" When did your loss start?" - A closer look at whether people truly appreciate their own hair loss

Many people with hair loss don’t realize they have loss

I generally like to believe that my patients know their hair quite well. After all, they see if every day. It seems true that patients know their hair well once they become patients (and realize they do have hair loss). However, several studies however, support a notion that many people in the general population don’t realize they have hair loss for quite some time once it develops. Furthermore, studies suggest that when they do realize they have hair loss they tend to underestimate its severity rather than overestimate it. This is such a good lesson for many physicians who see hair loss patients who mistakingly believe that patients worry excessively and inappropriately about their hair.

Bondo et al 2004, British Journal of Dermatology

A 2004 study by Biondo and colleauges found that 44 women on the waiting list for hair loss actually tended to underestimate the severity of their hair loss rather than overesimate it.

Tosti et al 2005, British Journal of Dermatology

Tosti and colleagues found similar results to the Bondo study. The authors recruited 629 young women who were interviewed by a trained dermatologist the end of secondary school and university. Of these 629 women, 31 of those interviewed had FPHL.

Study participants completed various questionnaires investigating, among other points, the severity ratings of their AGA. Each of the 31 women who had hair loss were asked to describe her alopecia by choosing one of the following descriptions: ‘my scalp is clearly visible’ (12 subjects chose this answer); ‘my scalp is slightly visible’ (12 subjects); and ‘my scalp is not visible’ (seven subjects). Interestingly, 39 % of the women (12 of 39) denied their was a problem, and 39 % underestimated it.

Conclusion

These studies are important because they provide information that women tend to underestimate the severity of their hair thinning before seeing a physician. Although it still needs to be proven, the authors proposed that the tendency to deny hair loss may be considered as a self‐defence mechanism against the psychological stress caused by this problem. This is such a good lesson for many physicians who see hair loss patients who mistakingly believe that patients worry excessively and inappropriately about their hair.

REFERENCE

Tosti et al. Tendency to underestimate the severity of androgenetic alopecia. Br J Dermatol. 2005 Jun;152(6):1362-3; author reply 1363.

Biondo et al. Women who present with female pattern hair loss tend to underestimate the severity of their hair loss.Br J Dermatol. 2004 Apr;150(4):750-2.

Alopecia areata and Sclerotherapy: Coincidence or Connection?

Alopecia Areata And Sclerotherapy for Venous Veins

Alopecia areata is an autoimmune disease that causes hair loss on all part of the body. A large proportion of the disease is felt to be due to genes the patient inherits at birth. However, a minor proporiton of the disease is due to various environmental ‘triggers.’ Dozens upon dozens of triggers exists ranging from stress, infections, medications.

In 2017, Whiteley and colleagues published a report suggesting that perhaps sodium tetradecyl sulphate foam sclerotherapy might be added to the long list of potential triggers.

The authors described a 40-year-old woman with a history of alopecia areata who underwent treatment for bilateral primary symptomatic varicose veins. Her first procedure entailed pelvic vein embolisation of three pelvic veins using 14 coils and including foam sclerotherapy of the smaller vein tributaries (using 3% sodium tetradecyl sulphate). Following this procedure, she had an exacerbation of her alopecia areata. . Seven months later, she underwent foam sclerotherapy of leg and labial varicose veins again using sodium tetradecyl sulphate. Two days following this procedure, she had a severe exacerbation of alopecia areata with gross shedding of hair.

The authors raised the possibility that two episodes of exacerbation of alopecia areata appear to be associated with sodium tetradecyl sulphate foam sclerotherapy of veins. This is an interesting article and clearly demands larger studies. A large retrospective review among vein clinics world-wide could easy answer the question as to the real magnitude of risk.

ARTICLE: SCLEROTHERAPY FOR ALOPECIA AREATA

REFERENCE

Whiteley et al. Exacerbation of alopecia areata: A possible complication of sodium tetradecyl sulphate foam sclerotherapy treatment for varicose veins SAGE Open Medical Case Reports Volume 5: 1–4

Estrogen, Anti-estrogens and Frontal Fibrosing Alopecia: What have we learned ?

Loss of Estrogen and Use of Anti-Estrogens May have a Role

Frontal fibrosing alopecia is a type of scarring alopecia which is becoming more common around the world. The condition typically affects peri-menopausal and post menopausal women. The disease may start with reduction in eyebrow density and recession of the frontal hairline. Other areas including eyelashes, body hair and hair on other regions of the scalp may be affected.

It is increasingly clear that hormonal factors are involved in the development of frontal fibrosing alopecia. Abnormalities in androgens and estrogens are thought to be involved.

Declining estrogens may have a role in women who are predisposed to develop this condition. The peri-menopausal period is well understood to be associated with steadily declining estrogen. A 2018 case control study by Buendia-Castrano and colleagues showed that menopause occured earlier in women with FFA. This data came from examining records of 104 female FFA patients and 208 controls. The same authors found additional data that interruption of estrogen signaling may have a role - the anti-estrogen tamoxifen was found to be associated with a nearly 15 fold greater risk of developing FFA.

Other studies have also supported the notion that low estrogen environments are somehow associated with the development of FFA. Imhof and colleagues in 2018 showed that 13 % of women in their study had a history of surgically induced menopause through hysterectomy. This data has raised the question as to whether the incidence of hysterectomy is higher than we previously had considered. In the same line of thinking, studies dating back to 2014 showed the early menopause was detected in 14 % of FFA patients.

Premature menopause is defined as menopause occurring in women under 40 years of age. Overall, about 1 % of women in the general population have premature menopause making the condition not really all that rare. The fact that 14 % of women with FFA may have early menopause draws attention to this as a contributing factor.

Conclusion

It is increasingly clear that the decline of estrogen has some sort of a role in FFA. It’s too simple to say that it’s the main reason. All women enter menopause but yet only 1 in every 5000 to 10000 develop FFA. it may be that the decline in estrogen in women who have some sort of a genetic predisposition promotes the development of this autoimmune hair disease. More studies are needed.

Reference

Buendia-Castrano D et al. Hormonal and Gynecological Risk Factors in Frontal Fibrosing Alopecia: A Case-Control Study. Skin Appendage Disord. 2018 Oct;4(4):274-276. doi: 10.1159/000484210. Epub 2017 Dec 8.

Imhof et al. Frontal Fibrosing Alopecia in Women: The Mayo Clinic Experience With 148 Patients, 1992-2016. Mayo Clin Proc. 2018 Nov;93(11):1581-1588. doi: 10.1016/j.mayocp.2018.05.036.

Vano-Galvan et al. Frontal fibrosing alopecia: a multicenter review of 355 patients. J Am Acad Dermatol. 2014 Apr;70(4):670-678. doi: 10.1016/j.jaad.2013.12.003. Epub 2014 Feb 5.

Can I use Latisse on my Thinning Hair? Will it Help? Is it Safe?

Latisse for Thinning Hair

I’m often asked if Latisse, containing the active ingredient bimatoprost 0.03 %, can be used for women and men with androgenetic alopecia. The short answer is it just doesn’t help enough to even make it even worthwhile.

Research over the last few yeas has shown that these so called ‘prostaglandin agonists’ do help to grow hair. Latisse contains the ingredient bimatoprost and this too has been shown to grow hair. In fact, it’s FDA approved to help eyelash growth at a concentration of 0.03 %. Application is nightly to the upper eyelid.

The main issue with Latisse is that the concentation of bimatoprost is quite good for growing longer eyelashes when placed on the delicate eyelid skin. However the concentration is just much too weak to be used on the very thick scalp. Latisse has much too low of a low concentration of bimatoprost - and it ​simply not enough gets into the scalp.

The Allergan company is studying much higher concentrations (3 % instead of 0.03%) and this is showing great promise. Indivdiuals using Latisse right now at the low concentration of 0.03 % on the scalp are going to find that it does not help enough to make it worth while.

Here’s another way of looking at it

1 mL of minoxidil costs 30 cents Canadian and this helps a bit for some people

1 mL of 0.03 % bimatoprost costs about 40 Canadian dollars and this helps hardly any for hardly any people

Interested readers may wish to refer to a previous article

BIMATOPROST FOR ANDROGENETIC ALOPECIA

Black Seed Oil (Nigella sativa) and It's Potential Anti-Inflammatory Properties.

Black seed Oil and Its Potential as an Anti lymphocytic treatment.

Black seed oil (Nigella sativa) is a 'herb with many pharmacological properties. The active constituent ‘thymoquinone’ (TQ) is thought to have the therapeutic effects and TQ are shown to possess multiple useful effects for the treatment of patients with several diseases, such as inflammatory and auto-immune disorders. It continues to be studied in other areas of medicine due to its potential effects in the setting of metabolic syndrome, its anti-cancer effects as well as its antimicrobial, anti-nociceptive and anti-epileptic properties. There is some evidence that it reduces fibrosis (scarring) in various models of lung scarring, kidney scarring, liver scarring and wound healing.

Whether black seed oil has any benefit in autoimmune scarring alopecias is unknown but warrants further study. In patients with autoimmune and inflammatory issues who do not wish to use more evidence based treatments (which have the best evidence) typically recommend does of 500 mg daily for 2 weeks and then 1000 mg daily after if the patient is tolerating it well.

I continue to follow ongoing studies of black seed oil. It is not possible at present to say that this herb has any benefit in the treatment of any of the autoimmune hair issues I treat. However, there is good reason to continue exploring this area. As just one example, I present a nice 2016 study by Kheirouri and colleagues. The authors reported results from a randomized, double-blinded placebo-controlled, 2 months, parallel-group clinical trial of black see oil. Forty-three female patients (20-50 years) with mild to moderate rheumatoid arthritis were recruited and assigned into black seed oil groups (n = 23) and placebo groups (n = 20) groups to receive 1000 mg of black seed oil (500 mg twice daily) capsule or placebo capsule. The disease activity scores of 28 joints (DAS28) were calculated and percentages of CD4(+), CD8(+), and CD4(+)CD25(+) T cells were examined using flow cytometry.

This study showed that treatment with black seed oil resulted in a significant reduction of the serum high-sensitivity C-reactive protein (hs-CRP) level and DAS-28 score and an improved number of swollen joints compared with baseline and study subjects using only the placebo. The treatment also resulted in reduced CD8(+) T cells, and increased the CD4(+)CD25(+) T cell percentage (i.e. the so called beneficial T regulatory cells) and increased the CD4(+)/CD8(+) ratio as compared to placebo and baseline. An increased CD4 to CD8 ratio is felt to be associated with better immune function. The overall conclusion of the study was that black seed oil had the potential to benefit an inflammatory disease through modulating T lymphocytes.

Conclusion

Black seed oil continues to be studied and for good reason. There is evidence that it has potential inflammatory effects and benefits in various auto-immune disorders. Whether it has any effects in patients with autoimmune hair loss is unknown but something that warrants further study.

REFERENCE

Kheirouri et al. Immunomodulatory Effect of Nigella sativa Oil on T Lymphocytes in Patients with Rheumatoid Arthritis. Immunol Invest. 2016 May;45(4):271-83. doi: 10.3109/08820139.2016.1153649. Epub 2016 Apr 21.

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The Potential Antiandrogenic Effects of Stinging Nettle

Stinging Nettle: More studies needed of this interesting herb.

Stinging nettle has been around a long time. It has been used in traditional medicine circles for it’s anti-inflammatory and diuretic effects.

There are no good studies to date pertaining to its effects in hair loss. However, there are interesting studies in other areas of medicine that support a potential antiandrogenic benefit at doses of 300-600 mg daily. In a very small 2014 study, levels of testosterone and free testosterone and DHEAS were found to be reduced by this herb and clinical parameters like acne, irregular menstrual cycles and oily skin were improved in women using the herb.

THE ANTI-ANDROGENIC EFFECTS OF STINGING NETTLE:

It’s still far to premature to say that stinging nettle might have benefits for hair loss. However, this is a first small study that will hopefully fuel additional studies.

Reference

Najafipou et al. Therapeutic effects of stinging nettle (Urtica dioica) in women with Hyperandrogenism. International Journal of Current Research and Academic Review, 2014.

Using Low Dose Naltrexone for Lichen Planopilaris (LPP)

LDN for Lichen Planopilaris: Practical Points in Home Compounding

Interest in low dose naltrexone arose in 2017 when a US group report some benefits in a small number o patients. It’s clear that LDN helps some patients but it does not appear to help all patients. What remains to be seen is whether it actually stops hair loss effectively or whether it is merely better at suppressing symptoms.

The typcial dose of LDN is 3 mg nightly at 9 pm. The medication can be made up in tablets by a compounding pharmacy or patients can make up a solution of 1 mg per mL themselves in water provided they are comfrotable doing this. We’ve had many patients dissolving 50 mg tablets in glass bottles containing 50 mL of water and using 3 mL every day.

This video is a nice video on how this can easily be done at home. All patients should review this directly with their physicians or pharmacist to ensure that they understand how this is properly done.

MAKING UP LOW DOSE NALTREXONE AT HOME

Reference

https://donovanmedical.com/hair-blog/ldn

Strazzulla LC et al. Novel Treatment Using Low-Dose Naltrexone for Lichen Planopilaris. J Drugs Dermatol. 2017 Nov 1;16(11):1140-1142.

Lichen planopilaris or Pseudopelade of Brocq: Does anyone care?

Lichen Planopilaris and Pseudopelade of Brocq are Different Conditions with the Same Treatment.

Lichen plaopilaris and pseudopelade are both types of scarring alopecia. They can look similar - but there are many unique differences as well too. Patients with lichen planopilaris often present with scalp itching and burning and the central area of the scalp is typically affected. Increased scalp shedding is common in the early stages. Other areas can be affected too. Some patients have other areas affected as well including eyebrows, and eyelashes. Some patients have oral, nail and vaginal lichen planus but this is present only in a small proportion. Examination of the scalp in a patient with LPP shows redness in the scalp and redness around hairs. There is often scaling and flaking in the scalp as well with scaling notably seen around the hairs in active disease (perifollicular scale).

Pseudopelade of Brocq: A type of primary lymphocytic scarring alopecia

Pseudopelade is a scarring alopecia which also presents with itching and burning. The scalp is often pink in color although may be surprisingly normal in appearance despite the ongoing loss of hair. Patients with PPB often have circular or oval areas of hair loss with strikingly close resemblance to alopecia areata. In fact, pelade is the french word used for alopecia areata. Pseudopelade is different than LPP because it typically lacks the thick perifolliuclar scale seen in LPP and often has more skin atrophy. The skin dips downs with tiny depressions which are referred to as “foot prints in the snow.”

So is it LPP or PPB?

I’ve been part of countless numbers of discussions over the years with patients, physicians, and dermatology trainees as to whether the patient in question has lichen planoplaris of pseudopelade. There is often a great intensity of discussion around the subject. In formal dermatology rounds, physician can debate for extensive amounts of time as if the true answer will be found at the end of the spirited battle.

The reality is that PPB and LPP are distinct conditions. Microarray studies from 2010 showed this clearly. PPB is not just a type of LPP. Generally speaking the less scale and redness around hairs and the more atrophic the skin is - the more likely PPB will be given as a diagnosis. There are histological features too that differentiate these conditions - with PP typically showing a preserved elastic fiber network whereas LPP typically shows a destroyed elastic fiber network. Some physicians and reserachers even feel that PPB is so different from LPP that it should not even be called a scarring alopecia but rather should be called a permanent non scarring alopecia. This is subject to ongoing debate.

LPP or PPB: Leaving our Patients Confused

The active debate that physicians like to have between PPB and LPP often leaves patients confused. Discussions often go something like this;

“I went to see Dr. X and he said I don’t have Pseudopelade of Brocq and what I have is actually LPP”

“I went to see Dr. X and he said what I have is LPP”

Ending the Absurdity: Using the Term “Primary Lymphocytic Scarring Alopecia”

Sometimes, I refuse to use the terms PPB and LPP. These are usually patients with massive files and patients who have seen many physicians to date. These are the patients where 5 doctors have said LPP and 5 doctors have said PPB. These are the patients who are not getting better and what to know two things 1) What is the proper diagnosis and 2) what is the best treatment?

Many physicians fail to recogniize that there is not one LPP and there is not one PPB. It’s not a matter of selecting the right answer. There are probably 20 different presentations of LPP and 5-10 presentations of LPP. Debating over whether a patient has LPP or PPB is good for academic purposes and teaching and good for understanding potential treatments. But at the end of the day, what the patient in front of us has is a scarring alopecia that is caused in part by inflammatory cells called lymphocytes doing things they should not be doing.

In the present day, the treatments for PPB and LPP are the same!! The question that must be asked is what is the purpose of so much extensive debate when the treatments in the present day are the same. Topical steroids, steroid injections, doxycycline, retinoids, hydroxychloroquine, methotrexate are among the options. Physicians far too often spend far too long debating and one upping other colleagues with an attempt to present to the patient what they think the diagnosis is that we forget that the treatments for LPP and PPB are generally the same.

One can argue on an on as to the relevant merits of honing down the diagnosis. Knowing that a patient has LPP prompts one to ask about lichen planus of other areas. But nail, mucosal, vaginal symptoms should be asked of all our patients. Knowing that a patient has LPP might prompt one to screen for certain blood tests including thyroid abnormalities. But these same tests are still appropriate in a patient with presumed PPB.

Conclusion

As a clinician, it is helpful to practice in a manner that strives for accuracy. Accurate diagnosis are fundamental to practicing good medicine. But there are times where we can not always make accurate diagnoses because not everything is always so clear cut. In the case of LPP, and PPB there are classic presentations of these diseases and there are aytpical or non-classical presentations of these diseases. We should strive to recognize the classical cases and strive in these cases to give them the proper names (either LPP or PPB). However, there are other times were the efforts that go into pigeon holing our patients into certain disease categories only serves to remove us further from focusing on actually providing care to the patient. There are dozens of variants of LPP not one. There are many variants of PPB not one.

The term “primary lymphocytic scarring alopecia” serves us well in cases where pigeon holing and efforts to force a diagnosis just doesn’t work.

Reference

Yu M et al. Lichen planopilaris and pseudopelade of Brocq involve distinct disease associated gene expression patterns by microarray. J Dermatol Sci. 2010 Jan;57(1):27-36.

Prescribing Dutasteride in Males with Balding: Are there any criteria ? Should there be any criteria?

Prescribing Dutasteride in Males

The most effective medical treatments for male balding (at the time of this article being written) are oral finasteride and oral dutasteride. There is no debate about this particular comment. In the present day, as the world grapples with the meaning of “post finasteride syndrome”, dutasteride is increasingly a choice for many physicians where it never might have been a choice before. I see it - and I see more now than I did 2 years ago. I see dutasteride being used and 0.5 mg three times weekly. I see dutasteride used at 2.5 mg once weekly or twice weekly. I see dutasteride being used at 0.5 mg daily. I see dutasteride being used more often - and I too prescribe it more now than I did 10 years ago.

Dutasteride is not formally FDA approved for treating male balding but is still widely used. It’s used “off label” though and certainly has a large number of studies to back up its effectiveness. In some countries, dutasteride does have formal approval.

The public is also increasing asking about dutasteride - and increasingly requesting it. After all, we don’t have a great deal of data implicating dutasteride in the same set of issues that finasteride has. Furthermore, it’s more effective than finasteride. These two points lead many to turn to the drug. Some data suggests side effects like sexual dysfunction are greater with dutasteride than finasteride but certainly not all studies show this. Some in fact, show that side effects of dutasteride are similar to placebo.

We don’t yet fully understand everything behind post finasteride syndrome to even begin to dig into what might be called a post dutasteride syndrome or a general 5 alpha reductase syndrome. More studies are needed.

So, will you prescribe me dutasteride or not?

Many patients come in the clinic wanting to know if I’ll prescribe them dutasteride. Some have been on finasteride and haven’t found that it works - and they want dutasteride. Some don’t want to try finasteride at all - they want dutasteride. Some want both. Some know the dose they want.

it all comes down to understanding the medical evidence and the 20 years of science that comes before. There is not a “yes” or “no” answer to whether I will prescribe dutasteride. I don’t know when a patient walks in the door if these medications are right for them - but I do know before the patient walks out the door if these medications are right for them.

The following are the criteria I use in the clinic for determine if the patient is a candidate for dutasteride. These are my criteria and may not necessary be the guideline principles for everyone.

Top 10 Criteria for Prescribing Dutasteride (Donovan)

1. The patient understands the treatment is life-long if he wishes to maintain active medical treatment of his androgenetic alopecia.

2. The patient is aware of the array of possible side effects that have been reported with use of 5 alpha reductase inhibitors including mood changes, depression, anxiety, sexual dysfunction, enlargement of breast tissue (gynecomastia), penile shrinkage, loss of penile sensation, weight gain, muscle weakness and others. The potential effects of dutasteride on males wishing to father are not completely understood. The patient accepts the risk of these side effects if he chooses to use dutasteride.

3. The patient does not currently have severe depression or currently have severe anxiety that might otherwise present a contraindication to using dutasteride. The patient has not been suicidal in the past or been hospitalized for depression and mental illness within the past 5 years.

4. The patient is aware of reports that some patients have experienced persistent (long lasting) problems even when the drug has been stopped. These are mainly studied in the context of finasteride but should be assumed for now to be relevant to the use of dutasteride. The patient accepts the risk of these side effects if he chooses to use dutasteride.

5. The patient is aware that class action lawsuits have been launched regarding the persistent side effects related to finasteride use.

6. The patient is aware of alternatives for treatment including topical minoxidil, oral minoxidil, topical anti androgens (topical finasteride), low level laser, platelet rich plasma and hair transplantation.

7. The patient has no known issues currently related to male inferility or infertility in a female partner.

8. The patient understands the possibility of dutasteride causing a reduction in sperm count and the rare possibility that these reductions may be permanent or long lasting (even when the drug is stopped). The original dutasteride studies showed that after 6 months of stopping the drug, sperm counts had not returned to normal in all study participants and that the total sperm count in the dutasteride group remained 23% lower than baseline.

   Males who are concerned about the possibility of lower sperm count or fertility issues may consider having baseline semen analysis or baseline FSH, LH, Free T4 and testosterone measurements before starting. These lab tests may provide some guidance about baseline fertility. These issues in point 5 are relevant to males who may wish to father children in the future.

9. The patient does not wish to donate blood and understands that blood donation is not possible for at least 6 months after stopping the drug.

10. The patient understands that dutasteride may affect future prostate cancer screening by affecting the PSA value. These issues need to be discussed at the time of such screen and consideration might be given to baseline screening depending on the age of the patient when starting dutasteride.

Conclusion

I can’t say if a patient is a candidate for starting dutasteride when they walk in the office but after 20-30 minutes I can determine if they are likely to be a good candidate for the drug or not. The answers to the questions and issues above help guide the decision making that goes into figuring out if a patient is a candidate for dutasteride or not. It’s not something that can be ascertained in a matter of a few minutes.

References

Meeker JD, Godfrey-Bailey L, Hauser R. Relationships between serum hormone levels and semen quality among men from an infertility clinic. J Androl 2007;28:397–406.

Minoxidil, Collagen and Facial Aging: Where are we at?

Minoxidil and Facial Aging: Yes or No, …or we don’t know?

There is currently a great buzz on the internet world that topical minoxidil affects collagen synthesis and affects facial skin by promoting facial aging. To date, there is no good evidence in the medical literature that minoxidil promotes aging of the face.

As for affecting collagen synthesis - minoxidil probably DOES affect collagen synthesis in the scalp. The problem with the unsubstantiated claims on the internet is that nobody has dared to offer the potential explanation that the minoxidil-induced reduction in collagen synthesis might actually be, well... a good thing.

Androgenetic Alopecia and Fibrosis

The lay public is not always aware that androgenetic alopecia is associated with the body laying down scar tissue in the scalp or what we call “perifollicular fibrosis.” That’s right - male and female balding is associated with INCREASED collagen production in the form of ‘fibrosis’ around hair. And this is not a good thing as the infalmmation and scarring around hairs only serves to speed up the miniaturization process and speed up the destruction of the delicate stem cells. It seems, based on 2006 studies by Yoo and colleagues that a growth factor known as TGF beta is responsible for this increase in collagen production. A variety of studies suggest that minoxidil has the potential to REDUCE TGF beta levels and in turn REDUCE the likelihood of further fibrosis. It seems like it could be a really great thing that minoxidil reduces collagen production.

It’s certainly premature to jump to conclusions that minoxidil promotes facial aging. If it does, it’s rare - likely because not enough minoxidil reaches the facial skin. My office phone rings off the hook with people terrified that their minoxidil is causing their hair shedding or growing hair in the wrong spots. We have never received a call about facial aging concerns. But minoxidil probably does affect collagen and that’s most likely a really wonderful thing rather than a bad thing because it suppresses the formation of more and more scar tissue around hairs that ultimately destroy stem cells. Patients worried about the small unproven risk of facial aging should not of course use the product.

More research is needed to put the facial aging issue to rest or bring it to the forefront so that the FDA and various health regulatory bodies can re-examine this issue more thoroughly.

Botox for Reducing Scalp Sweating in Frontal Fibrosing Alopecia

Botox for Frontal Fibrosing Alopecia Scalp Sweating

Frontal fibrosing alopecia (FFA) is a scarring alopecia associated with hair loss along the frontal hairline. The eyebrows, eyelashes, body hair can also be affected. A 2017 study showed that some women with FFA experience increased sweating in the areas of hair loss. Standard treatments for frontal fibrosing alopecia including topical steroids, steroid injections, and antibiotics were found to be helpful. Interestingly, botulinum toxin treatments (Botox) were also found to be helpful.

We are seeing an increasing amount of women with scalp sweating associated with their FFA. Sweating is controlled in part by the nervous system and this raises the possibility that a specific type of inflammation known as ‘neurogenic’ inflammation may be relevant in FFA. I think we will be hearing more about this area of research in the years ahead.

Treatment of scalp Sweating with Botox in FFA

For the excessive scalp sweating that some patietns with FFA experience, Botox can certainly be considered as an off label (non FDA approved indication). There is evidence that some of the inflammation in FFA is part of what is known as ‘neurogenic inflammation’ and blockade of these nerves will block signals sent to the sweat glands eccrine glands.

 My advice for FFA patients with excessive scalp sweating is to consider Botox in the hairline starting with a conservative number of units before increasing the dose. There seems to be a great (huge) variation in the amount of Botox needed to reduce scalp sweating in FFA. There is no formal protocol for FFA, but I generally recommend starting with 40 units in the affected hairline areas and waiting several months to see how well this work to reduce the sweating. One can certainly increase up to 80-100 units - and even well beyond (100-200 units).  Many patients, but not all, require 100 Units and above. 

Again, even though there is no formal protocol, one might consider diluting a 50 U vial with 1.25 mL and starting with 10 injections (of a 4U / 0.1 mL concentration) spaced 10 mm apart (i.e. 40 units total).  In 4-6 months, a decision can be made as to how well this worked and either proceeding in one of three ways

OPTION 1. Increasing to 60-80 units instead of 40 units and increasing the size of the area injected. This would involve diluting a 100 U bottle in 2.5 mL saline and proceeding with the same technique but injections covering a larger area.

OPTION 2. Diluting the Botox by one half (i.e. diluting a 50 U via with 2.5 mL saline) and injecting more sites.

OPTION 3. Doing nothing different in the case of the patient reporting success with the first trial of Botox and simply waiting for the patient to report that sweating has returned at which point the Botox can be administered again. This is typically every 6-12 months for successfully treated patients.

Reference

Harries et al. Frontal fibrosing alopecia and increased scalp sweating: Is neuorgenetic inflammation the common link. Skin Appendage Disord May 2016; 1(4):179-84

Hair Transplants for Folliculitis Decalvans: Yes or No?

Can patients with folliculitis decalvans have a hair transplant?

Folliculitis decalvans (FD) is a type of scarring alopecia. It is less common than scarring alopecias such as lichen planopilaris. Treatments, such as oral antibiotics and oral isotretinoin, are viewed as the main (so called “first line”) treatments for folliculitis decalvans. They may help slow disease progression and in some cases stop the disease altogether. However, it can takes many months to even many years to stop the disease- and permanent arrest does not happen in all cases. When the disease completely settles and stops and the patient demonstrates that they are able to come off all medications (without their disease flaring) it may be possible for a hair transplant to be considered. Until that time, a hair transplant is contraindicated.

When might a hair transplant be possible?

In general, hair transplants for scarring alopecias are sometimes associated with poor growth. However, very carefully selected patients can sometimes do well with surgery and have reasonably good results - although in my opinion far too often patients with scarring alopecias undergo surgery when they are not (yet) good candidates. Some of the patients who undergo surgery when their disease is not yet calm (ie burnt out) have less than optimal outcomes. Large studies of hair transplant outcomes for patients with folliculitis decalvans have not been published in the medical literature but certainly I see the phenomenon routinely in my clinic (Post operative Complications Clinic, POCC).

Is poor growth the worst that can happen?

In contrast to the scarring alopecia lichen planopilaris, patients with folliculitis decalvans are more likely to have thick scar tissue in the scalp which further limits growth and survival of grafts. In addition to poor growth, disease reactivation can potentially occur after surgery. Most patients, and sometimes their surgeons too, incorrectly approach hair transplantation for patients with scarring alopecia with the overriding view that “the worst that can happen is poor hair growth.” This is incorrect as sometimes the disease reactivates even worse than if the patient had not gone ahead with surgery. The worst that can happen for the patient is persistent redness, pustules, itching, scalp itching, burning, pain and marked hair loss not to mention the psychological consequences. Of course extreme examples like this are uncommon but the point has been made. Severe complications and disease reactivation/flares are unlikely if the patient and his or her disease meets the criteria outlined below. FD must be inactive before surgery is considered.

Hair transplants are not often done in folliculitis decalvans.The medical literature contains few reports of successful hair restoration surgery in FD. In 2010, Tyagi reported 40 % graft survival in a patient with folliculitis decalvans who underwent FUE (follicular unit extraction). Follow up was only 6 months in duration which is insufficient follow up time for scarring alopecia. Some scarring alopecias reactivate 1-3 years following surgery leading the patient to lose all their grafts. 6 months carries little meaning in the world of scarring alopecia. If surgery is performed, I can not emphasize enough the importance of a consultation with a dermatologist prior to the procedure to confirm that the patient truly is a good candidate (and that they meet the five criteria below). This is too often overlooked as patients are eager to move forward with surgery. Such a consultation is essential. In addition, the importance of having an experienced surgeon perform the surgery. It is essential as grafts must be prepared properly, handled properly and inserted at the correct densities.

Criteria for Hair Transplant Candidacy in Folliculitis Decalvans

Several years ago, I published a set of helpful five criteria which helps guide physicians about whether or not they are good candidates for surgery.

1.  The PATIENT should be off all hair-related medications.

2. The PATIENT must not report symptoms related to the FD in the past 24 months. 

3. The PHYSICIAN must make note of no clinical evidence of active disease in the past 24 months. 

4. Both the PATIENT and PHYSICIAN must demonstrate no evidence of ongoing hair loss over the past 24 months. 

5. The patient must have sufficient donor hair for the transplant. 

interested readers can read more in the following link:

Donovan Hair Transplant Criteria - Folliculitis Decalvans

Conclusion

Hair transplants are possible for folliculitis decalvans but only for a subset of patients who have proven, beyond any doubt, that their disease is inactive. The patient and surgeon might hope for the best but be aware that outcomes and graft survival in folliculitis decalvans may be suboptimal.

Reference

Tyagi V, Singh PK: A new approach to treating scarring alopecia by hair transplantation and topical minoxidil. Indian J Dermatol Venereol Leprol 2010; 76: 215.

PADI3 mutations found in Patients with Central Centrifugal Cicatricial Alopecia

Gene Mutations in PADI3 found in about 1/3 of Women with CCCA

CCCA is a scarring alopecia that occurs in about 15 % of black women. It also occurs in some families (in an autosomal dominant manner) suggesting that there may be some underlying genes that predispose women to CCCA.

A new study by Malki et al identified mutations in the PADI3 gene in 14 of 58 patients with CCCA (24%). When the authors examined the frequency of mutations in patients with CCCA compared with a control group of 2702 women of African ancestry that did not have CCCA, it was found that mutations were slightly more common in patients with CCCA than controls (P=0.04).

Summary and Conclusion

This is an interesting study which opens up some important questions in the field of CCCA research. PADI3 plays a key role in formation of the hair shaft. The gene encodes peptidyl arginine deiminase, type III (PADI3), an enzyme that post-translationally modifies other proteins that are essential to hair-shaft formation.

Mutations in this gene appears slightly more common in CCCA than control groups. The PADI3 gene is well known to contribute to another hair shaft condition known as uncombable hair syndrome (UHS). Interested readers can review a prior article written on the UHS:

Uncombable: New Insights into a Rare Condition.

Reference

Malki et al. Variant PADI3 in Central Centrifugal Cicatricial Alopecia. New Engl J Med. 2019 Feb 28;380(9):833-841.

Donovan J. Uncombable: New Insights into a Rare Condition.

Milky Red Areas (MRA) in Lichen Planopilaris

The Milky Red Areas (MRA) in LPP



Trichoscopy (scalp dermoscopy) involves the use of a hand held dermatoscope to better assess the scalp. It has proven helpful for managing a plethora of scalp diseases. 

The field of trichoscopy is filled with bizarre terms. This photo shows the milky red areas of lichen planopilaris. These milky red areas correlate with disease activity. The more milky red areas that are seen the more activity the patient has.

Reference 

Lajevardi V, et al. Assessing the correlation between trichoscopic features in lichen planopilaris and lichen planopilaris activity index. Australas J Dermatol. 2019

Perifollicular scale in Lichen Planopilaris (LPP): Close Association with Disease Activity

The Scale in Lichen Planopilaris

Dermoscopy also called trichoscopy is extremely helpful to the proper evaluation and management of hair disorders. Hand held dermatoscopes not only help in making correct diagnoses but help in monitoring disease activity. I need my dermatoscope to properly do my job.

Perifollicular scale (scale around follicles) is one dermatoscopic feature of lichen planopilaris and frontal fibrosing alopecia. Identifying the amount of scale is important as such scaling correlates nicely with the amount of inflammation going on under the scalp as well as correlating with the so called lichen planopilaris activity index (LPPAI). The presence of perifolliclar scale in patients with LPP is not ideal as it means the patient is at significant risk to lose hair.

Reference 

Lajevardi V, et al. Assessing the correlation between trichoscopic features in lichen planopilaris and lichen planopilaris activity index. Australas J Dermatol. 2019

The Localized Telogen Effluvium

Why does everyone say I have a localized telogen effluvium?

Too often, I hear patients tell me that they have been diagnosed with some kind of localized telogen effluvium. The story typically goes something like this:

I’m losing hair in the front and my doc thinks it’s a localized telogen effluvium 

I’m losing hair in the crown and I’ve been told it’s some kind of localized telogen effluvium.

By definition, a true telogen effluvium affects all hairs on the scalp equally. The hairs at the back feel the same pressure to leave as the hairs in the front. The hairs in the crown feel the same pressures to shed as do the hairs in the sides and back. So when someone tells me they are having a localized telogen effluvium, I know to look for another diagnosis. A localized telogen effluvium does exist. So it is not that the patient or doctor is way off in how they have come to that diagnosis. It’s simply that the main diagnosis is something else.

Here are a few examples:

1. When a patient with alopecia areata sees alot of hair coming out of one area of the scalp and someone confirms they seem to be telogen hairs that are being shed- the diagnosis is still alopecia areata. It’s true there is some kind if “localized telogen effluvium” going on - but the telogen hairs are being shed due to the alopecia areata.

2. When a patient with scarring alopecia sees alot of hair coming out of one area of the scalp and someone confirms they seem to be telogen hairs that are being shed- the diagnosis is still active scarring alopecia . It’s true there is some kind if “localized telogen effluvium” going on - but the telogen hairs are being shed due to the scarring alopecia.

3. When a patient with androgenetic alopecia sees alot of hair coming out of one area of the scalp and someone confirms they seem to be miniaturized telogen hairs that are being shed- the diagnosis is still androgenetic alopecia. It’s true there is some kind if “localized telogen effluvium” going on - but the telogen hairs are being shed due to the androgenetic alopecia.

Conclusion

A localized telogen effluvium should prompt the clinician and patient to search for an underlying diagnosis.

Scalp Biopsies: Just a Piece of the Puzzle

Scalp Biopsies: Often Just a Piece of the Puzzle but Not the Whole Puzzle

Scalp biopsies are extremely helpful in some cases. When the right sized sample (4 mm) is taken from the correct spot and processed properly using the correct technique and interpreted by a dermatopathologist who understands scalp hair & scalp pathology.... a scalp biopsy can be an amazing help.

As an analogy, take a look at the photo. I see some kind of metal object about 5 in x 2 in. It’s hard to tell what it is because it’s not representative enough of the original object. I am not so skilled in identifying electronics to know what it was when I first saw this object. I knew it was not a watch and not a toaster oven. I did not look like the insides of all the watches (or toaster ovens) that I had seen in my life.

I highly skilled electronics expert might correctly identify this as the inside of an iPhone. There are some specific design features that give clues that this is an apple iPhone and nothing else. A true iPhone expert might identify this not only as an iphone but as an iPhone5.

Biopsies of the scalp are just samples of the scalp. A good sized sample taken from the right area increases the odds that the sample will have the necessary features to make the right diagnosis. But you need an experienced pathologist too.

A good electronics technician would not just say this piece of metal is from a smartphone, they would say it’s from an iphone. A good pathologist does not just identify the patient has a scarring alopecia but helps pinpoint that the features are more consistent with lupus than lichen planopilaris. 
A biopsy is not as helpful when the principles of taking and interpreting the biopsy are not followed. A really good sample given to a less experienced pathologist can sometimes still give the right diagnosis (and usually does) and an inadequate sample given to a brilliant pathologist can also sometimes give the right diagnosis (and usually does). But really tough cases need good samples (sometimes 2 or 3), taken from carefully chosen areas and placed on the microscope stage of a pathologist who thoroughly understands hair and scalp pathology.

Dry Shampoo: Good or Bad?

The Facts about Dry Shampoo

I was interviewed by Katherine Lalancette, beauty director with The Kit on the topic of dry shampoo .... Those interested may wish to click on the link below

DRY SHAMPOO: IS DRY SHAMPOO BAD FOR YOUR HAIR?

Pityriasis Amiantacea: A Reaction Pattern Not A Diagnosis

Pityriasis amiantacea: Many Causes

Pityriasis amiantacea, also known as tinea amiantacea, is not a diagnosis. Rather it is a reactive phenomenon that sometimes happens during the process of scalp inflammation. The scalp responds by producing thick sticky (“asbestos-like) scale that wraps around hairs like shingles in a roof. The condition was first described in 1832.

The scales can be difficult to remove and often take out hairs when the scale is removed. Many different conditions can lead to the skin responding in a manner that produces the end result of pityriasis amiantacea.

So what are some of the causes of pityriasis amiantacea? Well, the finding of pityriasis amiantacea is often seen in patients with psoriasis, seborrheic dermatitis, fungal infections, various eczemas and many scarring alopecias.

The photo here is a magnified photo of the scalp of a patient with "pityriasis amiantacea" from seborrheic dermatitis.

Treatment includes identifying the root cause and treating that scalp condition or disease. Treatment such as topical steroids, steroid injections, anti dandruff shampoos, salicylic acid, tar all play a role in treatment.  I view the treatment of pityriasis amiantacea as being somewhat urgent because this type of scale can lead to removal of hair and sometimes even chronic permanent hair loss if secondary infection and scarring are present. #pityriasisamiantacea #hair #scale#inflammation #hairclinic #trichoscopy

Air Travel and Immunosuppression: What is the effect of flying on the immune system?

Air Travel May be Slightly Immunosuppressive

Of the 2 billion people who fly on commercial airplanes every year about 1 in 5 of them report that they develop a “cold” within the first week of arriving back home. 

Is there any logic to this? Could it really be true? 

Well, the world of aviation medicine has an interest in understanding what happens to the human body in a variety of in flight situations (...let alone what happens when we all start traveling off to Mars). In 2012, a group of researchers hypothesized that hypobaric low oxygen (hypoxic) conditions associated with air travel may actually contribute to impairment of the immune system.

To test this, the researchers studied the effects of hypobaric hypoxic conditions during a simulated flight at 8000 ft cruising altitude on immune and stress markers in 52 healthy volunteers before the simulated flight and on days 1, 4, and 7 after the flight. 

The findings showed that the hypobaric hypoxic conditions of a 10-h overnight simulation flight are not associated with severe immune impairment or abnormal IgA or cortisol levels. However, there were associated with short term impairment in some measurements including transient decrease in lymphocyte proliferative responses combined with an upregulation in CD69 and CD14 cells and a decrease in HLA-DR in the immediate days following the simulated flight. 

All these immune system abnormalities normalized by day 7 in most instances.

The conclusion of the study is that the 400,000 or so travellers who feel they have some kind of respiratory infection or cold after air travel could in fact be correct. A short term suppression of some immune responses could be responsible.

Reference 
Wilder-Smith A, et al. Transient immune impairment after a simulated long-haul flight. Aviat Space Environ Med. 2012.