In this video, I review the latest in emerging treatments for hair loss.
Hair loss can either be localized (meaning one area of the scalp) or diffuse (meaning all over the scalp). There are many causes of hair loss at nape of the neck and the back of the scalp.
Traction alopecia refers to a type of hair loss due to the tight pulling of hair. The back of the scalp is particularly susceptible to loss of hair. Hair styling practices can frequently lead to traction including braids and weaves and pony tail. If traction alopecia is of recent onset, hair regrowth can occur even without treatment. If traction is longer standing, the hair loss can often be permanent. Some women with hair loss that looks like traction actually have a scarring alopecia known as cicatricial marginal alopecia.
PHOTO 1: Traction alopecia presenting as hair loss in the nape
Alopecia areata is an autoimmune disease that affects about 2 % of the world. Hair loss can occur anywhere. Alopecia areata can frequently cause hair loss specifically at the nape in some patients. The particular form that causes loss at a the back of the scalp is the 'ophiasis' form. The ophiasis form is frequently resistant to standard treatments although topical steroids, steroid injections and diphencyprone are typically first line.
PHOTO 2: Alopecia areata presenting as hair loss in the nape
3. Androgenetic Alopecia (photo 3)
Androgenetic alopecia (male and female thinning) typically causes hair loss at the top of the scalp. In men, the temples and crown are most often affected. In women, the mid-scalp region is generally affect first. The back of the scalp can also be affected although this is not typically thought of. Hair thinking along the nape is not uncommon in advancing balding in men and women.
PHOTO 3: Androgenetic alopecia (AGA) presenting as thinning in the nape
Frontal fibrosing alopecia (FFA) is a type of scarring alopecia. FFA typically affects women between 45-70. Most often hair is lost along the frontal hairline and eyebrow. However the back of the scalp (at the nape) and frequently be affected. The hair loss in the nape typically starts at the sides (left side and right side) just behind the ears. Treatments for FFA include topical steroids steroid injections, topical calcineurin inhibitors. Oral drugs include finasteride, doxycycline and hydroxychloroquine at the top of the list.
PHOTO 4: Frontal fibrosing alopecia (FFA) presenting as hair loss in the nape
Heat and chemical treatments can lead to hair shaft damage and hair loss at the nape. Frequently, heat and chemical overuse leads to an increased tendency to develop traction alopecia which si discussed above.
Acne keloidalis nuchae (AKN) is a condition that can affect both men and women. Small papule or bumps develop along the posterior scalp and are accompanied by hair loss in the region as well. The hair loss in AKN is often permanent and can lead to thicken and thicker scars some of which are disfiguring.
Some individuals are born with abnormalities in how the hair shaft is produced. This frequently leads to hair breakage. Monilethrix is one of the hair shaft disorders that frequently leads to hair loss along the nape.
Diphencyprone or "DPCP" is a chemical that causes allergic reactions. It is used as an off-label (non FDA approved) treatment for patients with alopecia areata whereby the DPCP is applied directly to the scalp and left on for 24-48 hours. After 48 hours the DPCP is washed off.
DPCP is not soluble in water so it is typically made up in acetone. Acetone is an organic solvent best known as the ingredient in nail polish remover. DPCP may also be soluble in other ingredients such as isopropanol.
What is often forgotten is that DPCP degrades in light and at room temperature. DPCP should be ideally stored at 4 degrees ceclius and protected from light. Usually DPCP is dispensed in brown light proof bottles but I recommend wrapping in aluminum foil to further protect from light.
Anyone who reads online will see that there are reported links between topical minoxidil use and erectile dysfunction. But is it accurate ? My opinion is that it's not impossible - but very unlikely for most users. Let's take a look at the data.
To date, there are no really good clinical studies that support an associated between topical minoxidil use an worsening erectile dysfunction. The original studies from the 1980s did not raise this issue. However a recent study did suggest that topical minoxidil was the cause of erectile dysfunction.
MINOXIDIL ASSOCIATED WITH ERECTILE DYSFUNCTION
Minoxidil is a blood pressure medication and was used orally in the 1980s as Loneten. It's certainly not out of the question for blood pressure medications to cause erectile dysfunction. Drugs like beta-blockers and diuretics like hydrochlorothiazide can sometimes cause erectile dysfunction. Blood pressure medications like ACE inhibitors, Angiotensin receptor blockers are less likely. Minoxidil was FDA approved in 1979 as an oral medication to treat blood pressure problems. Topical minoxidil however, does not impact blood pressure to any significant degree in most users. Erectile dysfunction is not a side effect that has been raised in clinical trials to date.
When a patient asks me whether their minoxidil could be causing sexual dysfunction, my answer is first that it is possible and that we really need to consider something know as the Naranjo Adverse Drug Reaction Probability Score.
Anything applied to the skin or taken by mouth has the potential to cause a side effect. Some medications rarely cause side effects and others tend to cause frequent side effects. Occasionally a patient will report a side effect that perhaps has never been reported before. The question then becomes - is this a real side effect from the drug or is it happening from something else?
The Naranjo Scale was created nearly 40 years ago to help standardize how clinicians to about assessing whether or not a drug could be implicated in an adverse drug reaction. It is used in controlled clinical trials. The scale is quite easy to use - and involves asking the patient 10 questions. Answers to the question are recorded as "yes", "no" or "don't know" and different points are assigned to each answer (-1, 0, +1, +2).
Scores can range from -4 to + 13. A score of 0 or less means the likelihood of the drug causing the side effect is doubtful, a score 1 to 4 indicates it is 'possible', a score 5 to 8 means it is 'probable' and a score 9 to 13 means it is 'definite'
Tanglertsampan C. Efficacy and safety of 3% minoxidil versus combined 3% minoxidil / 0.1% finasteride in male pattern hair loss: a randomized, double-blind, comparative study. J Med Assoc Thai. 2012.
Cecchi M, et al. Vacuum constriction device and topical minoxidil for management of impotence. Arch Esp Urol. 1995.
Radomski SB, et al. Topical minoxidil in the treatment of male erectile dysfunction. J Urol. 1994
Iron supplements are commonly prescribed for individuals with low iron stores and low hemoglobin levels. I always advise patients to check with their physicians before simply taking a pill. Some causes of iron deficiency are quite serious and need a proper evaluation. Here are some general principles.
I'm okay with my patients taking most supplements provided they are not having side effects and provided it’s doing a good job and helping to raise ferritin levels. There are over 100 iron supplements on the market. There is no right or wrong as a starting point for most people. If the supplement helps raise ferritin levels to the desired range and the patient feels good while taking the supplement, then it may in fact be the right choice.
Iron supplements range from 5-10 cents per pill to 1.25 to 1.50 per pill. If a patient generally has a good stomach and is not prone to constipation or diarrhea, I recommend to start with the least expensive forms. They often work very well and the patient has the potential to save a lot of money. Any of the formulations listed in the attachment below are reasonable starting points. Ferrous gluconate for example is just pennies per pill.
If my patient frequently experiences an upset stomach, or is prone to constipation from previous iron supplements I recommend they consider PROFERRIN or FERRAMAX. Others may also be acceptable. These pills are particularly helpful if patients use antiacids as PROFERRIN and FERRAMAX do not require acid to be absorbed and are therefore acceptable for patients who use antacid medications.
Regardless of which pill a patient chooses, I can't overemphasize the important of the following key message: go slowly! Start with one pill every other day for 5 days and then go up to daily for 2 weeks. I may advise patients to go higher than once daily but it depends on the exact pill they are using.
Vitamin C (ascorbic acid) helps increase iron absorption. Taking iron pills with a glass of orange juice or with an actual vitamin C tablet can help iron absorption. If a patient is using ferrous gluconate, fumerate or sulphate, I advise them to be sure to take their iron supplements 1 hour before a meal or 2 hours after.
If patients are having difficulties raising their ferritin levels, I may advise them to avoid milk, calcium, high fiber foods and caffeine containing beverages. These can impair iron absorption.
Iron absorption is much better if the dose is spread out throughout the day rather than taken all at once. In addition, this may help to limit gastrointestinal side effects, such as nausea and vomiting.
Liquid forms of iron may stain the teeth. If patients are using liquid iron they may wish to combine with fruit juice or tomato juice to limiting staining. Drinking the iron with a straw may also help.
Lysine is an amino acid (a building block of protein). Studies have shown that L-lysine can help increase iron absorption. If patients are having difficult with raising their ferritin levels, I may advise them to include L-lysine in their plan.
One should never ever start iron pills unless they plan to test their levels again at some point in the future. This is important. The precise time point to retest ferritin levels will differ from patient to patient but is never sooner than 3-4 months and never more than 9 months. Testing ferritin levels weekly or monthly is pointless. However, re-testing a few months down the road is a good idea.
Anyone with low hemoglobin and low ferritin needs to speak to their doctor about a range of tests. They may not be necessary of course, but one needs to consider celiac disease, excessive menstrual bleeding (women), gastrointestinal bleeding, dietary issues, and a range of other illnesses. In my clinic, I generally screen for celiac disease (gluten sensitivity) in all patient’s with low hemoglobin and low ferritin. Patients with persistently low levels need a full evaluation by physician.
Taking iron is easy for many individuals but presents its challenges to some people. For some, the ferritin levels simply don't budge upwards despite taking iron. For others, any amount of iron causes gastrointestinal upset. A slow are methodical approach such as that suggested above often helps increase levels.
Hydroxychloroquine is an oral medication used in a variety of autoimmune conditions. Side effects have been discussed previously but today we will focus on eye side effects. A number of side effects are possible ranging from vision changes to double vision to asymptomatic changes in various parts of the eye.
"Retinopathy" is one of the more worrisome side effects of Hydroxychloroquine. At appropriate doses, studies show that the risk appears to be about 1 % of patients at 5 years of use and 2 % at 10 years. After 20 years, the risk may rise to 20 %. Once the retinal toxicity from hydroxychloroquine occurs, it is believed that the changes in the retina are permanent. Furthermore, the disease can even progress even if hydroxychloroquine is stopped.
Retinal damage can occur in anyone. However, the risk may be increased if the following risk factors are present
It's clear that taking the appropriate dose reduces (but does not eliminate) the chance of side effects. The optimal dose is 6.5 mg for every kg of lean body weight (not simply what the patient weighs). "Lean body weight" is essentially the patients expected weight for their height and gender - it does not include the "extra" weight that some might carry. Instead of calculating lean body weight, some clinicians advocate simply using the patient's true body weight and multiplying by 5 (instead of 6.5). In our clinic we typically dose hydroxychloroquine according to the following grid:
The risk of eye related toxicity is low in the first 5-10 years of hydroxychloroquine use provided the dosing is respected. This study has had great importance as it has further helped to define risk and has encouraged changes in screening guidelines. These guidelines now include an initial examination but dedicated yearly screening to begin only after 5 years in otherwise healthy individuals deemed at low risk for eye problems.
Reference
(1) Melles & Marmor. The Risk of Toxic Retinopathy in Patients on Long-term Hydroxychloroquine Therapy. JAMA Ophthalmolol. 2014;132(12):1453–1460.
I was recently asked a very interesting question - and that is whether one needs to exercise caution when using prostaglandin analogues like bimatoprost (Latisse) or latanoprost (Xalatan) in patients with a history of melanoma. The short answer is that there is no good evidence to support an increased risk of melanoma in users of any of the prostaglandin analogues - which includes latanoprost (Xalatan) and bimatoporst (Latisse). However, a number of points are important to carefully consider here - especially for individuals who already have a history of this type of cancer.
In general, patients with a personal or family history of melanoma (especially eye melanomas or skin melanomas around the eye) should speak with their physician if prostaglandin analogue type drugs are to be prescribed. This includes latanoprost (Xalatan) and bimatorpost (Lumigan, Lattise).
It is well known that users of prostaglandin analogues can develop increased pigmentation. For example, users of Bimatoprost (Latisse), can sometimes develop pigmentation of the eyelid or skin around the eyelid. Bimatoprost is a drug that stimulates prostaglandin F2 alpha (PGF2a). There is a good scientific basis for the observation that PGF2a drugs can cause pigmentation. In 2005, a study by Scott and colleagues (see reference below) showed that PGF2-alpha stimulates the activity and expression of tyrosinase, the rate-limiting enzyme in melanin synthesis. The group showed that fluprostenol, a potent and specific analog of PGF2a, stimulates tyrosinase activity in normal human melanocytes, but does not affect melanocyte proliferation. They also showed that melanocytes produce PGF2a in response to UVR.
Given that the prostaglandin F2 alpha drugs can stimulate melanocyte pigmentation, health authorities have asked manufacturers of these drugs to submit data and monitor if there is any increased risk of eye melanoma (ocular melanoma) in users of these drugs. In studies and discussions in 2002 examining whether latanoprost (Xalatan) increased the risk of ocular melanoma , the conclusion was that it did not.
Latanoporst (Xalatan) and bimatoprost (Latisse, Lumigan) are both drugs that target the prostaglandin F2 pathway. Latanoprost and Bimatoprost are widely prescribed as "first-line" agents for glaucoma.
In 2009, Esteve and colleagues reported 1 case of eyelid melanoma associated with the use of latanoprost. Two group reported two other cases of choroidal melanoma and earlobe melanoma that was associated with the use of latanoprost.
In 2012, Sun and colleagues reported a 77 year old patient who developed eyelid melanoma. She had used bimatoprost (Lumigan) for 6 years prior. When she first presented to her physicians, the pigmented lesion she had on her lower eyelid was biopsied and felt to benign. However, it subsequently progressed to a superficial spending melanoma in situ.
Melanocytes express receptors for prostaglandins, including PGF2-alpha and PGE2 as well. PGF2-alpha binds to the FP receptor to activates signals in melanocytes. PGF2-alpha stimulates melanocyte dendricity. As mentioned above, PGF2α stimulates the activation of tyrosinase (the rate limiting step in melanin synthesis), and the formation of dendrites, which facilitate the transfer of melanosomes from melanocytes to keratinocytes
One study suggested that melanomas reduce their expression of the PGF2-alpha receptor (FP receptor) suggesting that the FP receptor is lost at the transcriptional level in melanoma and in nevi and melanoma in vivo. it appears the FP receptor is expressed only by melanocytes, but is lost in melanoma and in nevi. There remains some uncertainty as to whether melanomas increase their expression of PGF2 alpha on account of loss of the FP receptor.
To date, there is no good evidence to suggest that users of prostaglandin analogues like latanoporst (Xalatan) or bitmatoprost (Latisse) are at increased risk of skin or eye melanomas. However, individuals who are already diagnosed with melanoma of the eye or skin around the eye or face should speak to their physicians as the use of the drugs would need to be considered on a case by base basis. There are no guidelines for using these drugs if a patient already has a diagnose of melanoma and current prescribing guidelines do not offer it as a contraindication. Although previous case reports do not prove any cause, these findings simply prompt one to take pause and carefully consider the risks and benefits based on current scientific evidence.
1. Fricke A, et al. The PGF(2alpha) receptor FP is lost in nevi and melanoma. Pigment Cell Melanoma Res. 2010.
2 Scott et al. Effects of PGF2a on human melanocytes and regulation of the FP receptor by ultraviolet radiation. Exp Cell Res 2005.
3. Esteve E et al. Melanoma during latanoprost therapy: three cases. Ann Dermal Venereol 2009; 136: 60–1.
4. Sun LL, et al. Lower eyelid melanoma during bimatoprost (Lumigan) therapy. Clin Exp Ophthalmol. 2012.
What season do humans shed more hair? A new study in the British Journal of Dermatology suggests the answer is ... Summer. In fact, the order of most likely periods to have increased shedding is Summer followed by Fall followed by Winter. Spring was a time of least shedding in this study.
This study was interesting in its design because it looked at Google Trends over time. Searches for "hair loss" were found to fluctuate according to season.
Seasonal shedding is important to remember. If one starts a treatment in Fall and notice by Spring things are better... one must ask if the treatment did it or would the hair have just gotten better anyways on account of it being Spring. The same is true if worsening is observed in Summer.
Reference
Hsiang et al. British Journal Dermatology 2017.
https://www.ncbi.nlm.nih.gov/pubmed/18505526
Minoxidil is the only topically approved agent that is approved but the FDA for treating androgenetic alopecia. The drug does not help everyone but does help 25-30 % of users. I've written in previous articles about the future of minoxidil pre-testing kits. It is well known that in order for minoxidil to have a chance to work, the body needs to convert the minoxidil to minoxidil sulphate. Some people have the enzyme (known as minoxidil sulphotransferase) to do this; other people simply do not. Those who lack the enzyme are more likely to be non-responders.
I was interested to read today in a press release that kits to test minoxidil sulphotransferase activity are moving forward in the FDA approval process. The FDA journey can be lengthy, but the possibility exists that we might see these kits in the clinic in the near future. These will help physicians to predict if it's a good idea to prescribe minoxidil or not.
Read the press release here: Press Release
I'm honoured to speak this weekend at the 2017 "Dermatology Update" conference in Vancouver. I'll be speaking about "Emerging Therapies for Hair Loss." In the last 5 years we have witnessed a remarkable increase in new options for treating various types of hair loss - and I'll have an opportunity to summarize these for the attendees.
Concerns about long-term side effects of some medications and a demand for more effective therapies are driving the development of new treatments for androgenetic alopecia. Topical anti-androgens (particularly topical finasteride) are increasingly used for treating male patterned hair loss. Topical bimatoprost (ie higher concentrations of Latisse) is actively being studied. Drugs which inhibit PGD2 (Setipiprant) are being studied and are among the exciting therapies to watch for. Low dose oral minoxidil (0.25 mg to 1 mg) is increasingly being considered as an option. Platelet rich plasma therapy has evidence now to support a therapuetic benefit in some patients.
One of the biggest breakthroughs in the last 5 years has been the recognition that inhibition of the Janus kinase (JAK) pathway can facilitate hair growth in many patients with alopecia areata. Both ruxolitinib and tofacitinib, in both topical and oral formulations, have shown benefit in treating alopecia areata and I will review these studies at the conference.
Cold caps have been popular in Europe for well over a decade but were banned in the US in 1990 on account of a lack of data on safety and efficacy. The recent FDA clearance of the Dignicap in 2015 and the Paxman cooling system this year offer new options for preventing hair loss from chemotherapy.
Hair dyes, highlights and bleaching can rarely lead to chemical injury. It's not common of course but the story is always the same: within seconds to minutes of applying a hair dye or highlights, the patient complains of intense burning and/or pain and requests the product to be removed. Hours to days later hair loss starts and within a week or two the patient has permanent hair loss (such as shown in the figure to the right). I have seen this type of scalp injury phenomenon many, many times and I do even feel that it is increasing world-wide.
The most important thing to do in these situations of potential chemical irritation is remove whatever chemical could be causing the reaction. The dye or highlight must be removed, neutralized and rinsed off. In my opinion a dermatologist should be consulted for management and monitoring. Rarely skin necrosis can occur from ehuberant reactions. One can not predict on day 1 whether the patient will have hair loss and whether any hair loss will be permanent. This will not be clear until day 14-28. In the short term one must management skin health, prevent infection, and limit and control inflammation. These are within the skills of a dermatologist. A biopsy may be considered to determined the type of inflammation and evaluate for scarring if it is unclear.
Too often I hear it said in these scarring alopecias that a biopsy was done and because the biopsy said the disease was inactive the patient proceeded to surgery. Keep in mind that we determine if a scarring alopecia is inactive by simply following what it does over time. Relying on a biopsy alone to determine if it is acitve is not a good idea for most people. If the area of hair loss has not changed at all in any way shape or form (same size area) and is not itchy and has no burning or pain thena biopsy supports it is inactive. Even if a biopsy says the scarring alopecia is inactive but the area is expanding over time and is itchy or red... it is not inactive. This is a common scenario and a common error in managing scarring alopecia.
One needs to wait 12-24 months for a scarring alopecia before surgery. Photos need to be done every 2-3 months in my opinion even for chemical burn related hair loss. If the photos look the same when placed side by side over a one year period, one can say the scarring alopecia is probably quiet. Rarely, this can be shortened to 6 months for chemical injury but one year is a safer waiting period to be confident there is no evidence of a slowly progressive scarring alopecia in evolution.
All this background waiting and monitoring needs to be done before surgery. It sounds excessive and time consuming and unnecessary- but it is far from it. Surgery for scarring alopecia can be highly successful provided it's done in the right patient. Too often, it is not done on the right patient... and then it does not work well or does not work at all and physicians, patients and the medical community as a whole loses confidence in the value of surgical restoration options.
The only way to restore the appearance is surgical. Medical options do not help improve density once the area is permanently scarred. If the area is small surgery via a plastic surgeon can be a great option. Many burns from hair dyes are in the form of small coin shaped patches. A flap (rotational flap etc) can work wonders and may be superior to hair transplanting. For this a surgeon is needed with skill in such flaps. The above patient would be a good candidate for a flap.
For hair loss that occurs more diffusely (and not in the above mentioned classic hair dye chemical burn patches), hair transplants can sometimes ca a good option. In my opinion, the key factor in choosing a surgeon is their experience and dedication to hair transplantation. The actual credentials is not so important to me and some of the world's top surgeons are a range of family physicians, dermatologists, plastic surgeons, former emergency room physicians. If her or she is dedicated soley to hair transplanting and has performed a large number surgeries and has been doing it for many years and has a good before and after album of scar procedures, then it may be worth a visit to speak to that surgeon.
Hydroxychloroquine (Plaquenil) is a slow acting drug. It can take up to 8 weeks or more before the medication really starts to have an effect and actually help an individual using the drug. Because hydroxychloroquine is so delayed in its onset, I usually give it 4-6 months before really deciding if it is working ... and sometimes even longer. Clinical symptoms (like itching and burning) tend to go away (or at least be reduced) first in those who respond to the drug followed by clinical signs on the scalp (perifollicular erythema, perifollicular scale, scalp erythema). The actual stopping or slowing of hair loss is last.
Hydroxychloroquine is among the slowest acting of all the typical oral immunomodulators such as doxycycline, methotrexate, mycophenolate and cyclosporine (cyclosporine tends to be the most rapid).
For my patients I often tell them that the “timer” does not start until 8 weeks into treatment. So if I see them in September, I tell them we will actually set the 'real' starting point of treatment in November. I tell the individual on the medication that for the next two months they can 'consider/imagine/pretend' that they are not really even on treatment from the perspective of their scalp disease. (Of course blood tests need to be done because the body certainly knows from day 1 that the drug was started).
Hyrdoxychoroquine (Plaquenil) use requires patience from patients and physicians.
Scarring alopecia is a form of hair loss which can lead to permanent bald areas on the scalp. Treatments focus on helping to stop hair loss but do not improve hair in most. Some individuals elect to purchase a wig, hairpiece or hair system while receiving treatment. For the purposes of the discussion that follows, I will specifically use the term hair system to refer to a scalp camouflaging method whereby synthetic or human hair is attached to a layer of some sort and glued to the scalp with some type of adhesive. I will use the term wig or hairpiece to include a broad array of similar products that attach via clips, tape or elastic.
The are quite a few factors that go into deciding what type of wig, hairpiece or hair system is appropriate for someone with scarring alopecia. The two main factors to consider when I am meeting with a patient trying to decide what type of system they should purchase are the following:
(1) How active is the scarring alopecia right now?
(2) Does the patient need topical steroids, steroid injections or special shampoos as part of his or her ongoing management strategy?
If a patient has a very active scarring alopecia (with many symptoms and/or rapid hair loss), it will be important to consider choosing a hair piece or wig with clips or tape over a hair system that is attached to the scalp with adhesive. A patient with an active scarring alopecia needs to have the scalp examined often to determine if treatment is working and to modify the exact treatment. For some scarring alopecias like folliculitis decalvans it may be important in some cases to frequently shampoo the scalp with antibacterial agents. An easily removable wig or hairpiece is preferred.
As the scarring alopecia becomes "quieter" it may be possible to consider shifting to a hair system and more permanent types of adhesive-based attachments. I generally ask patients to coordinate removal of the hair system at their salon on the same day as their follow up appointment with me or if that is not possible to have good pictures taken at the salon in the day that their system is removed, washed and reapplied (generally referred to as a "servicing).
For patients who answer yes to the above question, a wig or hairpiece will be preferred over a hair system. Topical steroids and steroid injections can be the mainstay of treatment for many patients with scarring alopecia. Even in relatively quiet scarring alopecias, topical steroids may still be needed every few days. For very active scarring alopecias, steroid injections may be needed monthly. As mentioned above under point (1), for some scarring alopecias like folliculitis decalvans it may be important in some cases to frequently shampoo the scalp with antibacterial agent. Therefore, in such cases where there is active disease, a more permanent hair system becomes either impractical or inconvenient. It needs to be removed for these treatments to be properly administered and this is not easy if a hair system is glued to the scalp.
All in all, these are the discussions that patients will want to have with their dermatologist. If topical steroids are needed daily and steroid injections are needed monthly for example (for very active disease) use of a hair system with an adhesive is less preferred over wigs or hairpieces with clip attachments or tape. If possible, these are discussions the dermatologist might have with the wig salon itself to best coordinate the proper care of the patient .
Minoxidil is FDA approved for the treatment of male balding and female thinning. After using it for a period of time, some patients find that it no longer seems to be working the way that it once did. This leads many to ask :
"Has my minoxidil stopped working?"
The most likely explanation is that the minoxidil is, in fact, still working but the machinery that controls balding is working harder. It is likely that more and more genes are being expressed inside the scalp and hair follicles that are accelerating the balding process forward.
A recent study from the UK, however, has shown that male balding is far more complicated and many hundreds of genes contribute to balding in men. It identified 287 genetic regions linked to male pattern baldness. This large study examined data from over 52,000 men.
Consider the 30 year old male who started noticing balding at 21 and started minoxidil. At age 16 - 18 he might have had 4-6 genes expressed at the start of balding (before he even noticed) and 21 there may have been a dozen or so distinct genes pushing the balding process. At age 30, there could be dozens and dozens of genes expressed. For many users of Minoxidil, it is usually working the same - and while it was pretty good at stopping 4 genes, it can't fully hold back the genetic changes associated with 60 or 70 genes. These numbers are different for everyone - but it illustrates an important point. The scalp environment and hair follicle milieu changes drastically over time.
Reference
Hagenaars SP, Hill WD, Harris SE, Ritchie SJ, Davies G, Liewald DC, et al. (2017) Genetic prediction of male pattern baldness. PLoS Genet 13(2): e1006594
Doxycycline is an oral antibiotic belonging to the so called "tetracycline" class of antibiotic medications. Other members of the family include tetracycline itself as well as minocycline and a few others. I frequently prescribe doxycycline on account of its "anti-inflammatory" effects. I may use doxycycline for treating lichen planopilaris, pseudopelade, frontal fibrosing alopecia, dissecting cellulitis and folliculitis decalvans.
Doxycycline is fairly well tolerated but anyone prescribed this medication must understand how to use it as well as the more common side effects. I always counsel patients about nausea - and on account of this the medication should be taken with food. Unlike some of the other tetracycline members, absorption of doxycycline is not significantly worsened by food. I recommend taking doxycycline with a large glass of water and to remain upright for 1-2 hours afterwards. One shoukd never take doxycycline and go to bed (which some people often do in order to sleep through undesirable side effects.
In some cases vomiting can occur. Other side effects include increasing sensitivity to the sun, weight gain, rash, yeast infections, diarrhea and headaches (see commentary on headaches below). For a more complete list please see our Doxycycline - Handout For Patients.
Headaches are not common in patients using doxycycline. However, any headache that lasts more than a day or two needs to be given serious attention in users of doxycycline. This is because of a phenomenon called "benign intracranial hypertension."
Tetracyclines can rarely cause a condition known as benign intracranial hypertension. Patients affected develop headaches, vision problems and double vision. This occurs from increased cerebrospinal fluid pressure. Despite the name, the condition is not truly "benign" as loss of vision is one serious consequence. Some refer to this condition as "pseduotumor cerebri."
It is not clear why doxycycline causes this phenomenon in some users. It can occur with tetracycline, minocycline and doxycycline. Most research has focused on minocycline. Intracranial hypertension from doxycycline can occur at any age, males and females and regardless of whether a patient is thin or obese. Some have proposed that venous occlusion is responsible for the increased pressures in the brain.
Anyone with persistent headaches on doxycycline needs to consider immediately stopping and to see a physician for evaluation of benign intracranial hypertension. Visual acuity needs to be tested urgently and the pupils need to be dilated by a physician to determine if there is "papilloedema" (a serious condition involving swelling of the optic nerve). This condition can even occur in users who have been on doxycycline more than 1 year so one must always be attuned to the importance of seeking medical attention if headaches persist. Treatment of benign intracranial hypertension due to doxycycline involves first and foremost stopping the drug. Medical therapy including acetazolamide, methazolamide or furosemide are often used to lower pressures. Other treatments may also be recommended by the ophthalmologist, neurologist or neurosurgeon.
A variety of shampoos are available for treating dandruff and seborrheic dermatitis. The following is a helpful list we provide our patients. It includes both sulphate free and sulphate containing shampoos. To download the complete handout, click here.
Lichen planopilaris (LPP). In follow up to yesterday's post, here is another example of a hair follicle injured by the inflammatory and scarring reaction that occurs beneath the skin surface in LPP.
Lichen planopilaris ("LPP") is a scarring alopecia (scarring hair loss condition). Inflammation first develops around hair follicles which triggers the development of scar tissue (fibrosis) around hairs. This inflammatory reaction causes hairs to eventually die. One such injured hair is shown in the photo.
Many patients first develop scalp itching, burning and tenderness. Once a hair is destroyed, it can not regrow. Early recognition of the disease and aggressive treatment and frequent monitoring is essential.
Lichen planopilaris (also known as "LPP") is a scarring hair loss condition. Individuls affected by the condition develop hair loss, increased hair shedding along with scalp itching, burning and pain.
An up close examination with dermoscopy is shown here and shows classic features including white scale around hairs in early stages. This scale is known as "perifollicular scale" or "follicular hyperkeratosis." This scale is often prominent in active stages of the disease. It can be reduced by treatment and even reduced to some extent by a good shampooing of the scalp.
Treatments include topical steroids, steroid injections, topical calcineurin inhibitors, and oral treatments such as doxycycline, hydroxychloroquine (Plaquenil), methotrexate, mycophenolate mofetil, cyclosporine, and others. Lasers, including the 308 nm excimer laser may also provide benefit.
Gynecomastia or enlargement of breast tissue in men can occur with a number of causes. These include hormonal issues that affect testosterone production (like Klinefelter’s syndrome or a pituitary problem), normal aging, tumors of the adrenal glands, testes or pituitary gland, thyroid problems, liver and kidney problems. A variety of medications can cause gynecomastia as well. Overall about 10-25 % of cases of gynecomastia have a drug cause. Some of the drugs known to cause gynecomastia include spironolactone, other anti-androgens, cimetidine, ketoconazole, estrogens. For a full list of implicated drugs, click here. In all of these different causes there is an underlying hormonal issue - typically an increase in the estradiol/testosterone ratio.
Finasteride, which is FDA approved for treating male balding at a dose of 1 mg daily, is a medication that can sometimes cause gynecomastia. The risk is likely about 4 to 10 out of every 1,000 users. There are a number of misconceptions about finasteride-induced gynecomastia. The following points help clarify some of these.
Finasteride induced gynecomastia is often one-sided but can be both sides. This is especially true at lower doses like 1 mg compared to 5 mg.
Finasteride induced gynecomastia can start as early as a few weeks but is typically a few months delay (if it is going to occur). It can also be 1-2 years before the phenomenon is appreciated.
An important sign to watch for is the presence of pain or tenderness. This can occur prior to any actual enlargement.
The 1 mg dose is less likely than the 5 mg dose to cause breast enlargement in men. The concept of the dose response is important because it means than for some men, 0.5 mg daily (or every other day) could be assocated with a lower risk of gynecomastia (while still potentially benefitting their hair).
Finasteride induced gynecomastia can reverse in many individuals provided the drug is stopped in the early stages when the gynecomastia is noted. If the drug is not stopped, it can enter a irreversible stage (where only surgery will provide treatment).
Finasteride induced gynecomastia is more likely in obese indivdiuals and with advanced age.
Blood tests may be appropriate for some men depending on their history. However, most of the time blood tests and various hormonal tests are normal.
Gynecomastia is common in the population so one must be careful to immediately ascribe their gynecomastia to a drug or health reason without a full evaluation. Finasteride induced gynecomastia occurs in 4 to 10 out of every 1000 men using finasteride. It is dose dependent so risk may be less with 0.25 mg compared with higher doses. Anyone with concerns about this phenomenon should see their physician immediately to discuss.
A link is more likely to a drug cause when the breast enlargement is one sided and tender/painful. One way to determine a link is to stop the drug and wait for the tissue to return to normal before starting the drug again (this is called a rechallenge). If gynecomastia occurs again, one has more confidence of a link. This may not be appropriate for all individuals so one should always discuss with their physician.
REFERENCE
[1] Nuttall F (1979) Gynecomastia as a physical finding in normal man. J Clin Endocrinol Metab 48:338–340
9. Green L, Wysowski DK, Fourcroy JL. Gynecomastia and breast cancer during finasteride therapy. N Engl J Med. 1996;335:823.
