Scarring in Advanced MPB

Advanced Balding Associated with Scarring

Advanced late stage male balding (AGA, MPB) is sometimes associated with the presence of scar tissue beneath the scalp. This can sometimes cause an uneven and asymmetrical appearance of hair loss and even cause the physician to consider other diagnoses. 

Chronic sun damage (which is shown here in the photo with areas of hyperpigmentation, hypopigmentation and dilated blood vessels) accelerates the development of this type of scar tissue in many men with male balding. Therefore advanced androgenetic alopecia can be thought of as a type of "scarring alopecia."

Is Low Level Laser Therapy (LLLT) Helpful For Treating Hair Loss?

Is LLLT Helpful For Treating Hair Loss?

Is low level laser therapy (LLLT) helpful for treating hair loss? To date there has been a number of studies that suggest LLLT is helpful including 5 randomized double blind studies - 2 studies with so called "laser brush/comb" devices and 3 studies with helmet/cap devices.

The photo here shows a LaserCap. This LLLT device consists of 224 ‘pure’ laser diodes (no LEDs) of 650nm/5mW each. The device is worn every second day for 30 minutes. Several hemet/cap devices now exist and are marketed as FDA cleared LLLT devices.
 

How Many Genes Are Involved in Male Pattern Balding?

How many genes control whether an individual develops balding?

Studies by Hagenaars et al in 2017 showed that male balding is actually more complex than we ever imagined. The researchers identified 287 genetic regions that are linked to male pattern balding (androgenetic alopecia). This data came from studies of over 52,000 men.

 

Reference

Hagenaars et al. PLoS Genetics 2017
 

Do all males bald in the same way?

Do all males bald in the same way? 

The answer to that is no. Most men whonare going to bald first notice changes in the temples and/or crown and then ultimately bald according to the so called "Hamilton Norwood" scale. However this male shown in the photo has a pattern of balding that does not match up to any of the Hamilton Norwood patterns. He has what is known as a "female" pattern of male balding where the central scalp is involved first and the frontal hairline is relatively unaffected. This pattern of androgenetic hair loss is common in women and affects about 10-13 % of males.
 

Does stress accelerate balding?

There is not a lot of great medical evidence to support the notion that stress directly impacts MPB.  However, it probably has a minor role and only in some men and women with the right genetic background. Of course, we don't understand yet what that genetic background is at present.

When one examines studies of identical twins, one sees that 92% actually still look identical (same level of hair loss) years and years down the road. If stress, diet, and environmental factors played a huge role, one would not expect this number to be so high.

But for some males and females, it is likely that stress accelerates balding to a minor degree. A study by Gatherwright in 2013 suggested that higher stress could lead to worsening hair loss in the crown in men.  For women, a 2012 study suggested that higher stress was correlated with worse hair loss in the frontal area and divorce and separation were correlated with worsening hair loss in the temples.

Conclusion

Stress probably accelerates the rate of progression of balding in some individuals who have the right genetic predisposition.   We know that stress can cause an increased amount of daily shedding and such shedding can accelerate follicular miniaturization. It makes sense that stress can accelerate the balding process in some individuals. However, it's not likely to be a consistent phenomenon amongst all individuals.  

Reference

The contribution of endogenous and exogenous factors to male alopecia: a study of identical twins.

Gatherwright J, et al. Plast Reconstr Surg. 2013.

The contribution of endogenous and exogenous factors to female alopecia: a study of identical twins.

Gatherwright J, et al. Plast Reconstr Surg. 2012.

Treatment of Male Balding: A closer look at the three tiers of options

Treatment of Male Balding

A variety of treatment options exist for males with balding, also known as androgenetic alopecia. I like to think of the options in terms of three tiers or categories of treatments. Tier 1 treatments have the best evidence and are consistently the most effective. Tier 3 treatments have the least evidence.

Tier 1 Treatments

Minoxidil and Finasteride are the two FDA approved treatments. Dutasteride is off label in North America but is also not uncommonly prescribed as well. These are among the most effective treatments and what I would term "tier 1" treatments. 

Tier 2 Treatments

Other treatments can also be considered including low level laser and platelet rich plasma. Meta-analyses support a benefit of these over placebo or sham treatments so they are not without at least potential benefit. These are what I term "tier 2" treatments. Other tier 2 treatments with less evidence but still reasonable likelihood of benefit include oral minoxidil and topical finasteride. These are not FDA approved and off label.

Tier 3 Treatments

Then we come to "tier 3" treatments. Some treatments in this group might help some males but not all and tesults may be inconsistent. Some tier 3 treatments could be helpful, it's just that not enough studies have been done. The public loves many "tier 3" treatments as they wrongly assume some are completely safe. Many tier 3 treatments simply have not been studied to any significant degree to render conclusions about safety. Lack of studies does not equate to them being safe.

This tier 3 group includes a variety of treatments purported to have a DHT blocking and anti-androgen type effect. There is biochemical evidence of this effect for some of the treatments and even a hint of clinical benefit for others. There is far less study of this group of agents which includes saw palmetto, pumpkin seed oil, ketoconazole shampoo, topical androgen receptor blockers. In the last category are many agents that can be bought on the internet and that I see in my office at least once per week. The evidence for a clinical benefit from these agents is weak at best.

This summarizes the three tiers of non surgical treatments that can be considered in males with balding. A number of exciting options are on the horizon and only careful study will determine if we ever see them in the clinical setting. This includes topical prostaglandin F2 analogues (bimatoprost), prostaglandin D2 inhibitors, Wnt pathway activators, JAK inhibitors and a variety of cell based therapies.

Bimatoprost for Androgenetic Alopecia: An intensely researched area

Bimatoprost for Male Balding

Bimatoprost is a prostaglandin F2 alpha analogue that stimulates hair growth. Bimatoprost at 0.03 % is a well known eyelash growth stimulatory compound and marketed under the name Latisse. 

Bimatoprost has been studied for use in androgenetic alopecia. At low concentrations, it is not particularly effective. Allergan is currently studying higher concentrations (1 and 3%). Data released by Allergan and available to the public online suggest that these higher concentrations may be beneficial in treating hair loss. This is an exciting area to watch out for in the near future.

The graph shows how bimatoprost compares to minoxidil in these Allergan led studies. In their preliminary results, higher concentrations of bimatoprost was similarly or even slightly more effective that minoxidil (the gold standard FDA approved topical treatment for androgenetic alopecia).

Density Changes in CTE vs AGA over Time

Chronic Telogen Effluvium: How does density change over time?

Chronic Telogen Effluvium (CTE) and Androgenetic alopecia (AGA) are both commonly encountered diagnoses in women age 40-70 years. They are however, very different conditions. 

AGA: Androgenetic Alopecia

AGA presents with hair thinning and sometimes increased daily shedding as well. The loss of hair is sometimes just frontal in location or the crown but can be diffuse (all over). A key to the diagnosis is recognition of the progressive reduction in the caliber (diameter) of hairs. 

CTE: Chronic Telogen Efflvuium

Patients with CTE can appear to have a similar story. Many have a sudden onset of shedding. The shedding is diffuse. The temples may be particularly affected with reduced density to a much more significant degree than seen in AGA. Reduced hair caliber (miniaturization) is not a feature of CTE. CTE has periods where shedding appears to slow considerably or even stop. When one follows these conditions for many years there is a realization of another important difference: Density in CTE reduces initially but then plateaus and does not reduce further. Density in AGA continues to drop off over time. These points are illustrated in the graph.

Androgenetic Alopecia: Should I start two treatments at once?

 Androgenetic Alopecia: Should I start two treatments at once?

There are many treatments available for any particular hair loss condition. Let’s take androgenetic alopecia as an example. Individuals with androgenetic alopecia might consider topical minoxidil, oral hormone blocking medications, low level laser or even platelet rich plasma.  For some types of hair loss there may be an even greater array of choices.   

I’m often asked if patients should start more than one treatment at the same time. My personal view is not necessarily the right answer or the only view on the subject. However, my personal view is my view. My personal view is that whenever possible medications should not be started at the same times but rather staggered.  The intervals of staggering the treatments will depend on the specific situation and the urgency of treatment.

Example

Consider the 34 year old female patient with androgenetic alopecia who is considering topical minoxidil and oral spironolactone.  After a careful review of the patient’s medical history, blood tests, and examining the scalp, it is determined that both are good options for the patient.  I am faced with two options: Start both or start one at a time (stagger the treatments). Let’s look at the implications of both.

Treatment Option 1: Start Minoxidil and Spironolactone at the Same Time

Both Spironolactone and Minoxidil are recommended for the patient in this situation. What needs to be considered is that minoxidil has about a  30 % chance of helping the patient. It has a 70 % chance of not being all that helpful. Spironolactone has a 40 % chance of improving hair growth. If both are started at the same time and the patient experiences and improvement it will be difficult if not impossible to know which treatment was responsible for the improvement.

Was it the minoxidil?

Was it the spironolactone?

Was it both?

Treatment Option 2: Start Minoxidil First and Introduce Spironolactone in 6-9 months.

My personal preference in this situation was to start minoxidil first. After 6-9 months of treatment (once I determine if the minoxidil is working or not), I can make a decision to add spironolactone. In this case I can have a clear sense for the entire lifetime of the patient what helps and what does not.

Comment and Conclusions  

Treatments for some hair loss conditions (such as androgenetic alopecia) are life-long. A 33 year old woman who lives to 93 could potentially have 60 years of use of a given medication.   From a cost perspective alone, once can potentially save a patient $ 36,000 over their lifetime by confirming that a medication does not work and should be abandoned.

Erectile dysfunction in Minoxidil Users: What's the Naranjo Score?

Erectile dysfunction in minoxidil users

Anyone who reads online will see that there are reported links between topical minoxidil use and erectile dysfunction. But is it accurate ?  My opinion is that it's not impossible - but very unlikely for most users. Let's take a look at the data. 

One one study to date supports an association

To date, there are no really good clinical studies that support an associated between topical minoxidil use an worsening erectile dysfunction.  The original studies from the 1980s did not raise this issue. However a recent study did suggest that topical minoxidil was the cause of erectile dysfunction. 

MINOXIDIL ASSOCIATED WITH ERECTILE DYSFUNCTION

Blood pressure medications can cause impotence

Minoxidil is a blood pressure medication and was used orally in the 1980s as Loneten. It's certainly not out of the question for blood pressure medications to cause erectile dysfunction. Drugs like beta-blockers and diuretics like hydrochlorothiazide can sometimes cause erectile dysfunction. Blood pressure medications like ACE inhibitors, Angiotensin receptor blockers are less likely.  Minoxidil was FDA approved in 1979 as an oral medication to treat blood pressure problems. Topical minoxidil however, does not impact blood pressure to any significant degree in most users. Erectile dysfunction is not a side effect that has been raised in clinical trials to date.

The Naranjo Adverse Drug Reaction Probability Scale

When a patient asks me whether their minoxidil could be causing sexual dysfunction, my answer is first that it is possible and that we really need to consider something know as the Naranjo Adverse Drug Reaction Probability Score.

Anything applied to the skin or taken by mouth has the potential to cause a side effect. Some medications rarely cause side effects and others tend to cause frequent side effects. Occasionally a patient will report a side effect that perhaps has never been reported before. The question then becomes - is this a real side effect from the drug or is it happening from something else?

 

A Closer Look at the Naranjo Adverse Drug Probability Scale

The Naranjo Scale was created nearly 40 years ago to help standardize how clinicians to about assessing whether or not a drug could be implicated in an adverse drug reaction. It is used in controlled clinical trials. The scale is quite easy to use - and involves asking the patient 10 questions. Answers to the question are recorded as "yes", "no" or "don't know" and different points are assigned to each answer (-1, 0, +1, +2). 

Typical Questions in the Naranjo Scale (using minoxidil associated erectile dysfunction ("ED") as an example)

1. Are there previous "conclusive" reports of minoxidil causing ED? (yes) 
2. Did the ED (or worsening ED) appear after the drug was given or were their such issues before the patient started minoxidil?
3. Did the ED improve when the drug was discontinued or a specific antagonist was given?
4. Did the ED reappear upon readministering the minoxidil?
5. Were there other possible causes for the ED that were explored by the family doctor?
6. Did the ED occur again with administration of placebo?
7. Was the minoxidil detected in the blood or other fluids in toxic concentrations?
8. Was the ED worsened upon increasing the dose of minoxidil (from once to twice daily)? Or, was the reaction lessened upon decreasing the dose? (ie. does going to once daily minoxidil make sexual performance better?)
9. Did the patient have a similar reaction to  minoxidil or a related  blood pressure drug in the past?
10. Was the ED confirmed by any other objective evidence?

 

Determining the Naranjo Score

Scores 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'

 

Reference

Tanglertsampan C. Efficacy and safety of 3% minoxidil versus combined 3% minoxidil / 0.1% finasteride in male pattern hair loss: a randomized, double-blind, comparative study. J Med Assoc Thai. 2012.

Cecchi M, et al. Vacuum constriction device and topical minoxidil for management of impotence. Arch Esp Urol. 1995.

Radomski SB, et al. Topical minoxidil in the treatment of male erectile dysfunction. J Urol. 1994

Can we predict if minoxidil will work or not?

Predicting the chance of benefit before starting

Minoxidil is the only topically approved agent that is approved but the FDA for treating androgenetic alopecia. The drug does not help everyone but does help 25-30 % of users. I've written in previous articles about the future of minoxidil pre-testing kits. It is well known that in order for minoxidil to have a chance to work, the body needs to convert the minoxidil to minoxidil sulphate. Some people have the enzyme (known as minoxidil sulphotransferase) to do this; other people simply do not. Those who lack the enzyme are more likely to be non-responders.

I was interested to read today in a press release that kits to test minoxidil sulphotransferase activity are moving forward in the FDA approval process.  The FDA journey can be lengthy, but the possibility exists that we might see these kits in the clinic in the near future. These will help physicians to predict if it's a good idea to prescribe minoxidil or not. 

Read the press release here: Press Release

Has my minoxidil stopped working?

Has my minoxidil stopped working?

Minoxidil is FDA approved for the treatment of male balding and female thinning. After using it for a period of time, some patients find that it no longer seems to be working the way that it once did. This leads many to ask :

"Has my minoxidil stopped working?"

The most likely explanation is that the minoxidil is, in fact, still working but the machinery that controls balding is working harder. It is likely that more and more genes are being expressed inside the scalp and hair follicles that are accelerating the balding process forward. 

Genetic hair loss has many genes

A recent study from the UK, however, has shown that male balding is far more complicated and many hundreds of genes contribute to balding in men. It identified 287 genetic regions linked to male pattern baldness. This large study examined data from over 52,000 men.

Consider the 30 year old male who started noticing balding at 21 and started minoxidil. At age 16 - 18 he might have had 4-6 genes expressed at the start of balding (before he even noticed) and 21 there may have been a dozen or so distinct genes pushing the balding process. At age 30, there could be dozens and dozens of genes expressed. For many users of Minoxidil, it is usually working the same - and while it was pretty good at stopping 4 genes, it can't fully hold back the genetic changes associated with 60 or 70 genes. These numbers are different for everyone - but it illustrates an important point. The scalp environment and hair follicle milieu changes drastically over time.

Reference

Hagenaars SP, Hill WD, Harris SE, Ritchie SJ, Davies G, Liewald DC, et al. (2017) Genetic prediction of male pattern baldness. PLoS Genet 13(2): e1006594

Finasteride and Gynecomastia (Male Breast Enlargement)

Finasteride: What are the myths are realities when it come to gynecomastia?

 

Gynecomastia or enlargement of breast tissue in men can occur with a number of causes. These include hormonal issues that affect testosterone production (like Klinefelter’s syndrome or a pituitary problem), normal aging, tumors of the adrenal glands, testes or pituitary gland, thyroid problems, liver and kidney problems. A variety of medications can cause gynecomastia as well. Overall about 10-25 % of cases of gynecomastia have a drug cause. Some of the drugs known to cause gynecomastia include spironolactone, other anti-androgens, cimetidine, ketoconazole, estrogens. For a full list of implicated drugs, click here. In all of these different causes there is an underlying hormonal issue  - typically an increase in the estradiol/testosterone ratio.

Finasteride-Induced Gynecomastia: Myths and Misconceptions

Finasteride, which is FDA approved for treating male balding at a dose of 1 mg daily, is a medication that can sometimes cause gynecomastia. The risk is likely about 4 to 10 out of every 1,000 users. There are a number of misconceptions about finasteride-induced gynecomastia. The following points help clarify some of these.

1. Gynecomastia can be one sided or both. It is very commonly one-sided.

Finasteride induced gynecomastia is often one-sided but can be both sides. This is especially true at lower doses like 1 mg compared to 5 mg. 

2. Gynecomastia typically starts after 2-4 months

Finasteride induced gynecomastia can start as early as a few weeks but is typically a few months delay (if it is going to occur). It can also be 1-2 years before the phenomenon is appreciated.

3. Finasteride-induced gynecomastia can start with breast tenderness or even pain

An important sign to watch for is the presence of pain or tenderness. This can occur prior to any actual enlargement.

4. Finasteride-induced gynecomastia lower doses are less likely than higher but can occur any dose

The 1 mg dose is less likely than the 5 mg dose to cause breast enlargement in men. The concept of the dose response is important because it means than for some men, 0.5 mg daily (or every other day) could be assocated with a lower risk of gynecomastia (while still potentially benefitting their hair).

5. Finasteride-induced gynecomastia reverses in many with immediately stopping the drug but not all

Finasteride induced gynecomastia can reverse in many individuals provided the drug is stopped in the early stages when the gynecomastia is noted. If the drug is not stopped, it can enter a irreversible stage (where only surgery will provide treatment).

6. Finasteride-induced gynecomastia increases with age and obesity

Finasteride induced gynecomastia is more likely in obese indivdiuals and with advanced age.

7.  Most men with Finasteride induced gynecomastia have normal blood tests

Blood tests may be appropriate  for some men depending on their history. However, most of the time blood tests and various hormonal tests are normal.

CONCLUSION and FINAL POINTS

Gynecomastia is common in the population so one must be careful to immediately ascribe their gynecomastia to a drug or health reason without a full evaluation. Finasteride induced gynecomastia occurs in 4 to 10 out of every 1000 men using finasteride. It is dose dependent so risk may be less with 0.25 mg compared with higher doses. Anyone with concerns about this phenomenon should see their physician immediately to discuss.

A link is more likely to a drug cause when the breast enlargement is one sided and tender/painful. One way to determine a link is to stop the drug and wait for the tissue to return to normal before starting the drug again (this is called a rechallenge). If gynecomastia occurs again, one has more confidence of a link. This may not be appropriate for all individuals so one should always discuss with their physician.

REFERENCE

[1] Nuttall F (1979) Gynecomastia as a physical finding in normal man. J Clin Endocrinol Metab 48:338–340

9. Green L, Wysowski DK, Fourcroy JL. Gynecomastia and breast cancer during finasteride therapy. N Engl J Med. 1996;335:823.  

Anabolic Steroids and Hair Loss: Is one month okay?

Anabolic steroids can cause hair loss in genetically susceptible individuals

Anabolic steroids are frequently used as training aids for men and women looking to increase muscle mass. This includes body builders and athletes at various levels. Many individuals are aware of the side effects of anabolic steroids and judge in their own minds whether the risks and benefits of using the drugs are worth it to them.  These are known by a variety of names including  stackers, gym candy, Arnolds, roids, juice. They are not uncommon - and some  studies have suggested that even 4 % of high school students will have used anabolic steroids at least once. They are always on my radar. 

Hair loss from anabolic steroids

There is no doubt that anabolic steroids can trigger a worsening of hair loss in some individuals. It does not happen to everyone but happens to those with the right genetic background. It can be mild or very marked hair loss. In my experience, there can also be a worsening of seborrheic dermatitis in these individuals as well. 

How long is too long? 1 month? 2 months?

As patients weigh the risks and benefits of using anabolic steroids, I'm often asked questions such as:

How much is too much? How long is too long?

Is it 1 month? What about 2 months?

The short answer is that any amount can potentially be detrimental - but it all depends on one's underlying genetics and stage of hair loss. We can not accurately predict in the present day whether someone will experience negative hair loss related side effects. However, as I speak to patients about the duration of anabolic steroid use, I find it important to remind them that hairs don't work in months, they work in milli and microseconds. One month of steroid use is 2.5 million seconds - or as a hair would view it 2.5 Billion microseconds.

Does 2.5 Billion milliseconds of anabolic steroid use cause hair loss?

It's much easier to deal with the concept of hair loss occurring with 2.5 millions seconds of continuos exposure to anabolic steroids. While 1 month might not sound like much, 2.5 million does sound like a lot more.

Conclusion

Hair are made of proteins, which form cells. Cell don't work in months - they work in units of fractions of a second.  In my clinical experience treating many individuals using anabolic steroids, short term use of anabolic steroids is sufficient to trigger hair loss in susceptible individuals.

Finasteride Side Effects in Women

What are the side effects of finasteride in women?

First off, finasteride is not FDA approved for women. Any such use is therefore "off label" and any female considering finasteride will want to be guided by a knowledgeable and experienced physician if this is a route you wish to take. Depending in the patient's current age, type of hair loss and medical history and family history this may or may not be a good option.

Side effects

i'm often ask about the range of side effects that are possible for women who use finasteride. Side effects of finasteride in women include, but are not limited to: harm to a fetus (finasteride can not be used in pregnancy), fatigue, weight gain, depression, anxiety, decreased libido, sexual dysfunction, hair shedding, breast tenderness, breast enlargement.  Other side effects can occur but are less common. These include changes in platelet counts and muscle injury (myopathy).

The Speed of Progression of Male Balding

How fast does male pattern balding progress over time?

Today, we complete day 5 of our week long look at male balding by examining the speed at which it progresses. Male balding progresses at different rates. Most men who develop balding experience a slow and steady reduction in density starting in the front (temples) or crown. One can often detect a change in density every 1-3 years (patient 1 in diagram). There may even be long periods of time where there is no progression of the hair loss. Some men have extremely slow and almost undetectable changes in their density once hair loss starts (patient 2, green line). Some men have an extremely rapid course of hair loss, with noticeable changes in density every 6-8 months (blue line). More rapid hair loss can happen to any male who develops male balding but it is more common in men who develop balding in their teens and 20s. In summary, male balding progresses at very different rates in different individuals. However, once it does start it always moves forward.  

The Resistance of Hair in the Back to Balding

Why are hairs in the back of the scalp so resistant to balding?

Males with balding (androgenetic alopecia) frequently maintain a thick density at the back of the scalp whereas the front or top of the scalp may experience thinning. There are many reasons for these differences. Hair follicles in the back of the scalp have different androgen metabolism. There are fewer androgen receptors in these hairs. There is a reduced level of 5 alpha reductase activity. Furthermore, there are reduced DHT levels in the scalp.

On account of these differences between the back and front, a hair transplant becomes possible. Hairs moved from the back of the scalp to the front of the scalp maintain their characteristics and continue to be resistant to balding.

Does stress, diet and smoking have a key role in male balding?

Today we continue the third of our week long look at male balding. I am often asked how much of a role does diet, stress and the environment have in male balding?

We currently believe that factors such as smoking, alcohol, stress, and sun exposure and obesity do have role in accelerating hair loss but the key question is "how much" of a role do they have? To look at this question in more detail, we need to look back at some brilliant studies of identical twins.

Identical twins carry the same genetic profile. By studying the appearance of identical twins at various points throughout their lives, we can get a sense of how important factors like genetics and the environment actually are. If genes are the key important factor in balding progress then, identical twins should look ‘identical’ in terms of their hair density. In contrast, if environmental factors like smoking, stress and ultraviolet radiation are important, identical twins might not have the same hair density because their environment is different. 

The Hayakawa Study 1992

Studies in 1992 revealed that genetics is by far the most important factor and the environment only has a minor role. 92 % of identical twins have "no significant" differences in their hair density. 8% of identical twins have a slight difference. Interestingly , no twin had a striking difference!
There studies support the notion that one’s genetics is by far the most important factor in the balding process. 

Is there any role for 'non genetic' factors?

That answer is certainly yes, but at least in men it appears much more minor in terms of the magnitude of involvement in the balding process. Other studies have suggested that "epigenetic" factors like stress, smoking and diet and sun exposure do have a role - but it is likely a minor role.

Reference

Hayakawa K, et al. Intrapair differences of physical aging and longevity in identical twins. Acta Genet Med Gemellol (Roma). 1992.

What’s new in androgenetic alopecia research ?

What’s new in AGA based research ? 

It is indeed an exciting time in biomedical research! Several companies are actively researching new treatments with the hopes to bring to market new options for androgenetic alopecia. Here are just a few of the nearly two dozen companies actively pursuing new treatments for men with balding. Some of course may apply to female androgenetic alopecia too.

 

Who are some of the key companies?

Shisedo, Replicel and Tsuji-Rekin are studying cell based therapies for balding. Follica is studying how specific therapies in conjunction with microwounding can stimulate hair growth. Specific molecular pathways are being targeted by companies such as Samumed (WNT pathway), Allergan (prostaglandins), Aclaris (JAK inhibitors). Cassopia is studying novel topical antiandrogens. Histogen is studying how factors produced by neonatal cells grown under embryonic-like conditions can stimulate hair growth.

New treatments for male balding could be around the corner!

Can a biopsy showing AGA be wrong?

Can a biopsy of AGA be wrong?

I'm often asked if a biopsy can be 'wrong.' The short answer is that yes, a biopsy can potentially be wrong. Biopsies are simply "samples" and used to represent a larger area. However,  the long answer is that if a biopsy is done properly and from the right area, and read by a good pathologist, them no, it is very likely that if a biopsy returns showing that androgenetic alopecia is one of the diagnoses that this is correct. The identification of vellus hairs and a terminal to vellus hair ratio of less than 4:1 with telogen hairs less than 15% is typical of androgenetic alopecia. Many individuals (especially women) with androgenetic alopecia do not have a family history so this fact should not be given too much emphasis.

A biopsy can "sometimes" be wrong in these situations:

1. Diagnoses of Scarring Alopecia (Lichen planopilaris, Folliculitis Decalvans)

2. Some diagnoses of Telogen Effluvium

3. Some diagnoses of Alopecia Areata

Most of the time, of course, a biopsy is correct in these situations. However, there are many cases alopecia areata, telogen effluvium and scarring alopecia that are challenging. A biopsy is just a piece of the puzzle and one must put together all the facts from the clinical history. examination, blood test results to come up with the diagnosis. 

A biopsy is less likely to be 'wrong' in these situations

1. Androgenetic alopecia (especially with use of horizontal sections)

2. Tinea Capitis

3. Trichotillomania

4. Skin Cancers and Metastases