What is causing my beard, body and scalp hair loss?

What’s causing my beard hair loss?

I’ve selected this question below for this week’s question of the week. It allows us to discuss the importance of the speed of hair loss in the diagnosis of hair loss.

Here is the question….

QUESTION

I have diffuse thinning across my entire body. I am male, under 30. The hair loss initially started as rapid thinning on the entire scalp, soon spread across facial hair and body hair. Some distinguishable features of my hair loss are that my beard and body hair only have one hair per follicle, a lot of hairs remain as very short stubble and do not grow, eyebrows experience pain during periods of shedding. I've been to 4 dermatologists and had one scalp biopsy which was inconclusive. Hair loss has been very rapid, from initial onset I lost well over 50% of my hair density within 4 months. My beard presented with patches of hair loss which have grown in.

Beard photos, before (left) and right (after) hair loss

Scalp does not itch and I do not feel any burning. However I feel tenderness and itching in my eyebrows which are constantly shedding. I've been on finasteride ( discontinued ), oral minoxidil for 9 weeks, and steroid injections in the eyebrows which have helped with regrowth. Hair loss started 3 months after I experienced a very traumatic event and has continued well over 1 year now.. After the traumatic event I broke out with very severe cystic acne across my back, scalp neck and face and hair loss soon followed. The way I look today is completely indistinguishable from what I looked like 1 year ago.

What is the likely cause ?

ANSWER

Thanks for submitting your question. There are several possible hair loss conditions that could be causing this, but the most likely cause, by far, is alopecia areata. But it’s certainly not 100%.

To help definitively figure out what’s going on, I would need to (1) ideally see photos of the scalp and eyebrows, (2) know the answers to a lot more questions I have, (3) review your biopsy and (4) review all your blood tests. I’d like to know if you’ve had patches of alopecia areata in the past, whether you have a family history of alopecia areata, how thin the eyebrows were, whether their was redness in the eyebrows too, whether the eyelashes were lost, whether you’ve had changes in your nails, weight loss, or abnormalities in your blood tests. I’d want to know if you’ve started or stopped any prescription medications and supplements in the last 12-16 months, started or stopped any anabolic steroids, and whether you’ve had any skin rashes of any sort in the last 2 years. Fevers, night sweats are important to know about as well. Of course, your entire medical history will be important.

The full list of possibilities for the hair loss includes:

1. Alopecia areata alone

2. Alopecia areata with a telogen effluvium

3. Alopecia areata with seborrheic dermatitis

4. Alopecia area with a telogen effluvium with seborrheic dermatitis

5. Alopecia Areata with a telogen effluvium with seborrheic dermatitis with male balding of the scalp.

6. Telogen effluvium with seborrheic dermatitis

7. Frontal fibrosing alopecia/lichen planopilaris

8. Rare mimickers - syphilis, cutaneous T cell lymphoma

There are many features of the story here which fit well with alopecia areata. First, the speed of hair loss is fast. The loss of 50 % density in 4 months is seen in alopecia areata and sometimes telogen effluvium but this kind of rapid hair loss is more typical of alopecia areata. it’s far too fast for androgenetic alopecia but of course this may be a part of the hair loss that is happening as well (more chronically). It’s too fast for most scarring alopecias too (and I would not expect regrowth to occur in the manner you described if this were the case). It’s not impossible for FFA, but it is an uncommon story for FFA.

I’ve written about the importance of the speed of hair loss in the past. Alopecia areata is classically quite fast and has the potential to cause more rapid hair loss than telogen effluvium if the alopecia areata is active.

It’s possible of course, that a person has a telogen effluvium and alopecia areata too. A person can have two diagnoses or three or even four or five. The intense stress you had from the traumatic event can cause a telogen effluvium and if you are genetically predisposed, it could precipitate alopecia areata too.

The regrowth of your eyebrows with steroid injections is best in keeping with alopecia areata. I would need more information to know it it’s a little or a lot of regrowth. It would be helpful to know what the brows actually looked like before. If the regrowth has been really significant with the steroid injections, alopecia areata remains at the top of the list. That said, any inflammatory condition of the eyebrows can cause hair loss and steroid injections can help with regrowth. Seborrheic dermatitis of the eyebrow can cause a little bit of loss but it’s usually mild and steroid injections can settle down the redness and help get brows regrowing. Even frontal fibrosing alopecia can show some regrowth so the simple fact there was regrowth does not prove it is AA. Eyebrows can improve with steroid injections in quite a few conditions so this feature alone does not prove it’s alopecia areata.

The beard photos you’ve submitted are most in keeping with a diagnosis of alopecia areata. Are there mimicking conditions that can look 100% the same ? Yes, there certainly are. Rarely, a seborrheic dermatitis can cause beard loss but that’s quite unusual to be patchy in this manner. Rarely, an immune based issue can cause beard loss too (lichen planopilaris/frontal fibrosing alopecia) but regrowth is less likely in these types of situations. Frontal fibrosing alopecia really is one of the key conditions that you and your doctors need to rule out confidently. Beard hair loss or beard thinning happens in about 30-40 % of patients with FFA. Telogen effluvium affecting the beard in a patchy manner like shown in the photos is not typical so telogen effluvium would not explain the beard loss but could, of course, still be involved. Syphilis is not common cause of the hair loss pattern you are describing but this diagnosis needs to be considered by your doctors in a presentation like this. It is a great mimicker of alopecia areata. A rare condition of the blood cells (mycosis fungoides/cutaneous T cell lymphoma) needs to be considered if things don’t improve. I would not expect these latter two conditions to have spontaneous improvement you have described without treatment so they probably don’t fit well in your particular case. Alopecia areata is still at the top of the list of causes but your dermatologists can review these entities and perform a full skin examination.

The acne eruption you describe may or may not be related to the hair loss. I suspect it is related in some manner. Acne eruptions of this kind can be seen in alopecia areata. (See previous article alopecia areata and acne). In order to understand how hair could have a role in acne development, it is important to understand the function of hair. During the process of normal skin turnover, the shed skin cells from the hair follicle epithelium are carried upward in the follicular canal towards the skin surface. It is thought that the sebum that is secreted by the sebaceous glands helps in this process but helping the shed cells efficiency move out of the hair follicle canal.

Ringrose and colleagues first reported the relationship between acne and alopecia areata back in 1952. They described a male patient who developed acne, milia and cystic type eruptions only in the areas of alopecia. The authors proposed that the hair helps keep the follicular orfice open to allow sebaceous contents to be properly removed. They described the hair follicle as a “natural drain” to the removal of sebum.

These same authors performed some interesting histological studies by examining biopsies of these acne lesions. They found that acne lesions were not seen in areas that contained hair and were not seen in areas where the pilosebaceous unit was completely degenerated. The proposal here was the acne lesions of alopecia areata represented a transition period - between normal growth patterns and complete loss.

in 2007, Sergeant and colleagues proposed that the hair follicle acts as a type of ‘wick’ and acts to draw sebum up towards the skin surface. They stated that the hairs on the scalp may do this more efficiently that hairs on the face and therefore the hairs on the face may be predisposed to the formation of “micocomedones” and the typical lesions of acne. Microcomedones are a prerequisite for the ultimate acne lesion.

So in your case, there is a high likelihood a diagnosis of alopecia areata is present. It is certainly not 100 % but the likelihood is quite high. It will be really helpful to follow all hair bearing areas - as definitive signs of alopecia areata (or scarring alopecia or another condition) may show up over time. In my opinion, frontal fibrosing alopecia is the mimicker that really needs to be ruled out.

FINAL COMMENTS

At this point, the evidence would suggest alopecia areata but I would need more information to confirm or refute that. I would recommend that you speak to your doctors about these issues as they will know your case best. I would suggest you considering asking them about blood tests for CBC, TSH, ferritin, testosterone, B12, ESR, ANA, zinc, vitamin D, RPR, creatinine, AST, ALT, urinalysis if you have not already. if any of these are missing you might get them done. If the diagnosis is not clear, a repeat scalp biopsy can be considered. It may be that with trichoscopy a dermatologist can evaluate whether alopecia areata is present although I certainly do appreciate that your story is complex and you’ve probably had many evaluations (with trichoscopy too). Biopsies of the arm hair, leg hair and eyebrows are trickier and often given less information. If a repeat biopsy is needed, it should come from the scalp. The main thing we are trying to distuish in the biopsy is alopecia areata vs scarring alopecia (ie frontal fibrosing alopecia) .

If it is alopecia areata that you have, I suspect that over time, a patch of typical alopecia areata hair loss will occur that will allow your doctor to definitively tell you if that’s what it is. There are ways to explore the diagnostic possibilities further. Certainly, the blood tests above are important. You’ll want to make sure there are no systemic issues that increase the chances for cystic acne and hair loss. We’ve spoken about the possibility of having a repeat biopsy. This should be done on the scalp and be 4 mm and be done with horizontal sections and read by an expert dermatopathologist. Alopecia areata can be tricky to diagnose in some cases. However, an increased proportion of catagen and telogen hairs and eosinophils in the tracts and peribulbar inflammation can all point to the diagnosis. A biopsy will pick up immune based issues, lymphomas, and if the percent of telogen hairs is high the biopsies will give an idea of how high it really is.

Sometimes in a situation like this, we consider a "therapeutic challenge.” A therapeutic challenge means we give certain medications to observe what happens when those medications are given. If the response to the medications is exactly what we predicted, it suggests we are probably correct with our diagnosis. I would need to know more about your story to describe exactly what might be appropriate but you and your doctor could consider therapeutic challenges like steroid injections to the entire scalp, or a 4-6 week course of oral steroids is an approach therapeutic challenge if alopecia areata is considered. If you get significant regrowth during these types of therapies, it’s a pretty good indication that there is an inflammatory issue that was blocking the growth of hair. Alopecia areata would be the most likely diagnosis in such as case.

If alopecia areata is the final diagnosis, then continued beard injections together with other systemic options would be possible including dexamethasone, methotrexate, cyclosporine, tofacitinib. A return to oral minoxidil could be reconsidered depending on exactly what your story was when you stopped it

Thanks again for submitting your case. I hope this was helpful.

What's the reason for my hair loss? What does my trichoscopy show?

Why am I experiencing hair loss?

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 interpreting trichoscopy and how the clinical history must be interpreted together with all trichoscopic analyses.

Here is the question….

QUESTION

I really hope you can help me with the diagnosis of my hair loss that I've been experiencing for a year now without being able to get a real diagnosis, doctors can't seem to find anything else than '' light dermatitis'', yet I can' t help but notice everyday that this isn't normal and I have no clue so far. 
About a year ago I suddenly noticed that I had way less hair and I could see my scalp, which never happened before. A few weeks later I've started to notice redness in my scalp and itching that never left ever since. The itching seems to come and go without any logical pattern, and the more red and itching my scalp gets, the more hair I seem to lose. I did a trichoscopy 2 weeks ago, where you can see the results.

I'm quite desperate to get a real diagnosis because I don't think something innocuous would last that long and cause hair loss without stopping. Overall I am in good health. Blood tests were all okay 

ANSWER

This is a great question because it allows us to talk about so many things.

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.

I can’t be sure of what’s going on entirely without seeing your scalp up close myself and knowing your entire story. Your age, and details about your scalp symptoms all matter.

In my opinion there are 4 possibilities for what you have:

1. Androgenetic alopecia with seborrheic dermatitis (AGA + SD)

2. Androgenetic alopecia with mild telogen effluvium with seborrheic dermatitis (AGA + TE+ SD)

3. Mild telogen effluvium with seborrheic dermatitis (TE + SD)

4. Seborrheic dermatitis alone (SD alone)

I’d like to make a few comments about the type of thinking that is needed in case like this.

A few comments

1. It’s true that you have very nice trichoscopy pictures - but what’s also important is just getting a sense if the frontal density is truly the same as the back. There certainly is a suggestion that your frontal density may be less than the back (occipital area) despite all the numbers that you see in your measurements. If there truly is a significant difference in the density in the frontal and back then we need to think about a patterned hair loss (ie androgenetic alopecia).

2. A physician can get a better sense of density by parting the hair down the middle from front to back and comparing the part width in the front to the back. If the part width is wider in the front than the back that means there may be more hair loss in the front compared to the back - and this might be a suggestion that there is some degree of androgenetic alopecia.

3. It does seem that your blood tests have been normal so we’ll assume that. This does not mean that a person can not have telogen effluvium or androgenetic alopecia with normal blood tests. In fact, most people with hair loss have normal blood tests. I have not seen your blood tests of course, but I would hope that you have had CBC, TSH, ferritin, 25 hydroxyvitamin D. If your periods are irregular you should have a hormonal panel. If you have other symptoms, you might need other testing too.

4. There appears to be clear differences with the photos in the frontal areas compared to the occipital (back) areas including more single hairs and less density. While this could be simply suggesting diffuse loss as in a telogen effluvium, we need to consider the possibility that this could represent a pattern to the loss (and female pattern alopecia also called androgenetic alopecia).

5. Your average hair caliber seems to be lower than expected at 60 um. This depends on your background and your type of hair but it certainly does make me wonder if there is some change happening that affect caliber especially a diffuse process like a diffuse AGA. Of course, androgenetic alopecia is one of the more common hair loss conditions that affect caliber. Your data from the trichoscopy is not definite so I can’t completely rule in or rule out this particular diagnosis.

6. If you do not have much in the way of increased shedding, I would favour a diagnosis of AGA. If there is a lot of shedding that you have, it still could be AGA but a mild effluvium (TE) certainly does not need to be considered. Your story of suddenly “noticing” that you have less hair is more typical of AGA than TE. The degree that you are shedding today and the degree that you have been shedding in the past 6-9 months would sway me someone as far as how likely a diagnosis of TE really is.

7. I do favour options 1 and 2 but it’s by no means definite based on the information you have given. It will be helpful to follow the trichsocopy measurements over time. If you have a TE like in option 3, the measurements and numbers will likely get better over time. If it’s an AGA (option 1 and 2), the numbers will not likely improve and may get slightly worse in 6-12 months. Photos will also be very helpful. If it does become clear that the density in the frontal areas is slightly less than the back of the scalp, one needs to consider androgenetic alopecia.

8. If you are concerned a scalp biopsy or a 5 day modified hair wash test might help. Sometimes in the very early stages a a biopsy only slightly helpful so I am not of the opinion that you must have a biopsy. However, if the terminal to vellus ratio of your biopsy is shown to be less than 4:1 it indicates androgenetic alopecia is likely to be present. If the terminal to vellus ratio is above 4:1 is suggests that TE alone (option 3 or 4) is more likely. A biopsy can also capture any rare mimickers of redness such as lichen planopilaris, although I do not suspect that is what is going on (the density and changes are far too similar in the 3 areas to really support early LPP - and the story I have so far and the trichoscopy does not really support that diagnosis). A modified hair wash test can give a sense of how many hairs are being shed and whether any of these are small. What’s interesting in your photos is that it does appear that there are more vellus hairs in the photos from the frontal area than the measurements state in the information you were given. I am personally a big believer not only in looking at the measurements these computers give but also in looking at the images myself and looking at the scalp myself and getting sense if the measurements the computer gives makes sense or not. The presence of thinner and thinner hairs (miniaturized hairs) and the presence of thinner and shorter hairs (vellus hairs) is what androgenetic alopecia is all about.

9. I do think that there is likely a component of seborrheic dermatitis complicating the picture here. Your dermatologist can review with you at your next appointment. The trichoscopy would suggest this as well. SD is not typically a major cause of hair loss but can give a bit of shedding if severe enough. If you do have SD, it is mild and may contribute to symptoms like itching and tingling from time to time and then there will be periods where the scalp feels good again. The involvement of the temples is quite typical of SD and your photos are noticeably most red in the temples. There are no signs of scarring alopecia in the trichoscopy images provided but again a biopsy can help further clarify.

FINAL SUMMARY

Thanks for the great question. With the information provided, I can’t say one way or another exactly what is the diagnosis. However, a scalp biopsy or 5 day modified hair wash test could take you that much closer to understanding the diagnosis if there is really debate. I am suspicious about their being androgenetic alopecia here but I can’t tell for sure and ideally would want to see the scalp in a situation like this. Once you have the proper diagnosis, you can plan treatment. In addition, it is going to become much clearer over time what the diagnosis is especially if you do repeat trichoscopy measurements in 6 and 12 months. The frontal density and caliber of the hair in the frontal area will decrease and the number of single hairs is going to increase in the frontal if AGA is truly what is present. For now, treating the seborrheic dermatitis is quite reasonable. I would normally recommend that efforts be put into confirming the diagnosis with certainty. Some of the treatments for TE overlap with AGA treatments including laser and topical minoxidil and oral minoxidil so one can certainly get started with a plan once the diagnosis is made. Certain other treatments however, like anti androgens, are only effective in AGA and will not be effective if TE is the true diagnosis.

Thank you for your question.

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.
   
   

Constant hair shedding for 2 years: Is the diagnosis TE or something else?

2 years of constant hair shedding: Is this just a TE?

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 the topic of chronic hair shedding. Hair shedding is often felt by some to be synonymous with telogen effluvium. This is incorrect.

Here is the question….

QUESTON

Hello. Would I be able to ask you a question about TE? I first experienced this in July 2018 4 months after I had my son by c section. Since July 2018 my hair fall has continued at a consistent rate of 70-80 hairs a day. Mostly all falling out in the shower. I’ve had all my blood work done by my doctor and he did a hair pull test and just says it’s TE. What do I do now that it’s almost been 2 years of constant fall out? Mind you the hairs are growing back in, tapered at the ends, sticking straight up, ALL over my entire scalp. The excessive hair fall is not stopping, which makes my hair look extremely thin even though they’re growing back in when one falls out.  
Any advice would be appreciated. My doctor wants me to try rogaine 2% and I don’t know if that’s the solution or not. 

Thank you in advance... 

ANSWER

Thanks for the question and probably one of the most common scenarios I encounter with female hair loss. 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. I’d like to know what blood tests were done in your case and what the results were. I’d like to know if there is any itching, burning or pain in the scalp. 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 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. I’d like to know the precise age of thee patient. All these things matter in fully answering these questions.

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

You might have telogen effluvium. But the main point here and the entire reason I chose this as the question of the week, is you might not have TE as the diagnosis or a TE might not be the main reason. I feel strongly that you need another examination or a scalp biopsy.

First, let’s take a look at the reasons why your shedding is not stopping. There are several reasons why shedding does not stop in women. I don’t know anything about your story and don’t have photos of your scalp so I can’t say which of these 3 reasons (see below) it is. However, I’d encourage you to meet with an expert dermatologist as he or she might assist you in determining which of the following is applicable to you.

REASON 1: You have telogen effluvium, but you have not found the trigger

I’d possible you have telogen effluvium as the “only” diagnosis, but I doubt it. If, in fact, you do have isolated TE, then you may still be shedding because you have not found the trigger of the shedding. Causes of telogen effluvium include stress, low iron, thyroid problems, medications, crash diets, weight loss, illness inside the body. Which one is relevant to you?

I’m hoping you have had blood tests done already … but if not, you need them. A person with shedding of hair needs CBC, TSH, ferritin, vitamin D at minimum. In someone with your story, other tests like ANA, zinc, testosterone, DHEAS, ESR, VDRL may be important to consider. There could be other tests you need too! The exact tests that you need depend on your entire story. There are about 50 tests possible but most people need 5-10. It would only be possible for me to list the blood tests you need if I knew about your entire story from A to Z

it’s possible you are still shedding because there still is a trigger telling your hair to shed. If so, you are your doctor need to find it. Is there something in the blood test results? Do you need more blood tests? is there a medication causing your shedding - like birth control? like a prescription mediation? Do you have any medical issues that you do or don’t know about that are causing the shedding? Is your diet adequate to sustain hair growth?

REASON 2 You have telogen effluvium but also have another diagnosis or you don’t really have TE at all

You might have telogen effluvium but there may be a second diagnosis present that you are your doctor are not recognizing - or you might not really have TE at all. The most common scenario is a patient who has TE but also has evolving androgenetic alopecia (AGA). It’s not uncommon for AGA to start in some when after delivery of a baby and then progressively get worse. When the condition first starts up the only thing that is experienced by the patient is shedding. For many women with AGA, this shedding is all over the scalp so this fact alone does not just mean you could only have TE.

So, it could be that you have TE + AGA or it could be that you don’t really have TE but rather you have only AGA that is mimicking TE. If you feel there is less hair on your hair today compared to one year ago, then there is a reasonable high chance you have AGA as one of your diagnoses or the only diagnosis. If there is the SAME amount of hair on your scalp compared to 1 year ago, then it’s still possible that TE is the only diagnosis that you have.

Be sure to see a dermatologist who specializes in hair loss for the proper diagnosis. A skilled dermatologist might be able to determine if you have androgenetic alopecia (also known as female pattern hair loss) simply by looking at the scalp with dermosopy. If not, then a scalp biopsy can be done. If you want to get some clues yourself, then you might consider performing a test yourself known as the five day modified hair wash test.

You can read more about this in the link above, but it essentially involves collecting every single hair that exits your scalp exactly five days after not shampooing your hair. If you see mostly long hair, it’s like TE. As a person starts to see an increasing number of short hairs, the possibility of androgenetic alopecia goes up. Now, I always suggest that the 5 day wash test be explained to your properly by your dermatologist and then interpreted properly by your dermatologist. But it is an option to get further clues about what diagnosis might be going on .

We also need to keep in mind that there are many other conditions besides just AGA and TE that cause shedding. Scarring alopecias are one of them. Lichen planopialris for example can cause constant shedding. It woudl be unusual for a person with your story to have scarring alopecia but not impossible. If there is burning on the scalp or tender sore areas on the scalp or redness in the scalp, the chances that a person has scarring alopecia goes up a bit. Alopecia areata incognito (a form of alopecia aerate) is another cause of shedding that mimics TE. A consultation with an experienced dermatologist can help determine if you have any other mimickers of telogen effluvium.

REASON 3: You have chronic idiopathic telogen effluvium or what is termed “CTE”

A person with chronic shedding may have CTE. Your story is certainly not typical of CTE but you’ll probably hear that term thrown around a lot. Most women with classic CTE have thick hair that sheds and sheds and sheds. Thinning is not obvious. You are in the wrong age group for CTE. You have what sounds like progressive thinning. While you could ‘potentially’ have a TE that follows what we talked about under reason 1, you probably don't have CTE. Again, a dermatologist can assist you.

SUMMARY

In summary, you might want to see an expert dermatologist in your city for diagnosis. I’m suspicious that TE is the only diagnosis you have. It might not be. You need to make sure you’ve had a proper examination and determine if other issues like AGA, alopecia areata or scarring alopecia are at all present on your scalp. The most likely of all of these is AGA. You need to make sure that you’ve had all the blood tests ordered based on your story. There may be 5 tests you need or 25 tests -it depends on your story that you share with your doctor. If anyone is still not sure about the diagnosis or you yourself are not confident with the diagnosis being told to you, a modified hair wash test could be a first step, or a scalp biopsy. A biopsy woudl be preferred in your case. A properly done scalp biopsy with horizontal sections and determination of the so called terminal to vellus ratio (T:V ratio) is going to go a long way to helping. IF your T:V is above 4 with lots of telogen hairs in the biopsy (above 15%), then isolated TE may be what you do have. If your T:V ratio in the biopsy is less than 4:1 then you probably have AGA. The biopsy can also help determine if you do have scarring alopecia or do have alopecia areata.

I hope this helps.

Good luck,

Why am I shedding with zinc supplements?

Localized Shedding with zinc supplements

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 zinc on the human body and how to approach atypical or unexpected reactions in the human body.

Here is the question….

QUESTION

I shed hair when taking zinc supplements. I cannot find any information on this at all. Most suggest zinc helps the hair cycle not cut it short and shed. The shedding appears to occur in locations that already had issues. It is not global (all over the body).  Is zinc connected to the hair growth/shed cycle or is it inflammation? Thank you.

ANSWER

This is a terrific question. Not one that I encounter often - but a fascinating one. There’s a lot to review with this 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. It could be relevant if the patient takes zinc for one weekend because they heard it was good to boost their immune system or took zinc for one year to finish the bottle that they purchased one day on sale. It could matter if the patient is obese or thin, malnourished or well nourished and elderly or young. It could matter if the patients knows their actual zinc levels through blood tests or not. Finally, it could matter and probably does matter if the patient has early staged adnrogenetic alopecia, mid staged androgenetic alopecia or advanced androgenetic alopecia. All these things matter in fully answering these questions.

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

WHAT’S THE MOST LIKELY EXPLANATION FOR SHEDDING WITH ZINC?

Well, the most likely explanation (given that I don’t know anything else about you), is that:

1) you have some male pattern balding and you are not using finasteride or dutasteride to treat your male balding and that zinc has trigger a mild effluvium of hairs that are in the early balding phase. We call this phenomenon immediate telogen release and it’s common with every treatment that acts on male balding including minoxidil, laser therapy, PRP therapy, finasteride therapy …. and sometimes zinc.

2) The second explanation is that you actually do have diffuse loss of hair on the scalp and you are just noticing it more in the areas that are already thin. In this scenario, the male balding has nothing to do with the discussion, it just so happens you notice hair loss more in areas that are already thinner.

3) The third explanation is that you have something else going on that is not related at all.

It zinc related to my hair loss? A Closer Look at the Naranjo Scale

Before we go further, I’d like to introduce you and readers to a wonderful system of determining how likely it is that a person’s rare observation is linked to the drug or supplement they are taking. It’s called the Naranjo Scale. I always refer to the Naranjo scoring system when some observation a patient is experiencing is uncommon because it helps to get a better sense of just how plausible things really are. If someone tells me their new supplement is causing hair loss, I might pull up the Naranjo Scale. If someone tells me their new cat is causing them hair loss, I might pull up the Naranjo Scale. We’ll take a look at this scale in a moment.

Now, it seems pretty obvious that if you say that when you take zinc you get more shedding that I believe you that zinc is causing your hair shedding. First off, I believe you. I have seen this phenomenon before so I’m not introducing the Naranjo scale as a way to prove whether you are correct in your observation or not. Rather, the Naranjo Scale helps us look at causation with a little greater precision - something a bit more scientific.

The Naranjo scale involves use of 10 simple question. You might want to try it yourself. The questions are below and I’ve worded each questions specifically to pertain to zinc although the Naranjo scarring system itself pertains to any drug not just zinc. You answer “yes", "no" or "don't know" and different points are assigned to each answer (-1, 0, +1, +2). 

Typical Questions in the Naranjo Scale

1. Are there previous conclusive reports of zinc causing hair loss from areas that already have an issue?

Yes (+1) No (0) Do not know or not done (0)

2. Did the shedding appear after zinc was given?

Yes (+2) No (-1) Do not know or not done (0)

3. Did the shedding improve when the zinc was discontinued ?

Yes (+1) No (0) Do not know or not done (0)

4. Did the shedding appear when the zinc was readministered?

Yes (+2) No (-1) Do not know or not done (0)

5. Are there alternative causes that could have caused the shedding?

Yes (-1) No (+2) Do not know or not done (0)

6. Did the shedding reappear when a placebo was given?

Yes (-1) No (+1) Do not know or not done (0)

7. Was the zinc detected in the blood at higher levels?

Yes (+1) No (0) Do not know or not done (0)

8. Was the shedding more severe when the zinc dose was increased, or less severe when the zinc dose was decreased?

Yes (+1) No (0) Do not know or not done (0)

9. Did the patient have a similar shedding to the same or similar zinc pills in any previous exposure?

Yes (+1) No (0) Do not know or not done (0)

10. Was the adverse event confirmed by any objective evidence?

Yes (+1) No (0) Do not know or not done (0)

Determining the Naranjo Score

Scores for the Naranjo Scale can range from -4 to + 13. A score of 0 or less means the likelihood of the drug causing the side effect is doubtful, a score 1 to 4 indicates it is 'possible', a score 5 to 8 means it is 'probable' and a score 9 to 13 means it is 'definite'. The website http://www.pmidcalc.org/index.php provides a free online calculator for clinicians to calculate the Naranjo Score. It is easy to use and has been embedded below as an example. Individuals wanting to know if a specific drug caused hair loss should be sure to speak to their dermatologist. For you, I’m guessing you are somewhere between 5 and 8 and probably and 6 or 7. This just simply reinforces that what you are experiencing is probable.

What are the effects of zinc on the body and on hair ?

Zinc is well known to affect the human body in about 50 different ways. Actually, it’s best to say that there are at least these are the 50 different ways that have been studied. There are probably 250 ways that zinc affects the human body - we just haven’t studied them all. Here are some of the more common effects of zinc under different conditions. You can see that zinc has a profound effect on many hormones, inflammatory markers and immune system components.

Zinc and Hormones.

Zinc has a complex relationship with hormones. Zinc supplementation seems act as an anti androgen in most scenarios. In women with PCOS, it’s clear that zinc supplementation helps PCOS and reduces hirsutism and improves hair loss. However actually hormone levels (DHEAS) don't seem affected. In prostate cancer cells grown in the lab, it’s clear that zinc acts as an androgen receptor blocker. Zinc blocks male hormones.

Zinc containing shampoos have a positive effect on male balding. In a 2003 study, Berger et al showed a benefit for 1 % zinc pyrithione (found in Head and Shoulders and other shampoos). The researchers performed a 6 month randomized study in healthy men 18-49 with Hamilton Norwood type III vertex or type IV baldness to assess the benefits of daily use of 1 % ZP shampoo. The researchers compared growth with zinc pyrithione shampoo compared with three other groups: 1) those using minoxidil 5 % twice daily, 2) those using a placebo shampoo, and 3) those using a combination of minoxidil and the 1 % ZPC shampoo. The results of the study showed hair growth with zinc pyrithione shampoo alone was almost as good as with minoxidil. Whether these effects are due to the anti-inflammatory effects of zinc on yeast and Malassezia (the causes of dandruff and seborrheic dermatitis) or specific zinc effects on the scalp are not clear.

Depsite all the studies showing zinc has antiandrogenic effects, there are studies showing that zinc supplementation may have the effect to increase testosterone. Zinc supplementation to subfertile men increased testosterone and DHT levels and improved the chances that the female partners of these men became pregnant.

SUMMARY AND FINAL CONCLUSION

There is a lot we have learned about zinc so far and here is a lot we still need to learn when it comes to zinc.

For most people, taking zinc doesn’t have any effect on the hair in any way. However, there will be some people who experience a reduction in daily shedding - especially if they had low zinc to begin with. For a very small proportion a bit of shedding might occur for 1-4 weeks but this is not something that is seen commonly. We do see it in patients with early androgenetic balding - but again even then it’s not common. Most individuals with androgenetic hair loss who use zinc either have no effects or experience a slight improvement.

Your question suggests you have a degree of underlying androgenetic alopecia (male balding) and what you are experiencing is a telogen effluvium of the hairs in that area. Of course a dermatologist can help confirm this.

Hairs that are found in the balding areas of the scalp are notiously more loose than hairs that are found in other areas. They wiggle out of the scalp very easily. We refer to this medically by saying that the hairs are in the telogen phase. Taking zinc supplements certainly gives the hairs some 50 to 250 reasons to wiggle out (or shed) but why this happens for some people and not other is not clear.

There are many different so called genetic polymorphisms that people are born with hat affect how they process zinc and what zinc does to the body. These too have been researched over the years. Polymorphisms in IL6 (IL 6 -174) and ZIP2 Lue- (Arg43Arg) are all examples of genetic changes inside of a person’s DNA that affect how they respond to zinc and why one person might respond differently than another person.

If you have used treatments for male balding before (like laser, minoxidil, finasteride, PRP) and developed some shedding when you started these treatments, you are likely to be experiencing the same sort of phenomenon with your zinc. Although it is unusual to shed hair with zinc supplementation, I must add that it is extremely unusual for males who are currently on finasteride to shed hair with zinc supplements given that the androgens pathways inside hairs are so effectively suppressed. Not impossible but unusual in my experience.

If you shed more with higher doses of zinc and less with lower doses of zinc, and stop shedding completely when you stop the zinc pills, the Naranjo score tells us you are onto something. The fact that you shed when you start zinc does not necessarily mean you will continue to shed forever. Just like with finasteride, laser, PRP, minoxidil, most shedding when related to male balding actually settles down in 6-8 weeks. So most men who continue zinc will find their shedding eventually slows down.

I’m not a fan of my patients taking zinc forever. Zinc level should be kept above 85 µg/dL (13 mmol/L) and below 118 µg/dL (18 mmol/L). Excessive zinc causes copper deficiency which is also a rare cause of hair loss. Long term copper deficiency leads to a great number of problems in the body. Zinc should always be taken with the goal to measure zinc levels over time. If you notice shedding every time you take zinc for a few days, that’s one thing, but if you notice shedding everytime you take zinc for months at a time, that’s a different thing. If zinc is causing a pure telogen effluvium due to low copper for example, it is never going to settle down.

As mentioned in the opening it is going to matter if the zinc is taken for the weekend or for one year. The longer the zinc is used (beyond 4 months), the less likely the shedding is due to helpful actions on the balding process and more likely this zinc is detrimental (or something else entirely is going on). It could matter if the patient is obese or thin, malnourished or well nourished and elderly or young. The more obese the patient is (above a BMI of 30) the more likely the zinc supplementation is going to significantly change hormones, insulin sensitivity and lipid metabolism. Mind you, these changes are probably for the good, but there is a chance they are going to set off some shedding in these patients. It could matter if the patients knows their actual zinc levels through blood tests or not. If one is taking zinc, and the levels skyrocket above 150 ug/dl (23 mmol/L) we often see zinc issues with the hair.

Finally, I hope I’ve made the point that all of this probably does matter if the patient has early staged androgenetic alopecia, mid staged androgenetic alopecia or advanced androgenetic alopecia. The earlier the AGA the more likely that zinc is going to cause a bit of temporary shedding. It’s still an uncommon phenomenon overall - but it’s the patients with early AGA that are the most likely to report shedding with zinc supplements in our clinic.

I hope this helps. It’s an interesting question and you and your doctor may want to consider how zinc is potentially affecting the androgenetic hair loss issues on the scalp and how the levels of zinc are changing over time when you supplement. The actual levels of testosterone and DHT may or may not have any relevance because some people could have slight elevations without it actually causing hair loss (or actually inhibiting hair loss as time goes by.

Thank again for the question.

Reference

Barnett et al. Effect of Zinc Supplementation on Serum Zinc Concentration and T Cell Proliferation in Nursing Home Elderly: A Randomized, Double-Blind, Placebo-Controlled Trial. Am J Clin Nutr 2016 Mar;103(3):942-51.

Ebrahimi et al. The Effects of Magnesium and Zinc Co-Supplementation on Biomarkers of Inflammation and Oxidative Stress, and Gene Expression Related to Inflammation in Polycystic Ovary Syndrome: A Randomized Controlled Clinical Trial. Biol Trace Elem Res 2018 Aug;184(2):300-307.

Foroozanfard et al. Effects of Zinc Supplementation on Markers of Insulin Resistance and Lipid Profiles in Women With Polycystic Ovary Syndrome: A Randomized, Double-Blind, Placebo-Controlled Trial. Clin Endocrinol Diabetes. 2015 Apr;123(4):215-20.

Giacconi et al. Effect of ZIP2 Gln/Arg/Leu (rs2234632) Polymorphism on Zinc Homeostasis and Inflammatory Response Following Zinc Supplementation. Biofactors.. Nov-Dec 2015;41(6):414-23.

Hosui et al. Long-Term Zinc Supplementation Improves Liver Function and Decreases the Risk of Developing Hepatocellular Carcinoma. Nutrients. 2018 Dec 10;10(12):1955

Jamillan et al. Effects of Zinc Supplementation on Endocrine Outcomes in Women With Polycystic Ovary Syndrome: A Randomized, Double-Blind, Placebo-Controlled TrialTrace Elem Res. 2016 Apr;170(2):271-8.

Kahmann et al. Zinc Supplementation in the Elderly Reduces Spontaneous Inflammatory Cytokine Release and Restores T Cell Functions. Rejuvenation Res. . 2008 Feb;11(1):227-37.

Kim et al. Effect of Zinc Supplementation on Inflammatory Markers and Adipokines in Young Obese Women.Biological Trace Element Research 2014 Feb;157(2):101-6.

Lomagno et al. Increasing Iron and Zinc in Pre-Menopausal Women and Its Effects on Mood and Cognition: A Systematic Review. Nutrients. 2014 Nov 14;6(11):5117-41.

Mariani et al. Effect of Zinc Supplementation on Plasma IL-6 and MCP-1 Production and NK Cell Function in Healthy Elderly: Interactive Influence of +647 MT1a and -174 IL-6 Polymorphic Alleles. Exp Geront.  2008 May;43(5):462-71.

Mocchegiani et al. Zinc: Dietary Intake and Impact of Supplementation on Immune Function in Elderly. Age.  2013 Jun;35(3):839-60.

Ranasinghe et al . Zinc Supplementation in Prediabetes: A Randomized Double-Blind Placebo-Controlled Clinical Trial. J Diabetes. 2018 May;10(5):386-397.

Aggressive telogen effluvium in males: A common misdiagnosis of androgenetic alopecia

Question

I am a 23 year old male and have been diagnosed with fairly aggressive case of telogen effluvium. It started at age 21 and does not seem to be improving. I have been using biotin supplements recently but they too don’t seem to be helping. I am healthy and take no medications or drugs. What are your recommendations to stop the shedding?

Answer

Thanks for the great question. I think the most important consideration for you is whether, in fact, you have been given the correct diagnosis. I would need to see photos and know everything about your story and recent blood test results to tell you what diagnosis you have. However, androgenetic alopecia (male balding) needs to be considered in your case. In fact, I would state it even more boldly: in a situation like this with a 2 year history of hair loss in a 23 year old male, we need to prove that you don’t have androgenetic alopecia before moving any further. Once we deal with that, we can move on.

Far too many cases I see that are diagnosed as being telogen effluvium are misdiagnoses. Does telogen effluvium exist? Of course! In fact it is a common cause of shedding in patients with hair loss. Is 2 years of telogen effluvium common in a 23 year old healthy male? No, it most certainly is not.


Telogen effluvium happens from a variety of reasons. These include low iron levels, thyroid problems, stress, medications and illness. In most cases, they are temporary and once the trigger is identified and stopped or fixed- hair grows back. In your case we need to look for a trigger but the reality is that after two years of shedding in a healthy male, there may not be one. It’s still important to search.

Most cases of aggressive telogen effluvium in young males are in fact cases of aggressive androgenetic alopecia instead. It is commonly forgotten that androgenetic alopecia in males can be associated with shedding. In young males with strong genetics that is driving the balding process, shedding can be quite significant.

A male with shedding needs of course to have a full evaluation. One needs to know your history in precise detail. Underlying health conditions, medications, recreational drugs, sexual transmitted diseases, diet, eating disorders and psychological issues all need to be considered.

Young males with shedding need blood tests for CBC, iron (ferritin), thyroid (TSH) and vitamin D (25 hydroxyvitamin D). A hormonal profile is not useful for most males. Other tests could be relevant on a case by case basis including zinc, ANA, ESR and tests for sexually transmitted diseases but usually these are unnecessary.

If there is any doubt that exists, a scalp biopsy can be helpful in proving or disproving whether a patient has androgenetic alopecia - especially when so called “horizontal sections” are used by the pathology lab. Horizontal sections allow the pathologist to determine accurately something called the terminal to vellus (T:V) ratio. A terminal to vellus ratio of less than 4:1 indicates a high likelihood of androgenetic alopecia.

In summary, for a young male a diagnosis of “aggressive telogen effluvium” one must be absolutely certain that a diagnosis of androgenetic alopecia is not being missed.

Minoxidil Itching: What are the important considerations and actions?

Question:

Is it possible that patients using minoxidil get itching because of the minoxidil and that this itching in turn causes more hair loss. I have tried both foam as well as liquid form, but still get itching. Can you tell me a prescription for minoxidil compounded in glycerin, water and ethanol.

Do you have any suggestions?

Answer

Thanks for the excellent question. Itching is often experienced by users of minoxidil. An accurate diagnosis of the precise cause of the itching is important for anyone because there are actually many causes of itching in minoxidil users. The top three considerations for you and your physicians to sort out are 1) Is minoxidil worsening an underlying seborrheic dermatitis? 2) Am I allergic or irritated by minoxidil? 3) Do I actually have another itching diagnosis that has been missed?

1) Is minoxidil worsening an underlying seborrheic dermatitis?

We’ll begin by talking about seborrheic dermatitis. This is a common condition and minoxidil can make it worse for some users. For patients with itching associated with minoxidil use, one needs a full review by their physician. I often advise patients to shampoo daily and add a few anti-dandruff shampoos to their routines. Ketconazole shampoo on Monday, Zinc pyrithione shampoo Tuesday and selenium sulphide Wednesday and then repeat. These should be applied for 60 seconds each application. Often the itching improves dramatically with these shampoos.

2) Am I allergic or irritated by minoxidil?

If there is a concern about allergy, I advise patients to apply the minoxidil twice daily to the inner forearm for 1-2 weeks and observe if an irritation or true allergy develops. This is called a “repeat open application test” (ROAT). Photos should be take daily and shown to a physician. A dermatologist can guide if a true allergic contact dermatitis has developed. Some patients are allergic or highly irritated by the ingredients in the formulation (such as propylene glycol in the liquid form) but some a truly allergic to minoxidil. A dermatologist can perform a standard patch test if doubt still exists after the patient performs and analyzes the ROAT.

It irritation to propylene glycol is suspected, minoxidil can be made up (compounded) in 20 % glycerin, 20 % water and 60 % ethanol. The fact that the patient in this question is still itchy with the PG free “foam” formulation makes it less likely the glycerin compounded formulation is actually going to help. As an alternative 2 % minoxidil can be used as it often has less PG.

3) Do I actually have another itching diagnosis that has been missed?

In situations like this, one always needs to keep an open mind that another itching diagnosis is present too or instead. This is not a common scenario but one can imagine a patient with lichen planopilaris (LPP) who was misdiagnosed as having AGA. Minoxidil can make active LPP worse.

In summary, there are many reasons to be itchy from minoxidil. Only in more severe cases does it cause hair loss. A methodical approach often reveals the cause and best options to reduce itching. Readers may also be interested in my previous article

I’m Itchy from Minoxidil: What Should I do?

Finasteride Use and Breast Cancer in Women

Question:

I read your recent article discussing the risk of breast cancer in spironolactone users. Do women using finasteride place themselves at increased risk of breast cancer?

ANSWER:

Thanks for the question. We received quite a few inquiries last week when I posted this question:

Does Using Spironolactone Increase the Risk of Breast Cancer?

This week, I’d like to address the evidence for another group of antiandrogens known as the 5 alpha reductase inhibitors. This includes finasteride and dutasteride. To date, there is no good evidence to support the notion that use of oral anti-androgens such as finasteride or spironolactone are associated with an increased risk of breast cancer in women either in the general population or in women at increased risk of breast cancer. For finasteride, studies in women have never been done and we rely entirely on studies in males at low risk. For women, only a few studies have looked at breast cancer risks in spironolactone users. These studies have not suggested an increased risk of cancer in spironolactone users who are at low risk for breast cancer. 

 We do not have data on the risk of breast cancer in users of anti-androgens at highest risk. If the patient or her treating physicians feels that her risk of breast cancer may be higher than current estimates then the drug might not be used given that we have no information about the risks in these high risk groups.  I will first address what is known at present about the risk of breast cancer from finasteride and then address how a patient may come to get a better estimate of risk.  References for all the studies discussed are provided at the end.

Finasteride and Breast Cancer Risk: No studies in Women

For finasteride-related risk, the best means we have in the present day of addressing this question is by looking at the risk of breast cancer in men using finasteride and extrapolating the data the best we can to estimate the potential risk in female users.  We do not have studies in women. Male breast cancer is a rare condition with a lifetime risk of 0.1 %. In men, its behavior is similar to breast carcinoma in postmenopausal women.  So while studying male breast cancer and extrapolating the information to female breast cancer is not ideal, it is the best method we have in the present day.

There have been case reports and clinical trial results that suggested that treatment with 5ARIs may be associated with male breast cancer. Most studies to date however, suggest that it is not. All data needs to be taken into context with all available data to date. It should be noted that a warning label has been placed on finasteride packaging in many countries until this issue is further evaluated. An evidence review by the United Kingdom’s (UK) national drug agency resulted in a finasteride drug warning label for breast cancer in the UK and Canada and initiation of an FDA safety probe for all 5ARIs in 2010.

It is impossible to ascertain risk of cancer from the original short duration clinical trials. In other words, one is not going to get a sense of the risk of breast cancer by looking up a journal article about a 1 or 2 year study with finasteride. It’s far too short of a period. This is because such typical clinical trials are neither large enough nor have long enough follow-up to identify male breast cancer cases in men who use finasteride. The best type of studies we have at present are observational studies where men with breast cancer are compared to men without breast cancer. Such “case-control studies” are an invaluable tool to assess this important question. I will review many such case control studies below. 

A. 2016-2018 PUBLISHED STUDIES ON FINASTERIDE AND BREAST CANCER IN MEN

 

Meijer and colleagues recently assessed the possible relationship between finasteride and breast cancer by combining nationwide registers in 4 countries (Denmark, Finland, Norway, and Sweden) to assess the potential association between finasteride and male breast cancer.  A cohort of all males with dispensed finasteride (1,365,088 person years) was followed up for up to 15 years for breast cancer, and compared to a cohort of males not receiving finasteride.  An increased risk of male breast cancer was found among finasteride users (IRR = 1.44, 95% confidence interval [95% CI] = 1.11-1.88) compared to nonusers.  The analyses suggested possible ascertainment bias and did not support a clear relationship between dispensed finasteride and male breast cancer.  

Hagberg et al conducted a cohort study with nested case–control analyses using the UK Clinical Practice Research Datalink. 5ARI users did not have an increased risk of breast cancer compared to unexposed men (OR=1.52, 95% CI 0.61–3.80).

B. 2013-2015 PUBLISHED STUDIESON FINASTERIDE AND BREAST CANCER IN MEN

In 2014, Duijnhoven and colleagues in the Netherlands performed acase-control study with data from the United Kingdom Clinical Practice Research Datalink database among all men aged 45 years and older. Cases of men diagnosed with breast cancer were matched to up 10 controls. There were 398 cases were identified and matched to 3,930 controls. The “ever use” of 5-ARIs was associated with an adjusted odds ratio for breast cancer of 1.08 (95 % CI 0.62-1.87) compared to non-users. Increasing cumulative duration of treatment showed no increasing risks. The conclusion here in Duijnhoven’s study was that there was no evidence of an association between short- or long-term treatment with 5-ARIs and the risk for breast cancer in older men.

In 2013, Bird and colleagues in the United States published a cased control study of men age 40 to 85 years old. Here there were 339 breast cancer cases matched to 6,780 controls. There were no statistically significant associations observed between 5α-reductase inhibitors and breast cancer regardless of exposure assessment. Their conclusion was that the lack of an association in our study suggests that the development of breast cancer should not influence the prescribing of 5α-reductase inhibitor therapy.

 

C. 2003-2012 PUBLISHED STUDIESON FINASTERIDE AND BREAST CANCER IN MEN

In the 2003 PCPT study, Thompson and colleagues published data on 18882 men aged 55 years or older who were randomized to treatment with 5 mg/day finasteride (n = 9423) or placebo (n = 9459) for 7 years. One case of breast cancer was reported as an adverse experience in each treatment group during the study.  In this very large long-term study, an increased incidence of breast cancer in the finasteride group compared to placebo was not observed.

The main study that drew attention to a potential relationship between finasteride and breast cancer was a 2003 study by McConnell. In this study, 3047 patients were randomized to a double-blind, multi-center, placebo-controlled clinical trial for 4-6 years. The 4 different patient groups were administered different drugs: placebo; 8 mg doxazosin; 5 mg finasteride and a combination of 8 mg doxazosin and 5 mg finasteride. Three cases of breast cancer occurred in the finasteride-treated group and 1 case of breast cancer occurred in the combination group. No predisposing factors were identified. Duration of treatment ranged from 1.8 years to 5 years. The occurrence of 4 cases of breast cancer in 3047 patients was considered high considering the normal incidence in the general population of 1 case in 100,000 man-years. Treatment with finasteride appeared in this study to confer 200-fold risk for breast cancer in comparison to patients not receiving the drug.

D. 1996-2002 PUBLISHED STUDIES ON FINASTERIDE AND BREAST CANCER IN MEN

 

In 1996, Prescription Event Monitoring (PEM) Study was published. This study was conducted by Drug Safety Research Unit (DSRU) and involved a total of 14,772 patients (mostly male) under observation of General Practitioners from 1992–1994. There were 2 reported breast carcinomas. For one of the events, the time to onset from commencement of finasteride treatment was recorded as 5 months, the other was unknown. The PEM study in 1996 concluded overall that that finasteride is acceptably safe when used in accordance with the current prescribing information.However, it is not possible from this study to evaluate the cases of breast cancer and their causal relationship with finasteride, as enough data is not available regarding the 2 events of breast carcinoma.

In 1998, McConnell and colleagues published the Proscar long term efficacy and safety study (PLESS). There were 3040 patients were followed up for a period of 4 years. The patients were randomized in approximately equal proportions to receive either 5 mg finasteride or placebo for up to 4 years. In this study, there were no cases of male breast cancer reported in finasteride-treated subjects, and 2 cases were reported in placebo-treated subjects.

Summary and Conclusion

The evidence to date does not point to an association between finasteride or dutasteride use and breast cancer in women at low risk. It is absolutely critical to keep in mind that the studies I have mentioned above above were conducted in men with low risk of breast cancer and not in women (and not in women who have high baseline risks of breast cancer and not in women who already have breast cancer). Also most of the studies have looked at finasteride rather than dutasteride but of course some of the studies looked collectively at both types of alpha reductase inhibitors. This is important to keep in mind. Many physicians continue to avoid avoid prescribing any type of anti androgen to patients with a history of breast cancer (or at highest risk of breast cancer) given that no such studies have been done. However, for most women, there is no evidence to suggest that their use of finasteride or dutasteride increases their risk of developing breast cancer.

REFERENCES

1.    Hagberg KW, et al. Risk of gynecomastia and breast cancer associated with the use of 5-alpha reductase inhibitors for benign prostatic hyperplasia. Clin Epidemiol. 2017.

2.     Wiebe JP, et al. Progesterone-induced stimulation of mammary tumorigenesis is due to the progesterone metabolite, 5α-dihydroprogesterone (5αP) and can be suppressed by the 5α-reductase inhibitor, finasteride. J Steroid Biochem Mol Biol. 2015.

3.     Meijer M, et al.  Finasteride treatment and male breast cancer: a register-based cohort study in four Nordic countries. Cancer Med. 2018.

4.     Duijnhoven RG, et al. Long-term use of 5α-reductase inhibitors and the risk of male breast cancer. Cancer Causes Control. 2014.

5.    Bird ST, et al. Male breast cancer and 5α-reductase inhibitors finasteride and dutasteride.

J Urol. 2013.

6.    McConnell JD, Bruskewitz R, Walsh P, Andriole G, Lieber M, Holtgrewe HL, et al. The effect of finasteride on the risk of acute urinary retention and the need for surgical treatment among men with benign prostatic hyperplasia. N Engl J Med. 1998;338:557–63.  

7.    McConnell JD, Roehrborn CG, Bautista OM, Andriole GL, Jr, Dixon CM, Kusek JW, et al. The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. N Eng J Med. 2003;349:2387–98 

8.    Thompson IM, Goodman PJ, Tangen CM, Lucia MS, Miller GJ, Ford LG, et al. The Influence of finasteride on the development of prostate cancer. N Engl J Med. 2003;349:215–24.

9.    Wilton L, Pearce G, Edet E, Freemantle S, Stephens sMD, Mann RD. The safety of finasteride used in benign prostatic hypertrophy: a non-interventional observational cohort study in 14,772 patients. Br J Urol. 1996;78:379–84.  

10.  Mackenzie IS, et al. Spironolactone use and risk of incident cancers: a retrospective, matched cohort study. Br J Clin Pharmacol. 2017.

11. Biggar RJ, et al. Spironolactone use and the risk of breast and gynecologic cancers. Cancer Epidemiol. 2013.

12.  Mackenzie IS, et al. Spironolactone and risk of incident breast cancer in women older than 55 years: retrospective, matched cohort study. BMJ. 2012.

Does using spironolactone increase the risk of breast cancer?

Question

I have been prescribed spironolactone for female pattern hair loss but have heard confusing information about whether or not the drug increases the risk of breast cancer. Do women using spironolactone have an increased risk of breast cancer?

Answer

Thanks for the great question. I’ll answer this with some depth but I’ll begin by saying that the most recent well conducted studies do not support an association between breast cancer and the use of spironolactone in women at low risk for the disease.

Concerns about the possibility of an increased risk of cancer from spironolactone date back to 1975. Studies at the time showed that rats ingesting spironolactone (at 25–250 times the exposure dose in humans) for 2 years developed several types of tumors including benign adenomas of the thyroid and testes, malignant mammary tumors, and growths on the liver.

To date, there is no good evidence to support the notion that women using spironolactone are at increased risk for breast cancer. In the most recent 2017 study, McKenzie studied the risk of cancer among users of Spironolactone. The participants were 74 272 patients exposed to spironolactone between 1986 and 2013 using the Clinical Practice Research Datalink from the UK. In this study, there was no increased risk of cancer in spironolactone users. 

In 2013, Biggar published data specifically looking at the risk of breast cancer in female spironolactone users. The researchers used anationwide prescription drug registry between 1995 and 2010 and identified use of spironolactone in a cohort of Danish women (≥20 years old).  After studying 2.3 million women (28.5 million person-years), the authors concluded that with respect to breast, uterus, ovarian and cervical cancer, there is no evidence of increased risk with spironolactone or furosemide use.

In 2012, McKenzie published a study a retrospective cohort study evaluating whether exposure to spironolactone treatment affects the risk of incident breast cancer in women over 55 years of age. The study involved 1,290,625 female patients, older than 55 years and with no history of breast cancer, from 557 general practices with a total follow-up time of 8.4 million patient years.  Although the vast majority of women were using doses under 100 mg, 17.2 % of women in the study were using 100 mg doses and 3.6 % were using 200 mg doses. The data suggested that the use of spironolactone did not increase the risk of breast cancer.

Summary and Conclusion

The evidence to date does not point to an association between spironolactone and breast cancer in women at low risk. These studies above were conducted in women with low risk of breast cancer and not in women at highest risk and not in women who already have breast cancer. This is important to keep in mind. Many physicians continue to avoid avoid prescribing spironolactone to patients with a history of breast cancer (or at highest risk of breast cancer) given that no such studies have been done. However, for most women, there is no evidence to suggest that their use of spironolactone increases their risk of developing breast cancer.

References

Barker DJP. The epidemiological evidence relating to spironolactone and malignant disease in man. J Drug Dev. 1978;1(Suppl 1. 2):22–25.

Biggar RJ, et al. Spironolactone use and the risk of breast and gynecologic cancers.Cancer

Epidemiol. 2013.

Danielson DAN, Jick H, Hunter JR, et al. Nonestrogenic drugs and breast cancer. Am J Epidemiol. 1982;116:329–332. 

Mackenzie IS, et al. Spironolactone use and risk of incident cancers: a retrospective, matched

cohort study. Br J Clin Pharmacol. 2017.

Mackenzie IS, et al. Spironolactone and risk of incident breast cancer in women older than 55

years: retrospective, matched cohort study. BMJ. 2012.