Upright regrowing Hairs in Telogen Effluvium

Upright Regrowing Hairs (URH) in Telogen Effluvium: Many per Field of View

Seeing new pointy hairs is potentially good news as it indicates that a hair has regenerated after falling out just a few weeks prior. There are quite a few hair loss conditions associated with new hairs (what the public frequently likes to call “baby hairs”). The presence of many many new sprouts in close proximity to one another may be a sign of telogen effluvium (hair shedding).

Numerous upright regrowing hairs in a patient with telogen effluvium.

Telogen effluvium can occur from over 2000 potential triggers. Triggers like stress, low iron, thyroid problems, diets, medications, scalp diseases and internal disease are among the more common categories. In the case of a telogen effluvium, these tiny pointy hairs are formally known as “upright regrowing hairs (URH).” They indicate that previously shed hairs are doing their very best to regrow. They do not however, mean that whatever caused the hair to shed in the first place is gone and that the underlying cause is solved. They just mean that some hairs are able to recover despite the trigger. 

The Use Metformin in Lupus: How does this apply to our Discoid LE (DLE) Patients?

Metformin for Lupus: Will it help discoid lupus?

Metformin is a well known diabetes drug. Recent evidence has suggested that metformin may have a positive impact on the treatment of some autoimmune diseases.

Metformin is well understood to reduce glucose production by the liver and to reduce absorption of glucose in the gastrointestinal tract and to increase insulin sensitivity. However, metformin may also reduce production of reactive oxygen species (ROS) which help create inflammation in lupus. The possible benefits of metformin in lupus was demonstrated in 2015 where Wang and colleagues in the journal Arthritis and Rheumatolgy showed that metformin reduce the risk of disease flares by 51 % compared to conventional treatment.

In a 2018 poster by McLeod and colleagues presented at the 2018 meeting of the American College of Rheumatology, authors showed that metformin helps patients with lupus improve control of their disease. The researchers studied 15 patients with lupus using metformin and compared to 1331 patients not using metformin. The authors found there ws a difference in disease activity in patients using metformin.

Metformin for Discoid Lupus: Will it help?

These studies are interesting as they suggest that metformin has the potential to help patients with lupus. What we don’t know yet is whether metformin will help the various types of ‘cutaneous’ lupus including discoid lupus.

Metformin may have an impact not only on autoimmune diseases (including effects on monocytes, macrophages and neutrophils), but improve gut microbiota and have an antifibrotic effect as well. These effects together make them ideal to consider in the study of scarring alopecia. We already know that drugs as pioglitazone may be helpful in lichen planopilaris.

REFERENCES

Wang et al. Neutrophil Extracellular Trap Mitochondrial DNA and Its Autoantibody in Systemic Lupus Erythematosus and a Proof-of-Concept Trial of Metformin.Arthritis Rheumatol. 2015 Dec;67(12):3190-200. doi: 10.1002/art.39296.

McLeod C, Olayemi G, Bhatia N, Migliore F, Quinet R. The Impact of Metformin on Disease Activity in Systemic Lupus Erythematosus [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 10). https://acrabstracts.org/abstract/the-impact-of-metformin-on-disease-activity-in-systemic-lupus-erythematosus/. ABSTRACT NUMBER: 2645

Lichen Planopilaris Dormancy and Hair Transplantation: Caution! Caution! Caution!

Is my Lichen Planopilaris (LPP) Dormant? Can I have a transplant?

A common question I receive is a question from patients who want to know if there LPP is dormant or not - and whether they can proceed with a hair transplant. I generally need to see a patient up close to determine if their LPP is dormant or not. However, out of every 10 people who ask me if their LPP is dormant…I would estimate that 8 are not. Yes, the number is really that high. I consult with patients who have been given the green light to proceed with hair transplant surgery when they are not really good candidates. I consult with an equal number of patients who have undergone hair transpant surgery thinking their LPP was quiet only to experience poor growth or unfortunately even a flare of their disease. This flare sometimes leads to more hair loss than the patient had going into surgery.

Several years ago I published my own personal views on what constitutes being a good candidate for surgery. It has been used by many physicians around the world.

DONOVAN LPP HAIR TRANSPLANT CANDIDACY CRITERIA

So - is my LPP Inactive/Quiet/Dormant?

In order to increase the liklihood that a patient’s LPP is ‘inactive’ (and therefore increase the likelihood that they might actually be ready for consider surgery), the patient MUST answer ‘No” to these 4 questions:

1) Have you have ANY itching, burning or tenderness in the scalp in the last 2 years?

2) Have you been on ANY topical or oral medications for your LPP in the last 2 years?

3) Does your hair density look ANY different compared to 2 years ago?

4) Does the clinical examination by an experienced dermatologist who understands LPP show ANY evidence of disease activity during the last 2 years?

If a patient can really answer ‘no’ to these 4 questions, there is a good chance the LPP is dormant. It’s by no means a guarantee, but it increases the odds massively. My person feeling is LPP does not get the respect it so deserves. The recommendation that is too often given is that a little bit of this cream or a little bit of that lotion settles things right now and makes a patient ready for a transplant. It’s simply not accurate. That’s not how LPP behaves.

LPP is a disease to be respected. It does not have a timeline. It does not always become quiet although it is more likely to become quiet when treated with more aggressive medications and treatments (oral medications, steroids injections). LPP tells us when it is quiet but we need to do all the hard work and be patient to determine if it is or not. We need to take photos every few months. We need to follow the symptoms the patient has. We need to examine the scalp periodically. One can never ever determine LPP is quiet by meeting a patient one time. Never.

To say thatLPP can never be tranplanted is wrong but it’s a view held by some. To say LPP is ready to be transplanted after just a few months of dabbing some medications on the scalp is also wrong but it is also a view held by some. LPP requires a methodical approach to first suppressing and stopping the disease and then removing medications to see if the disease stays quiet over a prolonged period (ideally 2 years). Once the disease has been quiet and inactive and dormant for 2 years…. one can cautiously approach the possibility of a hair transplant.

Nobody Can Figure out the Cause of My Hair Loss

When Nobody Can Figure out the Cause of Hair Loss

There are some pretty challenging and unusual presentations of hair loss. Often I hear patients tell me that they have spent years trying to figure out the cause of their hair loss and nobody has been able to figure it out. While some of these truly are mysteries, I’d venture to say that the vast majority have simply not had a complete work up.

Mystery Causes of Hair Loss

I’m willing to say that a patient truly has a mystery cause of hair loss if four conditions are satisfied and the diagnosis is still not known:

CRITERIA 1: The patient has seen a hair specialist.

This is important. Tough cases need the expertise of someone who handles tough cases. When the heart does not seem to work right, one needs a heart specialist. When the kidneys are not doing what they should, one needs a kidney specialist. When the car breaks down, one needs an expert mechanic - the advice of the neighbours just doesn’t cut it. It only follows that when hair is not growing as it should, one needs a hair specialist. It’s simply but overlooked. One can not say that their diagnosis is a mystery case if they have not seen the right specialists.

CRITERIA 2: The patient has had blood tests for varioius contributors of hair loss.

If the cause of hair loss is unknown and blood tests have never been ordered, then one can not say that the cause is unknown. Every single patient with hair loss needs to be evaluated for what blood tests are appropriate to order. Most people with hair loss benefit from a basic hemoglobin (CBC), a thyroid study (TSH), and assessment of iron status (ferritin). But the list of potential tests that could be ordered is incredibly long. The exact tests that one needs depends on the information that the physician obtains during the visit (i.e. the so called medical history). A variety of hormonal test, autoimmune tests, minerals, and tests for sexually transmitted diseases could be appropriate.

CRITERIA 3. The patient has had a biopsy.

If a patients feels their case is a mystery case and they’ve never had a biopsy, then it can’t be called a mystery case. If a person is coughing for several months and he or she has never had even a simple chest x-ray, it’s inappropriate to say that nobody can figure out the cause of the cough. A variety of tests are available to determine the cause of the cough and unless a person has had those tests, it’s not appropriate to say it’s a medical mystery.

Let me say at the outset that not everyone needs a scalp biopsy. If the cause of hair loss can be determined after listening to the patient’s story of their hair loss, examining the scalp and examining the blood tests, they one does not usually need a biopsy. Most patients who step into my office don’t receive a biospy. i don’t need it to diagnose the reason for their hair loss.

With that said, it’s important to realize that if the cause of hair loss is still unknown after listening to the patient’s story of their hair loss, examining the scalp and examining the blood tests, then one needs a scalp biopsy. it’s that simple.

CRITERIA 4. The patient has had photographs taken one year apart.

Criteria 4 comes as a surprise to some people but to truly say the cause of hair loss is a ‘medical mystery’, (i.e. biopsies, blood tests are not helpful), I need to see photos of the scalp one year apart. These can either be photos the patient brings in or photos that I take one year apart. We need to figure out if the hair issue is contributing to ongoing loss or whether it has stabilized. Some hair loss issues like CTE do not change much over time. The patients loses massive amounts of hair first and then maintains that year after year after year. CTE can usually be diagnosed by history and if not a biopsy can usually capture it so photos are not really needed. However, there are a variety of hair loss situations whereby a photograph taken one year apart helps diagnose the condition that was once labelled a mystery. This includes some cases of scarring alopecia, some cases of androgeenetic alopecia and some psychiatric issues associated with a variety of hair issues.

Tough cases can’t be truly labelled mysteries unless sufficient time has been given to follow the pattern of loss.

Conclusion

There’s so many different ways that humans can lose hair. Some hair loss conditions can present a challenge to properly diagnose. However, many people who label their hair loss as a mystery have simply not had an appropriate evaluation.

Stress and Lichen Planopilaris (LPP): Did stress cause my LPP?

Stress and LPP

Patients often ask me if stress caused their scarring alopecia. In the present day and age, it seems that stress does not cause scarring alopecia but can certainly contribute to it being more active and flaring when it might otherwise be quiet.

An Analogy

As many of my patients know, I often use analogies in the clinic. Analogies are helpful means of thinking about otherwise complex or abstract topics in simpler ways.

Does stress cause scarring alopecia? Well, let consider as an analogy two campers that are camping in the wilderness in the middle of the Summer. It’s been a dry summer and there are signs posted everywhere not to build a campfire because of the concern that it could cause a forest fire. After returning from a long hike, one of the campers decides that he wishes to have a cigarette and proceeds to light and smoke the cigarette. Twenty minutes later both campters realize that somehow the cigarette has caused the nearby underbrush to catch on fire and there is now a small forest fire happening.

The forest rangers and firefighters are called in to put on the fire. During the conversation, one of the campers makes a comment that all this dry weather caused the fire.

Did the dry weather cause the fire? No, not at all. An improperly disposed of cigarette caused the fire. The dry weather did not cause the fire but certainly the dry weather contributed to the fire developing more easily and spreading more rapidly.

Now back to the role of stress in scarring alopecia. The cigarette is like the immune system and the dry weather is like stress. It is the aberrant immune system activation that causes the LPP just like the aberrantly disposed of cigarette causes the forest fire. The dry weather makes the fire flare when it might otherwise have just extinguished itself just liek stress causes the LPP to flare when it might otherwise have just stayed quiet.

Stress can contribute to a scarring alopecia becoming more active and contribute to flares but probably is not an underlying cause. In my experience, some conditions (like frontal fibrosing alopecia) seem to have a greater contribution from stress than other conditions (like folliculitis decalvans) The exact reason for this is not clear.

Articles of Interest

Interested Readers may wish to see previous articles by Dr. Donovan

Why is My Scarring Alopecia Flaring Again?

What Causes Scarring Alopecias Like LPP to Reactivate?

PRP for LPP: Perhaps Rethink the Plan

Platelet rich plasma (PRP) for LPP: Is it an option?

Does PRP help lichen planopilaris and other scarring alopecias? Maybe sometimes.. Does it help the disease alot? Rarely. Is is a good option for starting treatment for someone with LPP? No, it’s not.

That’s the jist of what really needs to be said and that’s where this article could end. But I won’t let it end there. In the present day, PRP is popular. If people are looking for a popular treatment, I say go for it. it If they are looking for a treatment that helps stop a disease and is effective, I’d say have seat and let’s chat. Popular vs effective - the choice is up to the patient.

To say that PRP is a consistently effective treatment for scarring alopecia is nonsense. In fact, even with the most potent of drugs we don’t always shut down this disease. Of course, we win a good amount of the time in treating scarring alopecia but not nearly enough.

PRP is popular nowadays because it is fairly safe (there are side effects of course that one needs to know about). Yes, it’s that patient’s own blood. Yes, it’s not a drug. Yes, it’s natural. I agree with all these points. Do I agree that it stops scarring alopecia on a consistent basis? No way. How do I know? I treat a lot of patients with scarring alopecia over the years and I have treated lot of patients with PRP over the years. But more importantly I have treated a good number of patients with scarring alopecia PLUS PRP over the years and never found it to really help that much.

The most effective treatments for lichen planopilaris are treatments that are found in the following list: hydroxychloroquine (Plaquenil), doxycycline, methotrexate, cyclosporine, topical steroids, steroid injections, tacrolimus, mycophonolate, isotretinoin, tofacitinib. Treatments like low level laser may also help a bit.

The most effective treatments for frontal fibrosing alopecia are treatments that are found in the following list: antiandrogens, isotretinoin hydroxychloroquine (Plaquenil), doxycycline, methotrexate, cyclosporine, topical steroids, steroid injections, tacrolimus, mycophonolate.

Conclusion.

When a patients says to me - “I want PRP for treating my disease” I say to them the following:

IF PRP treatment is something you want for treating your LPP, I will leave the ultimate decision to you. If you can answer the following 3 simple questions for me, you may in fact be a good candidate for considering PRP. If you answer no to any of the following, I would urge you to please rethink the plan:

QUESTION 1: Can you say out loud at least 5 types of medications that are typically used to treat your type of scarring alopecia? Yes or No.

QUESTION 2: Do you take photos of your scalp (or does somebody take photos) consistently every 3-6 months? Yes or No.

QUESTION 3: Do you understand that PRP may be required every few months for life and that it is not a one time treatment? Yes or No.

If a patient answers yes to ALL of these three questions, there is a good chance they have the background understanding that puts them in a position to make an informed decision about PRP for treating their scarring alopecia. Of course, I’d also like the patient to be able to state in question 1 how well the treatment is expected to work (i.e. percent of patients they are expeccted to help) but these 3 questions are pretty good screening questions.

IF a patient can not answer ‘yes’ to these three questions or answers no to even one of them, I would say to the patient - perhaps rethink the plan (PRP).

Dexamethasone Pulsed Therapy for Alopecia Areata in Children Under 12

Oral Dexamethasone Pulsed Therapy for Alopecia Areata in Children

There are over 25 treatment options for alopecia areata. Generally speaking, topical steroids, steroid injections and minoxidil are important therapies for patchy alopecia areata (early staged disease). This is by far the most common type of alopecia areata and so these three treatments are among the most useful.

For patients with more extensive and progressive alpecia areata, a variety of treatment options can be considered including oral steroids (dexamethasone, prednisone, prednisolone), and oral immunosuppressants such as methotrexate, tofacitinib, ruxolitinib, sulfasalazine. Topical irritant and allergic therapies such as anthralin, diphencyprone and squaric acid are also important parts of the treatment ladder.

Treatment of Alopecia Areata in Children

The principles of treating alopecia areata in children is similar to treating alopecia in adults. One wants treatments that work really well and at the same time are really safe, affordable and easy to administer.

See previous article: The S.A.F.E. Principle for Treating Hair Loss

In my practice, treatment of alopecia areata in children under the age of 12 involves use of 8 main treatments. Four of them are topical and include topical steroids, minoxidil, anthralin and diphencyprone (or squaric acid). Three of them are oral treatments and include oral methotrexate, oral oral steroids, and the JAK inhibitors. The last one is neither topical nor oral - and simply involves what I call “active observation:” (or what some might call doing nothing). Many children and adults with alopecia areata regrow spontaneously so treatment is not always necessary.

Oral Dexamethasone in Alopecia Areata

Dexamethasone is an oral steroid that may be helpful in some cases of rapidly progressing alopecia areata. It has been studied in children with various medical conditions for well over 30 years. Because of the long half life of dexamethasone compared to prednisone (54 hours vs 1-2 hours), the option exists to use dexamethasone less frequently in so called “pulses” rather than daily as in the use of prednisone.

One of the important studies of dexamethasone use for treating alopecia areata was a 1999 study by Sharma and Gupta. They studied 30 patients with alopecica areata including a mix of adults and children. 3 patients in the study were children under 12 and were treated with dexamethasone on two day of the week at doses of 2.5 to 3.5 mg.

Sharma’s study showed that patients who received treatment for the minimum 12 week study period had excellent growth in 63.3 % of patients. 20 % of patients had no growth. It took an average of 5 months to get to the stage of excellent regrowth indicating that the regrowth can take time in these more challenging cases. Relapse was observed in two patients after 3 and 6 months but hair did regrow with treatment. About 25 % of patients had side effects of some kind but these were generally mild.

Other studies of dexamethasone use in adults have been conducted more recently. Vano-Galvan and colleagues from Spain conducted a nice study in 2016 reviewing dexamethasone use in 31 adults with alopecia totalis (n=9) and alopecia universalis (n=22). The dose used in treatment was 0.1 mg per kg per day for the two days of the week. About 80 % of patients had some type of response and 71 % had a complete response. The mean time to see any type of hair growth happening was about 1.5 months. Side effects were observed in 31 % of patients including weight gain, Cushing-like phenomena, striae and irritability.

Conclusion and Summary

Pulsed therapy with oral steroids is an option for children with alopecia areata. When one is deciding about which oral steroid to use, options for both prednisone and dexamethasone need to be considered. The long half life of dexamethasone and option for twice weekly dosing makes it a useful option. I generally prescribe dexamethasone on Saturday and Sundays to make it easy to parents to remember. The dose in children is according to weight but generally 2-4 mg of dexamethasone on Saturday and 2-4 mg of dexamethasone on Sunday is quite common. Because the dose is 0.1 mg per kg, it’s quite easy to calculate the appropriate dose - a 20 kg child would receive 2 mg each day of the weekend and a 30 kg child would receive 3 mg on each day of the weekend and a 40 kg child would receive 4 mg on each day of the weekend. Dexamethasone is given with calcium and vitamin D to protect bone mass. Side effects seen in children are generally mild but one must monitor for side effects carefully include irritability, weight gain, blood pressure changes. Long term use is generally discouraged and the goal of dexamethasone therapy is to help reset the immune system in some way so that minoxidil and topical steroids can once again become the mainstay of therapy for the child.

References

Sharma VK and Gupta S. Twice weekly 5 mg dexamethasone oral pulse in the treatment of extensive alopecia areata. J Dermatol 1999; 26: 562-5.

Vañó-Galván S et al. Pulse corticosteroid therapy with oral dexamethasone for the treatment of adult alopecia totalis and universalis. J Am Acad Dermatol. 2016 May;74(5):1005-7.

Spano F and Donovan JC. Alopecia areata: Part 1: pathogenesis, diagnosis, and prognosis. Can Fam Physician. 2015 Sep;61(9):751-5. Review.

Spano F and Donovan JC. Alopecia areata: Part 2: treatment. Can Fam Physician. 2015 Sep;61(9):757-61. Review.

Taking Iron Supplements: What's the best way anyway?

Alternate Day Iron May be Most Effective

Many hair loss patients with low serum ferritin are advised to increase their iron intake. The most common means of doing so is through oral iron supplements. The ideal way of taking supplements continues to be researched. New research supports the notion that taking iron supplements every other day (alternate days) may be a better way to get iron into the body.

The whole reason why researchers began studying how best to take iron is because iron intake triggers the body’s liver to make a protein called “hepcidin” and this hepcidin protein in turn blocks iron absorption from the gut. It seems the body has a fascinating built in mechanism to help prevent too much iron getting into the body.

New research suggests that taking iron supplements on alternate days may be equally effective if not more effective way for patients with low ferritin to address their low iron stores

A recent study set out to determine if iron absorption is better when iron supplements are given on consecutive days vs giving them on alternate days as well as to determine whether iron absorption is better when pills are given as single morning doses or better when doses are split with half in the morning and half in the evening.

In order to answer these questions, researchers performed two prospective, open-label, randomised controlled trials assessing iron absorption using special isotope labelled iron in iron-depleted (defined as serum ferritin less than 25 μg/L) women aged 18–40. In the first study, women were randomly assigned to two groups. One group was given 60 mg iron in the morning on consecutive days for 14 days, and the other group was given the same doses on alternate days for twice as long - 28 days. In the second study, women were assigned to two groups. One group was given 120 mg iron in the morning and the other was given 60 mg in the morning and 60 mg in the afternoon for three consecutive days.


For study 1, 40 women were enrolled. 21 women received daily iron and 19 received iron every other day. At the end of treatment (14 days for the consecutive-day group and 28 days for the alternate-day group), cumulative total iron absorption was 131 mg in the daily group compared to 175 mg in the every other day group. Serum hepcidin levels were greater in the consecutive-day group than the alternate-day group (p=0·0031). In study 2, 20 women were enrolled. Ten women received once-daily dosing and 10 received twice-daily divided dosing. There were no significant differences seen in total iron absorption between the two dosing regimens. However twice-daily divided doses resulted in a higher serum hepcidin concentration than once-daily dosing (p=0·013).

Conclusion and Summary

The study was interesting and supports a notion that prescribing iron on an every other day basis such as Monday, Wednesday and Friday mornings might be ideal. These strategies may limit the body’s production of hepcidin and facilitate iron absorption. These strategies may also limit the gastrointestinal side effects that can happen with iron supplements.

Reference

Stoffel NU et al. Iron absorption from oral iron supplements given on consecutive versus alternate days and as single morning doses versus twice-daily split dosing in iron-depleted women: two open-label, randomised controlled trials. Randomized controlled trial. Lancet Haematol. 2017

What is my own risk of developing hair loss?

A closer look at risk when family parents are affected?

When one hears that a particular condition has a “genetic” basis, a common reaction that follows is “will the children in the family be affected?” The answer comes down to the type of inheritance and the nature of the actual genes. Some conditions carry a high risk and others a low risk.

In the world of hair loss, we are increasingly learning of a genetic contribution for many of the conditions. This means that an individual in the family could be at higher risk for developing that type of hair loss compared to an individual in the general population. However, the risk can range from very high to very low.

Two polar examples on both extremes are male pattern hair loss (high risk) and frontal fibrosing alopecia (low risk). Male balding is complex and over 256 genetic regions contribute to this polygenic condition. Most males who have a dad with balding will develop some amount of balding themselves. For example, in a study of 572 men ages 16-91, young men with a balding father had a 5.5 times increased risk of balding compared ti young men who did not have a balding father. In another study, only 1 of the sons of 50 non balding men had Hamilton Norwood type III balding or worse. In contrast, 32 of 54 (60 %) of sons whose fathers were bald had Hamilton Norwood scale type III baldness or greater.

On the other extreme, frontal fibrosing alopecia is less common. Although the cause is not clear, 4 genes may have a role. Despite now known to have a genetic contribution, the risk for a family member to also develop FFA is still low. In fact, I would estimate that out of every 200 women with FFA I see - maybe 1 or 2 have a mother who also has FFA. The risk is clearly much different than for male balding.

The diagram shows my estimates for risk. Abbreviations include androgenetic alopecia (AGA), central centrifugal cicatricial alopecia (CCCA), alopecia areata (AA), frontal fibrosing alopecia (FFA), lichen planopilaris (LPP), discoid lupus (DLE).

Chronic Telogen Effluvium: Photos don't help with Diagnosis

Chronic telogen effluvium (CTE)

Chronic telogen effuvium remains one of the most poorly understood and confusing of all the hair loss conditions. First, this is a hair shedding condition whereby women experience intervals in their life where massive shedding occurs followed by intervals whereby things feel pretty normal again.

CTE is frustrating because the scalp may look normal. I’m often asked by prospective patients if they can email me a photo to me so I can tell them what I think. This can work well for some types of hair loss - but not chronic telogen effluvium! Photos do not help in confirming the diagnosis of CTE! For patients with CTE, the scalp looks quite normal and so does the hair! Granted the patient may feel they once had double or triple the amount of hair on their scalp - but the patients still walks through the door looking as though they have fairly full hair.

How do we diagnosis CTE?

CTE is diagnosed by listening to the patient’s story and by examining the scalp up close to exclude other mimickers. The patient’s story is important because the patient reports episodes of increased hair shedding. The hair loss occurs from all over the scalp. There may be symptoms like burning, creepy crawly feelings sometimes and tenderness. These are all part of the so called trichodynia that some patients experience.

Examination of the scalp shows bands of regrowth as evidence of previous sheds but also shows that there is no miniaturization of hairs that would otherwise be consistent with androgenetic alopecia. There is no loss of ostia and evidence of scarring that would point to a diagnosis of cicatricial alopecia.

Biopsy is seldom necessary but can be used to confirm that the patient does not in fact have genetic hair loss, scarring alopecia or alopecia areata as the cause of their hair loss.

Conclusion: Photos don’t help in the diagnosis of CTE

Patients with CTE don’t usually look like they have hair loss. The patient with CTE certainly HAS hair loss - but they don’t look like they have hair loss to someone who has never met them before. The patient with classic isolated CTE will be told by family and friends that they look fine - despite the fact that that patient is frustrated with all the shedding they have and frustrated by amount of hair they have lost.

Frontal Fibrosing Alopecia and the HLA B gene

Specific HLA B gene variation carries five fold increased risk of FFA

A new study has put frontal fibrosing alopecia on the radar as another hair loss condition with at least some degree of a genetic basis. Researchers this month identified 4 genes that appear to be relevant to frontal fibrosing alopecia, a type of scarring alopecia which is increasing in prevalance.

Variations in the coding of 4 genes has been identified to be associated with the development of frontal fibrosing alopecia, a type of scarring alopecia.

Of the 4 genes (shown here) HLA -B*07:02 or simply “HLA-B” on chromosome 6 was found to have the strongest association. The pinpointing of HLA-B was important because it confirms the important immune basis of this elusive disease. HLA-B is part of thr major histocompatibility complex and is one of the so called “immune recognition genes.” This genes appears to influence how antigens get presented to our immune system. 

Patients with a certain variation in the genetic coding for this gene have a five fold increased risk of developing FFA. The other three genes were important but carried less significant risk for developing FFA than the HLA-B.

Reference

Tziotzios et al. Nature 2019.

Vancouver Chapter of NAAF

NAAF Meetings in Vancouver

I enjoyed attending the quarterly meeting of Vancouver Alopecia Areata patient support group last week. I serve as the medical advisor for the Vancouver chapter of the National Alopecia Areata Foundation (NAAF) support group.

Support groups can be powerful because they are generally focused on supportive listening. There is of course advice shared and knowledge gained, but it’s the supportive listening that is often most helpful to participants. The opportunity to simply share one’s experiences during his or her hair loss journey can empowering. 

Details on support group meetings for patients with alopecia areata in the Vancouver area and around North America are available through the National Alopecia Areata Foundation (www.naaf.org) or at phone number 415.472.3780 or by email info@naaf.org.

Aggessive hair shedding in young males: More than just a "TE"?

Androgenetic Alopecia in Males Often Mimicks a TE

I just posted a new answer to our “Question of the Week.” I was asked to comment on the best treatment strategy based on a scenario I as given.

The full answer to this week’s question can be read here:

Aggressive Shedding in Males: A Common Misdiagnosis of Telogen Effluvium

To submit a new question for consideration of our Question of the Week, simply visit complete our online form

Squaric acid, DPCP and Steroid Injections: Can then be used together?

Squaric acid, DPCP and Steroid Injections for Alopecia areata

Alopecia areata is an autoimmune hair loss condition. Patients often develop circular or oval shaped patches of hair loss first. However, some patients go on to develop more widespread hair loss while others regrow their hair back.

There are at least 25 treatment options for alopecia areata that a dermatologist can offer. One generally starts with the safest options before moving down the list of potential treatments.

See previous article: TREATMENT OPTIONS FOR ALOPECIA AREATA

Squaric acid, DPCP and Steroid injections

Alopecia areata is understood to be an autoimmune disease. What this means is that the body’s immune system is somehow primed to attack the hair. (It’s probalby also true to say that the body’s hair follicles are also ‘primed’ to call the immune system over to it as well).

When a biopsy is performed from the scalp of a patient with alopecia areata, what is generally seen are inflammatory cells called lymphocytes around the base of hairs. In this inflammatory soup, hair follicles simply can’t grow well and leave the scalp. Treatments that reduce a specific type of inflammation called lymphocytic inflammation are helpful for many patients with alopecia areata. These treatments include topical steroids, steroid injections, as well as a wide variety of immunosuppressive pills. Topical steroids and steroid injections are generally considered first line in the treatment of localized alopecia areata (i.e. alopecia areata confined to a few patches).

Squaric acid dibutyl ester (SADBE) and diphencyprone (DPCP) are unique weekly topical scalp treatments that do not directly reduce inflammation but rather redirect where in the scalp the inflammation ends up and also the specific type of inflammation that gets created. The same is true with anthralin, although anthralin causes ‘irritation’ rather than true allergy. When SADBE or DPCP are applied to the scalp, an allergic reaction develops on the scalp and this directs the immune system focus away from the hair follcile and towards the scalp skin instead. When anthralin is applied to the scalp, an irritant reaction develops on the scalp and this directs the immune system focus away from the hair follcile and towards the scalp skin instead.

Can Squaric acid or DPCP be used with Steroid Injection Treatments?

Even though squaric acid, DPCP and steroid injections are three important treatments for alopecia areata, the they can not be used together. The treatments work completely opposite each other. Squaric acid or DPCP activates inflammation and causes redness, scale and dermatitis. Steroid injections stop inflammation and remove redness, scale and dermatitis. The treatments essentially cancel each other if used too close together. The same is true with anthralin - anthralin and steroid injections don’t generally go together.

E -cigarettes and hair loss: Still a concern

E-cigarettes have the potential to accelerate androgenetic alopecia

Electronic cigarettes (or e-cigarettes) have become increasingly popular since they first arrived to the world scene in 2004. Nowadays nearly 4 % of adults in the US use them.

A e-cigarettes is a battery operated device that typically emits vaporized nicotine to the user. Doses of nicotine delivered to the user range from very low (even zero) to very high. They provide the user with a similar sensation to regular cigarettes without the tobacco smoke. There are many forms of e-cigarettes including those that resemble a classic cigarette as well as a pen, pipe and cigar. E-cigarette use is increasingly popular in adolescents, many of whom have never smoked regular (tobacco) cigarettes. In fact, a great deal of marketing efforts go into targetting younger age groups.

E-cigarettes are not without risk. In 2016, FDA clamped down on sellers of e-cigarettes and brought forth tougher rules on how they are sold and marketed. In the same year, the surgeon general stated formally that e-cigarette user is a significant public health concern.

E-cigarettes and Hair Loss

For many years, researchers have been trying to figure out whether smoking speeds up the process of genetic balding. The studies have been somewhat inconsistent but point to the possibility that smoking accelerates the process of male balding.

An important study examing the relationship between smoking and hair loss was a 2007 study by the Taiwanese group of Dr. Su and Dr Chen.  These researchers examined 740 patients between the ages of 40 and 91 over a 2 month period.  They found that smokers generally had worse androgenetic alopecia compared to non-smokers. In fact, smokers had nearly a two-fold increased risk of having moderate or severe genetic hair loss compared to non-smokers. In addition, the early development of male balding was more likely in smokers.

It’s not clear if e-cigarettes bring about the same risk for the hair follicle as traditional tobacco cigarretes. It’s certainly possible the risk is different but no one knows yet for sure. It has been proposed be that smoking is damaging to the tiny blood vessels and the there are toxic substances in cigarette smoke that damage the cells in the hair follicles. It's also possible that smoking causes inflammation which speeds up the process of genetic hair loss. Some of the toxic substances in traditional cigarettes may be absent in e-cigarettes. But what is not absent in most e-cigarettes is the nicotine component. It’s likely that nicotine affects blood flow and affects inflammation in hair follicles.

In addition to the effects on blood flow, there is no getting around the fact that nicotine is found in hair of individuals who use nicotine. In fact, one way to monitor in clinical studies how well a person is stopping smoking is to measure the nicotine content of their hair.

Nicotine may also promote inflammation. In 2000, a study performed in rats showed clearly that this is the case. Rats exposed to nicotine were showed to have chronic inflammation and fibrosis (scarring) in the skin and effects were seen around hair follicles as well.

Conclusion

There is still alot of unknowns when it comes to the effects of e-cigarettes on the hair and more good studies are needed. It is quite likely that nicotine affects hair in a negative way and that use of e-cigarettes may accelerate the process of balding in those who have a genetic predisposition.

Reference

 Su LH and Chen T H-H. Association of Androgenetic Alopecia with Smoking and Its Prevalance Among Asian Men. Archives of Dermatology 2007 143; 1401-1406.

Inaloz H et al. Teratogenic effects of nicotine on rat skin. Clin Exp Obstet Gynecol 2000; 27: 241-3

Genetic Testing for Frontal Fibrosing Alopecia (FFA)

Can we test for the FFA genes?

Since the announcement last month that 4 new genes were discovered to play a role in frontal fibrosing alopecia (FFA), I have been asked several times if patients can arrange to have these genes tested for themselves of their families. The short answer is that such testing is not available yet, nor do we know yet how to properly use this information.

There were four main genes identified but one in particular stood out as carrying the highest risk compared to the other 3 genes. This was HLA-B*07:02 on chromosome 6. This gene is part of the major histocompatibility complex (MHC). This appears to be highly relevant because the HLA-B is an important so called “immune recognition gene.” A variation in these genetic coding in these immune recognition genes is thought to contribute to autoimmunity - which in the case of FFA would lead to autoimmune destruction of the hair follicle. What was remarkable in this study was the observation that specific mutations in the HLA B gene carried a 4.73 fold increased risk of developing FFA. When I look at the data, this points to a really significant association. It is this gene that might influence how autoantigens get presented to the immune system.

We don’t yet know how to use this information and whether there are other environmental risk factors that are more important or equally important to be exploring or testing at present. These are exciting times for new research in FFA. However, these are still the early days of understanding this information and how to use it properly.

Reference

Christos Tziotzios et al. Genome-wide association study in frontal fibrosing alopecia identifies four susceptibility loci including HLA-B*07:02. Nature 2019. Online March 8, 2019

 https://doi.org/10.1038/s41467-019-09117-w

https://www.nature.com/articles/s41467-019-09117-w.pdf

Exam Review

Working with Graduating Derm Residents

I enjoyed working with the dermatology residents again today - this time with the senior final year residents who will soon graduate (.... and step out into the real world to help people with dermatological issues). I helped the residents review and consolidate a great deal of information on the pathogenesis, diagnosis and treatment of both scarring and non-scarring hair loss. It’s looking like Canadian medicine will soon welcome some pretty talented new dermatologists to the group. Honored to work with them today.

Lecture for Dermatology Residents

Lecture for Residents

I enjoyed working with our amazing UBC dermatology residents yesterday afternoon reviewing and navigating through some of the many challenges of scarring alopecia!

Scarring Alopecias: Not always Classic in Appearance

The Scarring Alopecias: Not always classic

Scarring alopecias are a type of hair loss associated with the development of permanent hair loss. Not every scarring alopecia looks “classic” or “textbook.” One needs to always consider a scarring alopecia in patients with many symptoms (especially scalp tenderness and burning). Rapid loss, shedding, and redness in the scalp may also cause one to at least consider the possibility.

This patient has lichen planopilaris despite the lack of more classic dermatoscopic features. There is not much in the way of perifollicular redness. There is no real perifollicular scale (and the little bit of scale that is present can be seen in the normal scalp and in seborrheic dermatitis). There is no pili torti (twisting of hair) and no loss of follicular ostia. There is so degree of ansotrichosis (variation in diameter of hairs) which is consistent with the underlying androgenetic alopecia that the patient has had for years prior to the new development of scarring alopecia. The patient presented with hair shedding, scalp burning, scalp itching, tenderness and redness. A black dot marks the spot that a biopsy was taken to prove the diagnosis of lichen planopilaris.

Telogen Effluvium: Upright regrowing hairs.

Telogen Effluvium and Regrowth

Upright regrowing hairs (URH) are a common dermatoscopic (trichoscopic) feature of telogen effluvium. They are by no means specific for telogen effluvium as telogen effluvium actually does not have any specific dermatoscopic features. URH represent hairs that have just started their journey of regrowth after being shed a few weeks/months prior. Upright regrowing hairs are easily confused for the normal regrowth that is seen on anyone’s scalp as well as the smaller vellus hairs of androgenetic alopecia.

What distinguishes URH is that there are lots of them and they are all the same size. The are pigmented, stand straight up to the sky and are about 1/2 the thickness of a neighbouring hair. A few new sprouts here and there does not constitute a true URH. True URH are found in abundance all over the scalp.