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Hydroxychloroquine: 10% stop from side effects

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10% Stop from Side Effects

How often do patients stop hydroxychloroquine treatment because of side effects?

Hydroxychloroquine (also known by the name Plaquenil and generics) is an oral anti-inflammatory medication frequently used in the treatment of a variety of autoimmune diseases. For autoimmune hair loss, hydroxychloroquine is used in the treatment of lichen planopilaris, frontal fibrosing alopecia, discoid lupus, and pseudopelade of Brocq.

Side effects include irritation of the liver, pigment changes on the skin, reduced blood counts and retinopathy. The eye side effects are among the more worrisome side effects.

It’s helpful when prescribing a medication to have a sense of how common a side effect might be an how commonly a patient will discontinue a given medication.

Tetu and colleagues performed a retrospective study between January 2013 and June 2014 of patients receiving hydroxychloroquine for a variety of skin issues (not limited to hair). The study included 102 patients (93 of whom were women, with a median age of 44.5; range: 22-90 years). At least one adverse event was reported for 55 patients (ie 54%). 11 patients (10.75%) discontinued hydroxychloroquine due to a side effect that was thought to be directly attributable to the use of hydroxychloroquine.
 

Conclusion

It’s nice to have this kind of information when prescribing medications. Although the study did not solely focus on the use of hydroxychloroquine for hair loss, it’s reasonable that a similar proportion of hair loss patients would be expected to stop their hydroxychloroquine due to a side effect. Other oral options include doxycycline and tetracyclines, mycophenolate, cyclosporine, methotrexate and other anti-lymphocytic agents.
 

Reference

Tétu P, et al. Ann Dermatol Venereol. 2018.


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Steroid Injections: A Closer Look at Triamcinolone Acetonide (Kenalog)

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A Closer Look at Triamcinolone Acetonide

Steroid injections are commonly used in dermatology and essential treatments offered by the hair specialist. Triamcinolone acetonide (TAC) remains one of the most common steroids used for treatment of alopecia areata, traction alopecia as well as scarring alopecias. Doses of TAC range from 2.5 to 40 mg per mL although doses of 2.5 mg/mL to 10 mg/mL are by far the most common. I frequently use 2.5, 3.3 and 5 mg/mL in my practice and limit steroids to no more than 20 mg total dose every 4-6 weeks.

Triamcinolone acetonide is a “suspension” meaning that it does not actually dissolve. In the photo, particles of TAC can be seen on the bottom of the syringe rather than dissolved in the solution. TAC particles range in size from 0.5 to 1000 micrometers. About 1/3 of particles are between 0 and 10 um, another 1/3 are between 10-20 um and the remaining 1/3 are greater than 20 um. Rarely particles can be as large as 1000 um but this occurs in less than 1% of all particles.

When preparing TAC solutions, one should ensure the steroid is well mixed before injection. If there is any difficulty injecting through a 30 G needle one should stop and ensure the solution is mixed well.

Reference

Benzon HT et al. Comparison of the particle sizes of different steroids and the effect of dilution: a review of the relative neurotoxicities of the steroids.
Benzon HT, et al. Anesthesiology. 2007.
 


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Steroid Injections: Atrophy (dents, depressions, holes)

Atrophy (dents, depressions, holes)

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Steroid injections are a relatively common treatment for many inflammatory and autoimmune scalp conditions. There is rarely a day in the office that I don’t perform steroid injections. These are very valuable treatments for many patients with alopecia areata, scarring alopecias and even some forms of traction alopecia.

One of the side effects of steroid injections is atrophy. Atrophy appears as an indentation in the skin at the site of injection. The patient may refer to it as a “dimple” or a “depression.” Others may call it a “dent” or even a “hole” The indentation can often be better felt than seen.

The chance of developing indentations (atrophy) depends on the concentration of steroid the doctor uses. Higher concentrations (10 mg/mL) give a greater risk of causing atrophy than lower concentrations (2.5 or 5 mg/mL). Some studies suggested that the risk may be as high as 3 in 10 patients when a dose of 10 mg/mL is used. 
The indentations occur because the steroid affects collagen and elastin underneath the skin. The steroids inhibit the growth of fibroblasts, which are the cells that collagen and elastin. Studies have shown there is less collagen made and it’s degraded more quickly. There is a reduction in diameter of collagen fibrils. The collagen bindles become atrophic snd separated. Similar to collagen, elastin fibers become thin and fragmented.

Atrophy typically is seen by 3 weeks if it’s going to occur. An important point to be made is that the atrophy is generally reversible provided more injections aren’t given to an area already showing atrophy. The skin usually returns to normal in 3-4 months. Steroid injections should not be readministered too soon to an area that has not “recovered” as further atrophy can occur - some of which can be very long lasting.

Treatment for steroid atrophy is mainly to wait for the body to start making more collagen and elastin again in a few months. If this does not happen, saline injections, dermal fillers and fat injections can be considered.


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Gynecomastia in Finasteride Users: The Basics

What is Gynecomastia?

Gynecomastia refers to the enlargement of breast tissue in men.  It's extremely common and throughout life, a majority of men will be affected. For some, it will occur during infancy or puberty and resolve. For others it will start in puberty and persist and for others it will occur in older ages.

 

Gynecomastia by Age

Gyneomastia is common in newborns. Due to estrogens from the mother, 60-90% of male babies have enlarged swollen breast tissue. It resolves in a matter of weeks for most. For young male adolescents, gynecomastia is embarrassing but common. It can start at age 10-12 but typically it starts around 13 or 14 years of age.  About 50 % of male adolescents may be affected.  The breast swelling goes away on its own in 6 months to 2-3 years. In 20 % of affected teens, the swelling persists into adulthood. In men, gynecomastia is present in men 20-40, but particularly peaks in incidence after age 50. In the 50 plus age group, about 25-30 % of men are affected.  The number may rises to well over 50 % in 60 + age groups.

 

What causes gynecomastia?

Gynecomastia is caused by a variety of factors including genetics, drugs and physiological causes. Regardless of the precise cause, it is though that some hormonal imbalance (especially favouring estrogen and increasing the estrogen to androgen ratio) triggers breast tissue enlargement.  The actual level of hormones in the blood stream is typically normal and it's the ratio of these drugs at the actual level of the breast tissue itself that is important. Drugs cause about 10-25 % of cases. Pubertal gynecomastia that persists into adulthood is responsible for another 25 % of cases. The causes is generally unknown in about 25 % of cases as well.  But the list of potential causes is long and a full review is needed for anyone with concerns about gynecomastia. A variety of genetic syndromes (i.e. Klinefelter syndrome), metabolic problems, cancers all reduce the bodies production of testosterone and increase the estrogen to androgen ratio.

 

Drugs causing Gynecomastia

For hair specialists, it's well know that finasteride is among the causes of gyneocmastia. About 4 to 10 out of every 1000 men using finasteride will develop gynecomastia on account of the drug. But a variety of other medications and products can cause gynecomastia including:

1. Anti-androgens. (Finasteride Dutasteride). This anti-androgens is commonly used for treating male pattern balding. 

2. Anti-androgens. (Spironolactone). This anti-androgens is typically used for women with hair loss but not typically for men. 

3. Ketoconazole (anti-fungal). Generally speaking the risks is greatest with oral ketocoanzole rather than topical products. Oral ketoconazole is rarely used nowadays in North American due to safer anti-fungal agents. 

4. Heart burn medications (H2-receptor blockers). Drugs used to treat ulcers and heart burn including Cimetidine has the greatest evidence as a drug of this class being implicated. The others less so.

5. Tea tree oil and lavender oils. These essential oils have been reported to increase the risk of gynecomastia in children. Tee tree and lavender are found in soaps, shampoos and lotions. 

6. Other drugs. A variety of other drugs may also be implicated. A 2012 review classified drugs into two main groups including those 'definitely associated with gynecomastia" and those "probably associated with gynecomastia." The first group (drugs definitely associated with the onset of gynecomastia) inlcuded spironolactone, cimetidine, ketoconazole, hGH, estrogens, hCG, anti-androgens, GnRH analogs and 5-α reductase inhibitors.  The second group of drugs "probably associated with gynecomastia" include risperidone, verapamil, nifedipine, omeprazole, alkylating agents, HIV medications (efavirenz), anabolic steroids, alcohol and opioids.

 

Finasteride Induced Gynecomastia

Finasteride is FDA approved for treating male balding at a dose of 1 mg daily. It is among the medications known to cause  gynecomastia. The risk is likely about 4 to 10 out of every 1,000 users. 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 1-2 weeks after staring the drug but is typically a few months delay. It can also be 1-2 years before the phenomenon is appreciated. Pain is not uncommon in men with finasteride induced gynecomastia - and this pain/tenderness 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. Finasteride induced gynecomastia can reverse completely in many individuals provided the drug is completely stopped in the early stages when the breast enlargement is noted. If the drug is not stopped, it can enter a irreversible stage (where only surgical treatment will provide treatment). Finasteride induced gynecomastia is more likely in obese indivdiuals and with advanced age. Most of the time blood tests and various hormonal tests are normal in men with finasteride - induced gynecomastia. 

 

 

Treatment: How is gynecomastia treated?

The treatment of gynecomastia depends on the precise causes. For most adolescents, a conservative (watch and wait) approach is usually taken as the condition usually resolves in most cases. Only 20 % of adolescent cases of gynecomastia persist into adulthood.  Medical treatments are usually not effective. However, in some hormonal abnormalities, medications such as aromatase inhibitors can be used.  Usually surgery is needed to remove the excess tissue if that is what is so desired by the patient.

 

REFERENCES

Rodriguez et al.  Risk of gynaecomastia associated with cimetidine, omeprazole, and other antiulcer drugs. BMJ. 1994 Feb 19; 308(6927): 503–506. 

Bera F, et al. [Impotence and gynecomastia secondary to hyperprolactinemia induced by ranitidine].Therapie. 1994 Jul-Aug.

Deepinder F, et al. Drug-induced gynecomastia: an evidence-based review. Review article. Expert Opin Drug Saf. 2012.

Fentiman IS, et al. Managing Male Mammary Maladies. Eur J Breast Health. 2018.

Soliman AT, et al.  Management of Adolescent Gynecomastia: An Update.Acta Biomed. 2017

 

 

 

 

 

 

 

 


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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PSORIASIS-LIKE REACTIONS TO ANTI-TNF DRUGS

 

POSSIBLE ANTI-TNF DRUG REACTIONS

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Anti-tumour necrosis factor (TNF) agents such as adalimumab and infliximab have been shown to have benefit in inflammatory bowel disease (IBD). It is now recognized that cutaneous reactions such as new onset psoriasis or psoriasiform-like reactions are among the most common adverse reactions. 

Researchers from Australia retrospectively reviewed cases of anti-TNF-induced psoriasis or psoriasiform manifestations in IBD patients. A total of 10 (six females) of 270 (3.7%). IBD patients treated with anti-TNF therapy developed drug-induced psoriatic or psoriasiform-like reactions: five patients were treated with infliximab and five with adalimumab; nine had Crohn disease. The duration from start of anti-TNF agent to onset of rash was about 8 months on average. The scalp was the most frequent distribution (7/10). Three patients discontinued anti-TNF treatment with resolution of the rash. Topical treatment of the lesions allowed continued use of biological agent in the majority. 


Reference

Peer FC et al. Paradoxical psoriasiform reactions of anti-tumour necrosis factor therapy in inflammatory bowel disease patients. Intern Med J. 2017.


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Can I eliminate the possibility of side effects from finasteride?

Eliminating a Drug is the only way to Eliminate the Possibility of Side Effects

I'm often asked how one can eliminate the side effects of a medication. "I want to take it doctor if it weren't for the side effects."  The reality is that it is possibility to eliminate the chances of side effects from any drug - and that is by not taking the drug.

 

Reducing Side Effects from Finasteride

The only way to really eliminate side effects from finasteride is not to take the drug. The chances of side effects with oral finasteride are low and in the order of 1-2 %. Nevertheless, all men need to be aware of the possibility of sexual dysfunction, mood changes, gynecomastia and other potential side effects as well.  The chances of side effects tend to be depenent on the amount of finasteride absorbed into the blood stream which in turn affects the degree of reduction in DHT.

 

1. Reducing the dose

Reducing the dose to 0.5 mg or 0.25 mg may be associated with reduced chances of side effects. DHT is still inhibited at these doses, albeit not as effectively as a 1 mg dose. Studies have suggested that DHT inhibition at 0.2 mg is about 80 % the level of 1 mg pill.

 

2. Reducing how often it is taken

Even though the drug half life is 6-8 hours, one needs to consider how long 5 alpha reductase inhibition in the scalp is actually occurring. Studies have suggested that 1 mg finasteride daily and 1 mg finasteride every other day are fairly similar in effectiveness although good studies still have yet to be done to really back this up definitely. Taking every other day can reduce side effects but may potentially alter effectiveness as well.

 

3. Using topical compounded finasteride

The other way to minimize finasteride side effects is to consider topical finasteride applied to the scalp. Absorption into the blood stream may still occur with topical finasteride (as systemic DHT levels are still reduced) but side effects are much less.

 

4. Taking time to understand the risk and benefits, long term studies

Studies also show that a broad and objective understanding of finasteride, its proper use also reduces side effects. Men who are alarmed about the drug and proceed into taking the drug without a full and balanced view of the risks and benefits also have a higher incidence of side effects. Studies have shown that risks increase in this situation from 2-5 % to above 60 % (i.e. nocebo effects).

 

Conclusion

Anyone wishing to minimize side effects of finasteride should have a thorough discussion with their physician. For more information on finasteride, download our handout. 

FINASTERIDE - HANDOUT


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Topical Finasteride: Are side effects possible?

Topical Finasteride: Don't forget the placebo studies!

If one is going to use topical finasteride,  they must be 'prepared' for the possibility of side effects. For patients to use topical finastseride (or physicians to prescribe topical finasteride) with the complete expectation that it comes with zero chance of side effects is simply incorrect. The "chances" of side effects in my experience are certainly very, very, very low (probably well under 1 in 1000) and much, much lower than oral finasteride. But they are likely not zero especially if one considers that even placebo pills have side effects! Side effects with topical finasteride have not been reported to date.

 

Topical finasteride: What is the risk of side effects?

Common sense dictates that someone will have a side effect to topical finasteride. Whether it's 1: 1000 men or 1 in 10,000 or 1: 1,000,000 is unknown but there is little doubt in my mind that side effects are possible. We know that DHT is still inhibited in the blood by up to 25 % with some topical finasteride formulations and about one tenth of the amount of finasteride is still absorbed. In other words, a lot less gets into the blood, but it's far from zero. 

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Analogies I use in my clinic

I completely understand that many physicians and many patients assume that topical finasteride is 100 % free of side effects (or at least close to it). But let's use a few analogies which help us all understand that a 25 % reduction in DHT is going to be a bit much for a small proportion of men.

Humans have a delicate physiology. There are some individuals that are sensitive to small changes in blood levels of anything. There are some individuals that are sensitive to small amounts of alcohol in the blood. Some individuals are sensitive to small amounts of caffeine.

Sexual physiology is likely even more complex. There is no doubt that some will be sensitive to small reductions in DHT. We see similar "DHT" related side effects even with saw palmetto - which is not supposed to even effects DHT at all! We even see DHT related side effects (erectile dysfunction, decreased libido) in 0.7 % of men using "placebo pills" in clinical studies - which inhibit DHT 0 %!! By age 30, about 30 % of men have some degree of sexual dysfunction. By age 50, it's 50 % , and by age 80, it's well over 80 % of men.  Factor this into the 0.7 % chance of sexual-related side effects with placebo pills and it's easy to understand that at least someone is going to present with concerns about side effects from topical finasteride. 

Consider now the following table. We know that oral finasteride inhibits DHT by 70 % based one studied done in the 1990s. The chances of side effects with oral finasteride are around 2 %. This includes sexual dysfunction and mood changes. A drug that inhibits DHT to no degree at all (i.e. 0%) would likely have lower chances of "DHT-related" side effects. But clinical studies using placebo pills in clinical trials of finasteride have suggested this could be as high as 0.7 %. Of course, other side effects could be possible.  We are then left with considering the chances of side effects in a drug that inhibitors DHT levels in the blood by 25 %. Are the chances of side effects zero? Probably not given that not even the placebo has a 0 % chance of side effects.. But fortunately, they are likely very low. We don't yet know that number. In my experience using topical finasteride, I have formed the opinion that it is likely very low and probably well under 1:000. But what is the real number? Is is 1:1000 men?  1:10,000 men?

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.Many different Topical Finasteride Formulations

If a male is very sensitive to a reduction in DHT then side effects may occur. If a formulation can be created with zero penetration into the blood then systemic DHT will not be affected. That does not exist yet. One must keep in mind that there is no "one" topical finasteride formula - there are dozens of different formulations. Some pharmacies just make it up however, they like. Polychem is studying a specific formulation. MorrF is available in India already through Intas Pharmaceuticals and consists of topical minoxidil and topical finasteride together. .

Topical finasteride is clearly safer than oral finasteride and we have used for several years in our clinic. To say it has zero possible side effects would be incorrect. In my opinion, it is just a matter of time before we hear of possible side effects.  There are side effects even with placebo (and it's as high as 0.7 %!).But overall, topical finasteride is much much safer than oral finasteride. But anyone who uses it must be aware that it is off label and long term effects are not known. There have been millions of prescriptions for oral finasteride to date and well over 1 million men use it every year for treating hair loss. This does not include finasteride use in prostate issues. Compare this to the fact that there are probably under 200,000 men worldwide (maybe quite a bit less) that have used topical finasteride. 

Physicians and patients need to be aware of the 'unknowns' of topical finasteride use and  counsel patients on the reduced chances of side effects but the possibility that a very small proportion of men will report side effects. Overall, the drug appears to have a very good safety profile in the topical formulation.

 

REFERENCES

M Caserini, et. al.  A novel finasteride 0.25% topical solution for androgenetic alopecia: pharmacokinetics and effects on plasma androgen levels. Int J Clin Pharm Th July 30, 2014 (1-8).

BS Chandrashekar, et. al. Topical minoxidil fortified with finasteride: An account of maintenance of hair density after replacing oral finasteride. Indian Dermatol Online J 2015 Jan-Feb; 6(1): 17-20.

S Sheikh, et. al.  A new topical formulation of minoxidil and finasteride improves hair growth in men with androgenetic alopecia. J Clin Exp Dermatol Res 2015, 6:1.


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Medication induced hair loss

Does Drug Induced Hair Loss Eventually Stop ?

If a patient's hair loss is truly from a medication the hair shedding is likely to continue while the medication is present. If the hair loss does not actually have anything to do with the medication and the timing is coincidental, anything is possible... including an improvement, worsening or continued same-rate shedding.

Hair loss from medications is complex. They have different mechanisms causing the loss and not just one. Some are true telogen effluviums, some are toxic responses and some are hormonal. Some are immune-based. Growth promoters like minoxidil and low level laser therapy are often considered for hair loss due to the true effluviums but is often ineffective or results suboptimal. If hair loss is due to hormone based mechanism, then anti-hormonal treatments may help. If immune-based, then immune modulators may help.

 

Blogs on Drug Induced Hair Loss

For further review see previous blogs

Drugs and Hair Loss: Is it common?

Drug Induced Hair Color Changes

Drug Induced Hair Loss: A Closer Look at Amphetamines

Hair Loss from Chemotherapeutic Drugs: Does it always grow back fully?

 

 

 

 

 


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Saw Palmetto: What are the side effects?

Saw Palmetto Side Effects

Saw palmetto (serenoa repens) is a natural herbal-based product commonly used for prostate problems in men and hair loss in men and women. 

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A number of studies have suggested that saw palmetto can help hair loss. These studies are small and few in number. Nevertheless, countless numbers of patients turn to these natural products. Furthermore, because they are natural, most assume they are without side effects. The side effect profile of saw palmetto is not entirely clear. It is however known that saw palmetto affects hormones in the body, and risks of mood changes like depression and sexual dysfunction may be real (albeit low) risk.

A recent report provided additional evidence that this natural product might best be classified among chemicals and molecules that affect the hormone and endocrine system of the body (so called "endocrine disruptors"). A 2015 paper from Italy reported development of hot flashes in a 10-year-old girl using saw palmetto. When she stopped treatment, the hot flashes stopped. When she started back up again ("ie a rechallenge'), the hot flashes returned. However, 4 months after starting saw palmetto, the 10 year old got her first menstrual cycle. 

This report reminds us that use of saw palmetto requires counselling of at least the low possibility of side effects. I advise my own patients of the generally well tolerated nature of saw palmetto but remind them of possible risks of mood changes and even the rare possibilities of sexual side effects. More studies are needed to not only document the successes of saw palmetto in medicine but the incidence of side effects.
 

Reference

Morabito et al. Pharmacology 2015.
 


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Alopecia Areata and Oral Contraceptives: 50 Years of Wondering

Do birth control pills cause alopecia areata? Can they be used to treat alopecia areata?

Alopecia areata is an autoimmune conditions that is not uncommon in the population. In fact, about 1 in 50 women will develop alopecia areata and usually before 30.  Oral contractive use is also common in women 18-40 years of age with 15-18 % of women in this age group using birth control. Given these relatively high frequency of alopecia areata and birth control there will be individuals who will develop alopecia areata fairly close in time to the start of an oral contraceptive pill. The question then arises :

Did starting the birth control pill cause the alopecia areata?

 

50 years of wondering

The question as to whether or not oral contraceptives can trigger a patch of alopecia areata has been with us since oral contraceptives first came to market.  In fact, oral contraceptives were first FDA approved in 1960. Reports questioning whether a possible connection could exist between alopecia areata and oral contraceptives surfaced in 1965 with studies published in the British Medical Journal in an article "Alopecia areata and Oral Contraceptives".

 

No good evidence

For most people, there is no good evidence that alopecia areata is triggered by oral contraceptives. That does not rule out the possibility that there are a proportion of individuals who do have this as a trigger - but for the most part medical studies can't conclusively pinpoint a link. 

 

Oral contraceptive and Autoimmune diseases

A compressive review by Willams in 2017 examined whether there was any link between hormonal type contraceptives and any of the known autoimmune diseases. The article indicated that ere was in fact substantial evidence exists linking the use of combined oral contraceptives to an increase in multiple sclerosis, ulcerative colitis, Crohn's disease, Systemic Lupus Erythematosus, and interstitial cystitis.  Oral contraceptives were associated with a lower incidence of hyperthyroidism. Alopecia areata was not on this list.

 

Alopecia areata and estrogen

We do know that the inflammation that is seen in alopecia areata can be influenced in some manner by estrogen.  One study has suggested that alopecia areata can actually be treated with a combination of oral contraceptives (especially those containing norethindrone) and metformin. In a 2013 study by Reisz and colleagues, 14 females with alopecia areata were given norethindrone or metformin (500-850 mg per day) or both and encouraged to take an over the counter vitamin D supplement. Five patients requested intralesional corticosteroids along with hormonal therapy, and nine patients opted for hormonal treatment only. Interestingly, seven of the 14 had complete regrowth of hair within 12 weeks. Another 4 fully regrew their hair but took at least a year to completely reverse their hair loss. 

 

Norethindrone containing oral contraceptives

The following oral contraceptives may contain norethindrone and ethinyl estradiol:  

Norethindrone & Ethinyl Estradiol Containing OCPs

 

CONCLUSION

It's clear that estrogen affect the immune system and at least for some immune based diseases (like multiple sclerosis, ulcerative colitis, Crohn's disease, Systemic Lupus Erythematosus, and interstitial cystitis) there is good evidence that oral contraceptive use increases the risk of developing these conditions. 

We don't have good evidence yet for alopecia areata and to date it would appear for the vast majority of patients there is no link. However, this does not exclude a small subset of individuals that in fact develop alopecia areata after starting a birth control pill. Detailed studies have not examined this and whether there are certain types of birth control pills that are protective against AA and some that are contributory.  The study by Reisz and colleagues discussed above would certainly cause us to give pause and consider that some oral contraceptives may actually be helpful.  For my patients who clearly feel that their OCP is a trigger, I may consider stopping if the alopecia areata is not responding to treatment as one might expect. If an oral contraceptive is restarted in the future, a different one might be considered with close monitoring of whether the OCP gives a flare of the alopecia areata.

 

 

REFERENCES

1) Williams WV.  Hormonal contraception and the development of autoimmunity: A review of the literature. Linacre Q. 2017.

2) Oral contraceptives and alopecia. 1968 Mar 9; 1(5592): 593. 

3) Oral contraceptives and alopecia areata. Br Med J. 1965 Oct 23; 2(5468): 1005. 

4) Wallace ML, et al. Estrogen and progesterone receptors in androgenic alopecia versus alopecia areata. Am J Dermatopathol. 1998.

 

 


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Side Effects from Hair Loss Medications:

Side Effects from Hair Loss Medications: What is the Chance?

Today, I’d like to review my personal view on medication and treatment-related side effects.

 

1.     Every single treatment has ‘potential’ adverse effects. (No treatment is risk-free).

Every treatment for hair loss has potential side effects. There is no treatment on the planet that is side effect free. How do I know that? Well, studies have shown that even patients using “placebo” treatments for their hair loss report side effects. This teaches us that any time a patient uses a treatment they have a chance to experience a side effect. Whether it’s a true side effect or not is sometimes challenging to decipher but a topic for another article.

 

2.     No medication or treatment for hair loss should ever be prescribed or used without patients understanding the “most common" adverse events

It is critically important for patients to understand the "most common" side effects of a treatment. The purpose of delivering such information to patients is to help them with informed consent.  A patient should only use a mediation if they feel that the benefits of using the medication are greater than the potential risks. It is the responsibility of the physician to transfer information about both the benefits and the risks to the patient so that the patient can offer their informed consent.

 

3.     It is not possible to explain all the potential side effects of a medication.

Despite the important role that we as physicians have in telling our patients about the side effects of medications, it is important for patients to be aware that a given presciber can not communicate the entire list of side effects that have ever been reported. However, it is imperative for the prescriber to advice on the most common ones. 

Take for example, the oral medication doxycycline. In the hair clinic, doxycycline is used for the treatment of scarring alopecia, folliculitis and a variety of other inflammatory and infectious conditions. A patient who is deciding on whether to use doxycycline or not should be made aware of the most common side effects including gastrointestinal upset, nausea, headaches, increased chance of yeast infections in women.

However, rare side effects are possible as well. For example, every year a small number of users of doxycycline around the world develop serious allergic skin reactions. It would be highly unusual for any prescriber or pharmacist to counsel a patient on this particular side effect.

 

4.     There may be side effects that are discovered years down the road.


One must also be aware that some side effects of a medication may not be apparent during clinical trials or even during the first few years that the medication is on the market. In some cases it may take 10, 15 or even 20 years to come to understand that rarest of side effects.  “Post marketing surveillance” is a term used to describe the monitoring that goes on after a medication is released on to the market. Post marketing surveillance has lead to some medications being removed from the market. One must always be aware that additional side effects of a medication may be revealed in the future through such post marketing surveillance.

 

5.     For any potential adverse effect, one must ask “how common” that side effect is.

 

For some medications, the chance of adverse effects may be very low, whereas for other medications, the chance of an adverse effect may be quite high. Let’s take topical minoxidil as an example. The most common side effects and headaches, dizziness, hair shedding (in the first few months), hair growth on the face and heart palpitations. However, in deciding whether to use the medication or not, patients need to understand the overall chance of these side effects.  For example, many women are extremely concerned to learn that hair growth on the face (hypertrichosis) is a potential side effect of minoxidil.  it is very important from women to note that 19 out of 20 women who use minoxidil will not have any problems with hair growth on face. However, 1 out of 20 users will. This information is helpful as it encourages many women to move forward with considering the medication with knowledge that their chance of hair growth on the face is quiet low.

 

Conclusion 

Hair loss medications have the potential to dramatically improve hair density or stop hair loss and may improve quality of life. However, anyone using a treatment, no matter what the treatment actually is, needs to be aware that every treatment has potential side effects. It is imperative that patients, together with their doctors, spend time understand how common the various side effects actually are.

 

 


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Erectile dysfunction in Minoxidil Users: What's the Naranjo Score?

Erectile dysfunction in minoxidil users

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

One one study to date supports an association

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

MINOXIDIL ASSOCIATED WITH ERECTILE DYSFUNCTION

 

Blood pressure medications can cause impotence

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

 

The Naranjo Adverse Drug Reaction Probability Scale

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

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

 

A Closer Look at the Naranjo Adverse Drug Probability Scale

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

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

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

 

Determining the Naranjo Score

Scores can range from -4 to + 13. A score of 0 or less means the likelihood of the drug causing the side effect is doubtful, a score 1 to 4 indicates it is 'possible', a score 5 to 8 means it is 'probable' and a score 9 to 13 means it is 'definite'

 

 

Reference

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

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

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

 

 


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Am I taking the right amount of hydroxychloroquine (Plaquenil)?

Hydroxychloroquine (Plaquenil): Am I taking too much?

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.

 

The Risk of Retinopathy with Hydroxychloroquine

"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.  

 

Risk Factor for Retinal Toxicity

Retinal damage can occur in anyone. However, the risk may be increased if the following risk factors are present

  • Longer Duration of use (cumulative dose)
  • Renal or hepatic functional impairment. Compromised kidney and/or liver function can lead to increased accumulation of hydroxychloroquine in the tissues.
  • Age over 60 years.
  • Preexisting retinal disease
  • Concurrent tamoxifen therapy

 

What dose should I take?

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:

Hydroxychloroquine Dosing

 

Conclusion

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.

 


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Doxycycline and Headaches: What everyone needs to know.

Doxycycline and Headaches: Caution Needed

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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.

 

Side effects of doxycycline

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 in Patients Using Doxycycline:  A closer look at benign intracranial hypertension

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."

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. 

 

Urgent medical attention needed if headaches persist

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.


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Finasteride and Gynecomastia (Male Breast Enlargement)

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

 

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

 

Finasteride-Induced Gynecomastia: Myths and Misconceptions

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

 

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

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

 

2. Gynecomastia typically starts after 2-4 months

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

 

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

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

 

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

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

 

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

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

 

6. Finasteride-induced gynecomastia increases with age and obesity

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

 

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

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

 

CONCLUSION and FINAL POINTS

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

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

 

REFERENCE

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

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

 

 


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Anabolic Steroids and Hair Loss: Is one month okay?

Anabolic steroids can cause hair loss in genetically susceptible individuals

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

 

Hair loss from anabolic steroids

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

 

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

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

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

Is it 1 month? What about 2 months?

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

 

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

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

 

Conclusion

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

 

 


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Hair loss from steroid injections: Is it possible?

Steroid injections: Is it possible to cause hair loss?

Steroid injections are frequently used for treating two conditions: alopecia areata and scarring alopecia. Medications such as triamcinolone acetonide (sometimes referred to by the popular name Kenalog) are injected into the scalp. The purpose is either to grow hair (in the case of treating alopecia areata) or to stop further hair loss (in the case of scarring alopecia). 

Steroid injections can sometimes induce hair loss (telogen effluvium) in some individuals. It's not common but some individuals actually develop small circles of hair loss around the areas injected. Some will even develop small 'indentations' in the skin in these areas as well. This hair that has been lost may grow back with time but indicates that a lower concentration of triamcinolone should be used for that patient in the future.  


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Plan b: Is There a Plan B to Treating Hair Loss?

The first step in determining how to help someone with hair loss is figuring out his or her diagnosis. There is no bypassing this step.  The second step is determining a treatment plan that is based on the best medical evidence. 

 

Plan B: What is Plan B, Doc?

After reviewing a treatment plan with my patients, I'm often asked what treatment will be considered next. "What's plan B, doc?" Well, every treatment plan needs Plan B as well as a Plan C and Plan D.

Consider the 28 year old female with androgenetic alopecia. The best treatment option for her based on all her facts, review of her blood tests and scalp exam might be topical minoxidil. Plan B might be oral spironolactone with or without minoxidil. Plan C might be the addition of a laser comb or changing the anti androgen used. Plan D for her might be a trial of PRP. A solid treatment plan has an alphabet of plans. Not guesswork and not a random pull out of a hat option. But rather options based on a delicate combination of medical science and expert consensus, and personal experience.

What about the 53 year old female with frontal fibrosing alopecia? Plan A for her might be finasteride & steroid injections with hydroxychloroquine as Plan B. Doxycycline is reserved for her as Plan C. For another patient with FFA, Plan A might start with hydroxychloroquine & steroid injections. For her, finasteride is not on the list given the past history of breast cancer the patient had. Plan B is doxycycline and plan C is methotrexate.

 

Conclusion

Every treatment plan should have an alphabet of plans. That does not necessarily mean one will need to move down the list but the physician should have a clear plan for how to navigate.


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Can drugs accelerate androgenetic alopecia (AGA)?

Medications can potentially accelerate androgenetic alopecia. Common examples are anabolic steroids, the use of testosterone injections and topical androgen gels (commonly used for men with "low testosterone"), androgenic progestins in birth control pills, danazol as well as many other medications.

This individual whose scalp is shown in the picture has been using anabolic steroids for body building and has experienced rapid hair loss mainly due to a conversion of his large terminal hairs (some labelled by green dot) to thinner miniaturized hairs (labelled by yellow dot). Treatment of drug accelerated AGA involves either stopping the androgen or blocking the effects of the androgen on the hair follicle using 5 alpha reductase inhibitors... or both. Less specific treatments like minoxidil may provide some benefit. Many individuals can improve with this plan but full regrowth is unlikely.


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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Anti-coagulants during hemodialysis: Can they cause hair loss?

Blood Thinners and Hair Loss

Dialysis is a medical procedure used to filter waste from the blood in patients with kidney disease. Close to 500,000 Americans and 25,000 Canadians are receiving dialysis. The most common reasons for dialysis is end stage kidney disease due to diabetes and high blood pressure. 

Hair loss and hair changes occur time to time in patients receiving dialysis. One needs to consider a range of nutritional issues (including protein intake, zinc deficiency, iron deficiency), thyroid abnormalities, as well as hair loss from systemic disease itself (ie. autoimmune disease). The use of medications must be considered. 

Anticoagulants are a group of blood thinning medications used during hemodialysis to prevent blood clotting when blood is filtered through machines. Several different types of anticoalgulants may be used and many can rarely cause hair loss. The mechanism by which they cause hair loss is typically a telogen effluvium although other mechanisms may occur as well. 

Apsner and colleagues, in 2001, reported 5 hemodialysis patients who had hair loss from the low molecular weight heparin blood thinner dalteparin. All patients reported that their hair loss stopped when the dalteparin was stopped and a different method of anticoagulation (regional citrate anticoagulation) was used. 4 of the 5 patients even regained hair. In 2003, Sarris and colleagues reported a hemodialysis patient who had hair loss after switching from one low molecular weight heparin (enoxaparin) to tinzaparin. Hair regrowth resumed after switching back to enoxaparin. 

 

Conclusion

There are many potential reasons for hair loss in patients receiving hemodialysis. Careful review of all factors is needed. Anticoagulants used during hemodialysis, including the low molecular weight heparins, need to be considered. 

 

Reference

Sarris E, et al. Am J Kidney Dis. 2003.

Apsner R, et al. Blood. 2001


Dr. Jeff Donovan is a Canadian and US board certified dermatologist specializing exclusively in hair loss. To schedule a consultation, please call the Whistler office at 604.283.1887
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