and in the literature so now I feel like I should stop and it is not working for me! I know topical Rogaine dread shed is common.

Is oral minoxidil shedding common as well and for how long might I expect it?

Thanks!

Answer

Thanks for the question! This is so important! Thanks for taking the time to present your question.

Shedding on oral minoxidil is common yes - just not talked about much. In fact, it’s rarely talked about because many in the medical community and lay public have somehow come to view oral minoxidil as low risk and just decided to ignore any side effects. Not everyone of course - but a common view.

In fact, shedding issues are often not talked about in the medical community with many treatments. PRP shedding is not talked about much either!! Try to find studies on shedding with PRP and you won’t find much ! Not a day goes by that I’m not on the phone discussing post PRP shedding with someone somewhere in the world. Why don’t we talk about it? No idea.

So yes, oral minoxidil shedding is not talked about much. The attention is all put on the famous “Rogaine dread shed” which leaves people wondering “do these other treatments cause shedding?
They absolutely do.

I don’t know your reason for hair loss as I haven’t seen your scalp up close and don’t know the whole story AGA is quite likely with a story like this. CTE is pretty unlikely with a story like this. But of course the exact diagnosis comes with a full review of one’s medical information and proper review of the scalp.

Sanabria and collegues remind us about shedding, shedding shedding

Dr Sanabria and her colleagues from Brazil reminded us in 2021 that shedding from oral minoxidil is not really that uncommon. Give oral minoxidil to 2 female patients and guess what? One of them is going to get shedding? Is that rare? No. 1 in 2 people is not rare.

Here are some of the side effects that Sanabria taught us about in her study (see right column) and side effects Dr Vano taught us about in his study (see left column)

Summary

I appreciate your question. Oral minoxidil certainly does give shedding. It can last 3 months or so. It could be that you are not quite on the right dose (yet) so you and your dermatologist can decide if going up to 1.25 mg is right for you or not. If you are not having side effects (other than shedding), sometimes going up makes sense.

In addition, you’ll want to make sure all the other issues are addressed like seborrheic dermatitis, and any other triggers of telogen effluvium (stress, low iron, thyroid problems, medications, supplements, allergic contact dermatitis from shampoos and conditions and products you are using). By the sounds of it your blood tests are good so most causes in the list above seem unlikely. But seborrheic dermatitis always needs to be considered.

Everyone loses more hair on shampooing days so don’t gauge things too much by that. It’s normal to lose double or triple the hairs on a shampooing day especially if you are not shampooing all that often these days. Photos of the top of the scalp are going to be really important (in addition to the shedding patterns you are seeing).

At age 23, the key is to be patient with making adjustments - if possible. I don’t know the details of your hair enough to give much further but generally speaking sticking to a plan for a few months proves more helpful that jumping to another plan too quickly. Giving 0.625 mg a solid three months is not at all unreasonable (and you and your doctors may consider going up to 1.25 mg or even 0.625 mg alternating with 1.25 mg). Stopping minoxidil too quickly usually just creates more confusion than it helps.

You’ll want to review with your doctors if perhaps another COVID infection in Spring or Fall 2022 is contributing to any shedding now or whether seasonal shedding is throwing a bit of confusion into the picture. Any recent vaccinations add to the complexity. Any other medications you’ve used recently need to be factored in.

I thank you for the question and wish you the best.

REFERENCE

Sanabria B et al. Adverse effects of low dose oral minoxidil for androgenetic alopecia in 435 patients. JAAD 2021; 84: 1175-78

Pumpkin Seed Oil: Not a Substitute for Finasteride

Pumpkin Seed Oil for AGA

 
I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in the use of pumpkin seed oil for treating AGA.

Question

I have side effects on finasteride will now reduce to 3 times weekly instead of daily in hopes this will help. iI will also start pumpkin seed oil the other days to help block the DHT. What do you think of this plan?

Answer

Pumpkin seed oil may have minor benefits for treating AGA - but it is not a substitute for finasteride so directly. There are no good studies that really guide us as to how much worse it is than finasteride but it’s certainly not the same at all.

To make things worse there are thousands of brands and purities and methods of processing of pumpkin seed oil. So the kind one person buys is not likely to be the same as the kind another person buys. These are not the same. Running 5 minutes from my parking lot to my office is not the same for health and fitness routine as running 60 minutes across town. They are both considered exercise but one clearly does more than the other.

Both pumpkin seed oil and finasteride and considered (by some) as “DHT blockers”, bu they are not the same - clearly one does much more than the other.

Can I use Oral Minoxidil and Spironolactone Together?

Oral minoxidil and Spironolactone Lower Blood Pressure - But Only Slightly

 
I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in use of oral minoxidil and spironolactone.

Question

My doctor won’t prescribe oral minoxidil and oral spironolactone as he says the two can lower blood pressure to dangerous levels. Is that true? I see many patients combine them.

Answer

Thanks for this question. I can’t say whether you should use them or not as I haven’t reviewed your whole story and haven’t examined your scalp. however, I can say a few pertinent points here!

You’ll want to review a recent prior article on the subject as I think you’ll find it helpful.

SEE ARTICLE: ORAL MINOXIDIL AND SPIRO: CHANGES IN BLOOD PRESSURE

I think you and your doctors just need to ask the key question: how much to they lower blood pressure? Spironolactone lowers blood pressure about 3 mm Hg and oral minoxidil about 1 or 2 mm Hg. So a person might get 5 mm Hg change. For most humans, this is not significant although a small proportion of people really do feel this drop and don’t like that sensation.

Overall, 5 points change in blood pressure is pretty small!

Blood pressure drops a great deal throughout our every day. That’s important to understand.

It drop about 15 points when we are sleeping! It is highest in the morning and drops in the afternoon and evening. It rises when we are stressed and rises quite a bit when exercising. Some have swings of 40-50 points at times during the day!

For the vast majority of people, a few points drop in blood pressure is not harmful. Be sure to discuss with your doctors! I don’t know enough about your story to say if it’s right for you or not. But lots of patients use both oral minoxidil and oral spironolactone at carefully selected doses and proper monitoring.

Hope this helps!

Diagnosing Hair Loss with Trichoscopy: Only Part of the Story

Clinical Decision are Never Made with Trichoscopy of a Single Area

 
I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in how to diagnose hair loss.

Question

In an area of thinning on my scalp I see miniaturization!!

Does it mean I will will need a hair transplant soon.

How do I know how extensive it is?

Answer

First, one should never use trichoscopy photos to make that kind of a decision or give those answers. No.

If this photo you are looking at is from the temples it has a dramatically dramatically different implication than if from the mid scalp and dramatically dramatically different yet if it’s from the back of the scalp. We don’t let the appearance of 50 little hairs dictate what’s happening to the other 95,000!!

You need a full history and a full examination. There are no substitutes for a proper diagnosis. There are many causes of miniaturization. Of course, AGA is the most common but it’s not the only cause and that’s why you need a proper examination ! If your miniaturization is from alopecia areata - a hair transplant is completely off the data.

Don’t be tricked into thinking trichoscopy is the final answer to how we make clinical decision. Not at all. It’s one of many parts of the proper work up and evaluation of hair loss. But one needs a full story and full examination of the scalp in order to make decisions. Your stage of hair loss can only be determined when one has a chance to see the full scalp and see the other 95, 000 hairs too.

Topical vs Oral Minoxidil: Which do you like?

Should I use topical or oral minoxidil?

 
I’ve selected this question below for this week’s question of the week. It allows us to review some concepts in the use of topical and oral minoxidil.

Question

What is your opinion on use of topical vs oral minoxidil as montherapy?

Answer

Thanks for the question.

Both good options to consider. They’ll are not options for everyone, but they are definitely on the table for discussion with your doctors. If you are lucky to be one of the low proportion who get great results with topical minoxidil, I often say go with that. But some just don’t get such good results - and oral can give better results for some people (but certainly not all).

We tend to forget that oral minoxidil has way way more side effects so be sure to review all with your doctor and make sure it’s right for you.

Here are some of the side effects of oral minoxidil that everyone person needs to be aware of.

The frequency of these side effects is approximately shown in the prior studies shown in the table below:

As far as monotherapy, some people have mild AGA that stays mild. A single treatment is sometimes all that is needed. Some have some pretty strong genetics driving AGA and just can’t completely stop it long term with a single treatment. Another treatment is needed also.

Again be sure to review with your doctors.

I make my decision on topical vs oral based on the precise details of the patient and their health and medical history. A 67 year old female with heart failure and 2 prior heart attacks can’t use either. A 32 year old trying to conceive with her second child can’t use either. A 42 year old male who wants a short term option before having a hair transplant at age 44 shouldn’t use either.