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Vision Changes from Topical Steroids: A Closer Look at Central Serous Chorioretinopathy (CSCR)

Central serous chorioretinopathy from Topical Steroids

Topical steroids are an important aspect of managing many scalp conditions. Many different topical steroid strengths from class I (strongest) to class VII (weakest) are available.

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I was interested in a few reports from the last decade that mentioned the development of an eye condition known as central serous chrorioretinopathy (CSCR) from prolonged or even short term use of topical steroids. Central serous chrorioretinopathy is associated with visual impairment, often temporary, and usually affects a single eye. Blurry vision is often the symptom that affected patients report but it may even be asymptomatic. Other symptoms that patients with CSCR reports are a dark area in the central vision, objects appearing smaller than they really are, objects appearing further away than they really are, the change of straight lines to crooked or bent lines, and a duller color to objects that are white.

It is a common retinal disease that can cause loss of vision as a result of accumulation of fluid behind the retina (subretinal) leading to localized serous retinal detachments. In simple terms, CSCR causes a blister-like swelling in the retinal layers. Males aged 20 to 50 are the most commonly affected (94 % in one 2016 study) but it may also affect women. Some studies have suggested that emotional stress, smoking, hypertension, sleeping problems, heart disease, migraine headaches, medications (stimulants, erectile dysfunction medications), autoimmuen diseases and peptic ulcer disease may be among risk factors that are sometimes (but certainly not always) present.

CSC occurring after prolonged use of topical steroids is not common. Most cases typically occurring in patients using oral or inhaled steroids.

In 2011, Ezra and colleagues in the Journal of Drugs in Dermatology reported a 25 year old male who had been using a corticosteroid ointment for 15 years. He presented to the eye clinic with vision impairment from central serous chrorioretinopathy.

In 2016, Chan et al reported 2 patients who developed CSCR in 2 patients who were using topcial steroids on limited areas of the body.

in 2018, George et al reported an interesting case where CSCR developed quite quickly. The patient was a female patient with oral lichen planus who was started on a topical steroid in the mouth (triamcinolone acetonide 0.1%). One week later, she reported with blurring of vision of both eyes. She was referred to the ophthalmologist and was diagnosed to have acute central serous retinopathy (CSR).. The topical steroid was discontinued and she was advised ketorolac eye drops (0.3%). At a follow up appointment 2-months later, there was significant improvement in her ocular condition.


Central serous chrorioretinopathy is not common but it is important that dermatologists are aware of this condition. It appears that steroid induced CSCR may happen in patients who have some sort of a predisposition to begin with - and can even happen with very lower doses. Treatment of CSCR involves stopping the steroid as the first step. Many cases resolve on their own in a few months and many patients regain vision fully. However, it has been suggested that patients who develop CSCR on account of steroid use may have slightly poorer prognosis than some other groups so close follow up is advisable. If symptoms persist, a variety of options are available including lasers, photodynamic therapy, oral treatments (methotrexate 5 to 10 mg, finasteride, beta blockers, aspirin), and injections (anti VEGF agents like bevacizumab). Agents like doxycycline have not been well studied in CSCR.

The main message here is that all patients who use topical steroids and develop vision changes should be referred for a proper eye examination.


Chan et al. Localized topical steroid use and central serous retinopathy. J Dermatolog Treat. 2016 Oct;27(5):425-6. doi: 10.3109/09546634.2015.1136049. Epub 2016 Jan 29.

Ezra et al. Central serous chorioretinopathy associated with topical corticosteroids in a patient with psoriasis.J Drugs Dermatol. 2011 Aug;10(8):918-21.

Fernandez CF et al. Central serous chorioretinopathy associated with topical dermal corticosteroids.Retina. 2004 Jun;24(3):471-4.

George et al. A potential side effect of oral topical steroids: Central serous chorioretinopathy. Indian J Dent Res. 2018 Jan-Feb;29(1):107-108. doi: 10.4103/ijdr.IJDR_694_16.

Islam et al. Frequency of Systemic Risk Factors in Central Serous Chorioretinopathy.J Coll Physicians Surg Pak. 2016 Aug;26(8):692-5. doi: 2407.

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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10 Signs You Are Probably Not On Track In Treating Your Scarring Alopecia

Scarring Alopecia: Clues that You’re Off Track and How to get back On Track

Scarring alopecias are hair loss conditions that have the potential to cause permanent hair loss. Patients often have scalp itchiness and may also expeirence burning in the scalp as well. Increased shedding is common. There is a lot of misinformation about these conditions becasue all too often they are grouped in the bigger category of ‘hair loss.’ It’s too often felt that what worked for one person with hair loss should work for another person. That’s just not the case if that other person has scarring alopecia.

After treating many patients with scarring alopecia over the years, I can say that there are often signs that that tell me that a patients needs a bit of help with how they are approaching their own scarring alopecia. These may be patients who contact our office, or patients who post concerns on social media or patients who come to the office.

Treating scarring alopecia is not only about connecting patients with effective treatments but also about dispelling myths and misinformation - some of it quite strongly rooted in the mind of the patient and sometimes their doctors too. Treatments can help the patient but knowledge also heals too.

Here are these 10 signs.

10 signs

CLUE 1: The patient has no idea what they should be monitoring.

Many patients with scarring alopecia tell me that they leave their doctor’s office with prescriptions but don’t know exactly what they are supposed to be monitoring until their next appointment. Alternatively (as in CLUE 3 below), they leave the office with the expectation that their hair will grow back.

Patients with scarring alopecia should be monitoring SEVEN main things at home - scalp itching, scalp burning, scalp tenderness, scalp redness, scalp pimples (pustules), hair shedding and density in various areas of the scalp. Of course, not all patients want to monitor these things and leave it up to the doctor to ask about these things at the follow up appointments. However, for those who want to actively play a role in montiroign their disease at home, we encourage them to complete the following form at home on a weekly or monthly basis


CLUE 2: The patient knows what to monitor but does not know how soon to expect it all occur.

Some patients come to understand the basics of what sorts of things they should be monitoring at home. They know to keep track of scalp itching, scalp burning, scalp tenderness, scalp redness, scalp pimples (pustules), hair shedding and changes in density in various areas of the scalp. However, they are not sure when all this is expected to improve or when they are to notice a change.

It is import to review these sorts of things with the dermatologist as they may differ slightly with the exact type of scarring alopecia. I normally expect scalp symptoms to improve within 2-3 weeks and scalp shedding to improve within 2-3 months. Changes in hair density however, may take 2-7 months depending on the type of treatment that the patient has chosen.

For lichen planopilaris, for example, these changes might occur as follows (according to various treatment)


CLUE 3: The patient is expecting hair regrowth.

Many patients with scarring alopecia tell me that they have been doing all the things that their doctor recommended but are just not seeing an improvement. These patients are essentially telling me that they have not been educated on what it is they should expect.

While it’s true that hair regrowth does occur in many scarring alopecias, especially when treated in the early stages - the expectation should be that we STOP further hair loss rather than get new growth back. I tell patients that if they look the exact same as they do today in 6 or 12 months from now - it means the treatment is working well. Of course, I also tell some patients that a bit of regrowth might occur too. But this does not happen for everyone.

CLUE 4: The patient has never taken a photo of the hair & scalp to date.

If a patient has scarring alopecia and has never every taken a photo of the scalp since their diagnosis, they are missing out on an important step. Patients simply MUST take photos at home for optimal management. Of course, the doctor should take photos in the office but not all do. In today’s busy world, patients simply must be their own advocate and must take photos themselves or get someone else to take them.

When a patient of mine emails our office and says they are doing worse, the first thing I want to see is photographs.

Photos should of course be taken of the areas of hair loss, but should also be taken of normal appearing areas in the event these are slowly changing or in the event loss occurs in the future.

A patient who has never taken photos of their scalp needs to be educated on the importance of this step in scarring alopecia.

CLUE 5: The patient is shampooing the hair less and less.

Most patients with scarring alopecia react to their hair loss by shampooing less often. Many of these patients develop worse and worse seborrheic dermatitis on account of shampooing less and less. Some even develop thick scale in areas (pityriasis amiantacea) that traps bacteria and other microorganisms and worsens inflammation. In addition, some patients who shampoo less and less start to see more and more hair coming out after showering which prompts them to shampoo the scalp even less. A vicious cycle sometimes develops. For example, a patient who shampoos the hair once per week is going to see a lot more hair loss compared to if they shampoo the scalp daily.

I recommend that patients with scarring alopecia be gentle on their scalp but generally speaking shampooing every 2-3 days is appropriate for those with fine or straight hair and shampooing every 4-6 days is appropriate for those with curly hair. If seborrheic dermatitis is present, an anti-dandruff shampoo should be added to the shampooing routines. It thick scale is present, a salicylic acid based shampoo may be needed to help lift the scale.

CLUE 6: The patient has never used a topical corticosteroid.

Corticosteroids are the mainstay of treatment for many types of scarring alopecia. That’s not to say by any means that they are the most effective treatments. Not at all. However, for most types of scarring alopecia, especially lichen planopilaris, frontal fibrosing alopecia, discoid lupus, pseudopelade, they are a an improtant treatment to consider given their relatively safety and reasonable effectiveness.

A patient who has never used a topical steroid is quite likely to be misinformed, or poorly educated about their scarring alpecia. On average. Of course, there are exceptions. Yes. But we are talking averages here. A patients who has used this supplement or that supplement in hopes it will help their scarring alopecia or done this cosmetic non sense or that cosmetic non sense but has never used a topical steroid is all too common.

The purpose of this article is to help patients and physicians recognize the clues of being off track with treating scarring alopecia - and this is certainly one of them.

CLUE 7: The patient has never had any blood tests after your diagnosis.

Many scarring alopecias are diseases of the immune system of the body. Yes, it’s true many just have effects in the scalp (and the rest of the patient is perfectly healthy. But not all. We know that many scarring alopecias are associated with an increased chance of having blood test abnormalities - including thyroid abnormalities and low vitamin D. If a patient has not had blood tests since their diagnosis, they need them. Plain and simple. The basic tests are CBC (blood counts), TSH (thyroid studies) and ferritin (iron storage) and 25 hydroxyvitmain D (vitamin D status). Yes, other tests might be needed too - but these are the four basics that everyone needs. If a patient has never had blood tests, they are not quite on track yet.

CLUE 8: You have not seen a dermatologist to date about your hair loss.

This one often prompts some to take offence, but it should not. Many physicians treat hair loss and do a great job. Many hair transplant surgeons treat hair loss and do a great job. Many endocrinologists treat hair loss and do a great job. Many trichologists treat hair loss and do a great job. But most scarring alopecias are best handled by dermatologist.

A hair transplant surgeon, general practioner, endocrinologist and trichologist are not equipped with the tools to fully battle this group of diseases. A hair transplant surgeon does not usually prescribe systemic medications. For example, it’s rare that a hair transplant surgeon prescribes hydroxychloroquine, mycophenolate, cyclosporine, isotretinoin, clindamycin, rifampin. Are these really needed sometimes? They most certainly are.

A hair transplant surgeon treats hair loss with surgery and surgery is never ever an option in the early stages of scarring alopecia. An endocrinologist may have great strategies for some cases of female pattern androgenetic alopecia and may offer minoxidil, spironolactone and other systemic hormonal based options. But no, most endocrinologists don’t prescribe systemic medications for scarring alopecia and do not have the experience to monitor these systemic medications in the setting of scarring alopecia.

I’ll leave this topic now, but it’s one I feel strongly about. The only physician group with advanced skills to battle scarring alopecias are dermatologists. The exception of course would be physicians with advanced training in the field of hair loss dermatology. It’s simple. Yes, this concept rubs some the wrong way. But it shoud not. Patients are confused with available treatments. Bold statements are needed to help patients. And my primary concern is to help patients. The vast majority of patients with scarring alopecias are best treated by a dermatologist.

CLUE 9: The patient is using treatments but you don’t know what ingredients they contain.

It’s common for a patient to tell me they are using this treatment and that treatment. This vitamin and that vitamin. Many go on to say they are using something their hairdresser gave them or something they ordered from the internet, but they are not sure what it is.

If a patient is using something that they don’t know what it is, they need to stop. The treatment of scarring alopecia is a finely tuned process. At every single step, we need to know what we are doing. Taking things that one does not know what it contains is unsafe.

The immune system however, does know what the patient is taking - and so does the rest of the body. Some treatments activate the immune system, some have no effect and some actually weaken it. This includes natural products, herbs and random supplements.

CLUE 10: The patient is buying more and more products from the internet.

Patients who find themselves buying more and more treatments from the internet are probably not on track. This supplement, that supplement - it probably does nothing in the case of scarring alopecia. Fancy packaging and elevated prices are not associated with a great chance of helping scaring alopecia.

Do I ever recommend various supplements? Sure. Some may have benefit in non scarring alopecias, especially those associated with increased shedding (telogen effluvium). Rarely do they help scarring alopecia.

If a patient is increasing turning to amazon or various online website stores for options for their hair loss, it’s probably an indication that they should be seeing a dermatologist who treats scarring alopecia.

Conclusion and Summary: How do I get back on track?

There is a great deal of misinformation about scarring alopecias out there in the world. After treating many patients with scarring alopecia over the years, I can say that there are often signs that that tell me that a patients needs a bit of help with how they are approaching their own scarring alopecia.

I feel strongly that patients need to know what it is they should expect and how best to monitor their scarring alopecia. Not everyone follows there symptoms like our chart enables them to, but I certainly encourage patients to take photos. Everyone with primary scarring alopecia needs blood tests and there simply are no exceptions. Some types of scarring alopecia may need more tests than others, but everyone needs blood tests. Most patients with scarring alopecia benefit by a visit with a dermatologist. it’s true that future appointments and ongoing monitoring may be handled by many different types of specialists, but scarring alopecias are fundamentally dermatological diseases. I understand that it can be difficult to access a dermatologist in many parts of the world. It still does not change the view that dermatologists are the group of physicians with the skills to battle the toughest cases of scarring alopecia.

Treating scarring alopecia is not only about connecting patients with effective treatments but also helping dispel myths and misinformation. Helping the patients starts with education - long before I reach for a prescription pad.

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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Treatment Options for Lichen Planopilaris: What to consider?

Lichen planopilaris: What are the treatment options to consider?

Lichen planopilaris is a scarring alopecia with the potential to cause permanent hair loss. Treatment helps stop the disease in many but may or may not actually help the hair to grow back. Treatment, however, may help reduce symptoms such as scalp itching, burning or tenderness.

Lichen planopilaris: A variety of options are available although some are clearly better than others.

Lichen planopilaris: A variety of options are available although some are clearly better than others.

The Main Nine Treatments of LPP

There are a variety of treatment options available for LPP. In fact, taken together there are well over 25. This list in this figure is not complete by any stretch. However, several options would be considered "standard options" or “first-line options” and have the best medical evidence. These options include topical steroids, topical calcineurin inhibitors, steroid injections, and oral medications such as hydroxychlorqouine, doxycycline, methotrexate, cyclosporine and mycophenolate and isotretinoin. These are by far the most helpful nine treatments. Oral cyclosporine is probably the most helpful treatment for LPP overall but rarely we start with this due to side effects (it's viewed as a “third-line option” in my pratice). It may help up to 80 % of patients. The next best is probably methotrexate and hydroxychloroquine with up to 60 % benefiting.


The First Step: Where does one start?

Typically, I start with topicial steroids, (sometimes with topical calcineurin inhibitors), and steroids injections and give careful discussion to whether to start doxycycline or hydroxychloroquine. Other options that can be considered (especially if these 9 options do not work) include low level laser, low dose naltrexone, pioglitazone, excimer laser, anti-androgens, azathioprine, and tofacitinib.

These treatment options do not help everyone and it may take 4-6 months to get an idea if it’s helping stop loss. Symptoms however can go away very quickly on the right treatment (3-4 weeks). In discussing treatment options with one’s physician, side effects, ease of use, and cost must be taken into account. Some treatments like topical steroids and steroid injections have a fairly good side effects profile if used correctly. However, they rare stop the disease completely if used alone (but rarely can). Nevertheless they may provide some degree of benefit. Other options such as the oral immunomodulating medications are superior to topical steroids and steroid injections but have greater potential side effects that must be weighed.


Cautionary Tales

Starting with treatments like platelet rich plasma for LPP is common but not based on solid evidence. Rarely do patients really benefit. Over the counter supplements don't shut down the disease and are not first line either. Hair transplantation for LPP can be done but only when the disease is 100 % quiet (patient has no symptoms and has not lost any hair and taken no medications) and has shown itself to be 100 % quiet over 2 years of extremely careful monitoring. If photos of a patient taken two years apart look identical, a patient with LPP may be a candidate for surgery. Even then the disease can still flare and long term dermatological monitoring is needed.

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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Spironolactone for Hair Loss: Should we be measuring potassium levels in patients or not?

Potassium Levels and Spironolactone: Measuring May be More Relevant for Women over 45.

Spironolactone is an oral medication often used off label for treatment of androgenetic alopecia in women. Previous recommendations in patients using spironolactone for acne (not hair loss) suggested that routine monitoring of serum potassium levels was important. However, more recent studies have suggested this is not necessary for healthy women. This includes a 2017 study by Layton and colleagues that evaluated 10 randomized controlled trials (RCTs) and 21 case series pertaining to acne.

See Previous Article: Spironolactone and FPHL: Are routine measurements necessary?

Similar conclusions were found by Plavanich and colleagues in a retrospective study of healthy young women taking spironolactone for acne. The findings of the study were that young women receiving spironolactone had a hyperkalemia rate of 0.72%, equivalent to the 0.76% baseline rate of hyperkalemia in the general population.

Although there is increasing evidence that measuring potassium levels in young healthy women who do not use any other medications is probably not necessary, a key question is whether we should or should not be measuring potassium levels in women in the late 40s, 50s (and beyond) who are prescribed the drug.

Thiede and colleagues recently reported data on potassium levels in 124 women both before and after spironolactone initiation. 112 women were in an 18 to 45 years age group, and 12 were in a 46 to 65 years age group. All women had potassium levels within normal limits before starting the drug. Interestingly, 17 % of women in the 46 to 65 years age group had high potassium levels (hyperkalemia) after starting spironolactone compared with less than 1 % of women 18 to 45 years of age.

Routine monitoring of potassium levels is probably not necessary in young healthy women who don’t take other medications.

Routine monitoring of potassium levels is probably not necessary in young healthy women who don’t take other medications.


Overall, this was a very small study and there were only 12 patients in the older age group which limits how we interpret this data. Nevertheless, the study has important lessons which are likely relevant not only for women using spironolactone for acne but hair loss as well. First, routine potassium testing in young healthy women is probably not necessary. Second, women with cardiovascular disease, kidney disease, diabetes and women taking certain medications that affect potassium levels (ie potassium sparing diuretics) may or may not be deemed good candidates for spironolactone in the first place but if they are they will certainly require periodic potassium measurements. Third, even healthy women over 45 could potentially be at increased risk of hyperkalemia from spironolactone and one should at least consider whether or not monitoring is warranted.

Thiede RM et al. Hyperkalemia in women with acne exposed to oral spironolactone: A retrospective study from the RADAR (Research on Adverse Drug Events and Reports) program. Int J Womens Dermatol. 2019 Apr 25;5(3):155-157.

Layton AM et al. Oral Spironolactone for Acne Vulgaris in Adult Females: A Hybrid Systematic Review. Am J Clin Dermatol. 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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Top 10 Things You Need to Know about Oral Minoxidil for Hair Loss

Oral Minoxidil: Top 10 Points for Prescribers and Patients.

Here are the top 10 points that prescribers and users of minoxidil need to know.

1. Oral minoxidil is not FDA approved for hair loss.

The use of oral minoxidil is FDA approved for high blood pressure. Its use in hair loss is entirely off label.

2. If you are going to use or prescribe oral minoxidil, you need to know a thing or two (or three) about it - including who should not be prescribed the drug.

If one is going to use or prescribe oral minoxidil they need to know everything about it. The same is true for any treatment - prescription, non-prescription, cosmeceutical, holistic, natural or ayurvedic. No treatment should be used without solid understanding of risks and benefits, indications and contraindications. If you can’t list 5-6 common side effects of oral minoxidil, I believe you should not be using it or should not be prescibing it. Plain and simple.

One should also have a clear sense who should not use this medication. The following are contraindications or reasons not to be using or prescribing minoxidil:

1. Minoxidil should not be used if women are pregnant or trying to conceive. 

2. Patients over 60 years of age can use oral minoxidil only with caution as they may be more sensitive and could potentially have underlying cardiovascular disease which can precipitate angina if blood pressure were to drop.

3, Patients with underlying chronic health issues, especially kidney, heart and liver problems should not use

4. Patients with heart disease include those with previous heart attacks but also those with angina, heart failure and rhythm problems should not use

5. Patients with pheochromocytomas should not use oral minoxidil

6. Patients with porphyria should not use oral minoxidil

7. Patients who have not used or considered other standard hair loss treatments first should not jump not necessarily jump into using oral minoxidil.

8. Patients with low blood pressure to begin with or those using other anti-hypertensives may not be ideal candidates for oral minoxidil. This needs careful review.

3. Oral minoxidil can be a very helpful second-line treatment for many conditions when used properly. This includes androgenetic alopecia, alopecia areata, chronic telogen effluvium, traction alopecia and post-chemotherapy permanent induced alopecia.

As mentioned above, oral minoxidil is not FDA approved for hair loss. Oral minoxidil can help some conditions and can have an amazing role in managing various conditions. However, it is rarely a first-line agent. Other options might be considered first for many of these conditions, including consideration given to topical 2 or 5% minoxidil. However, if various first-line treatments do not prove completely helpful or can not be used for various reasons, oral minoxidil might be considered. Oral minoxidil at doses 0.25 to 5 mg has shown benefit in treating androgenetic alopecia, alopecia areata, chronic telogen effluvium, traction alopecia and post-chemotherapy permanent induced alopecia.

4. When minoxidil pills are taken by mouth, most of the drug is quickly absorbed into the blood.

Oral minoxidil is easily absorbed from the gastrointestinal tract. The peak levels in the blood occur at around 1 hour after taking the medication and then levels slowly drop after that. Minoxidil is metabolized by the liver. The half life of oral minoxidil is around 4.2 hours. The concentration of minoxidil that appears in the blood depends on the dose used. With 5 mg pills, a concentration of of 157 ng/mL can be measured in the blood about 1 hour later before levels start to drop off. If one-half the amount of minoxidil is ingested (ie a 2.5 mg pill), the concentration in the blood at the one hour time point is actually much less than simply one half the amount. It’s about one-fifth the amount at approximately 28 ng/mL. This is important information because it reminds us that it’s not appropriate to say “Oh you did well on 2.5 mg, I’m sure you’ll do just fine if we go up to a 5 mg dose …. let’s go up on the dose.” Likely the patient will do just fine, but we need to monitor things just the same. There may be more than twice the amount of minoxidil in the blood at certain times with twice the dose.


5. There are many ‘potential’ side effects of oral minoxidil. The most common ones are easily remembered by the mnemonic “HAIR “- (headaches, ankle edema, increased hair on the face, and rashes/urticaria). Other side effects potentially occur as well.


The headaches may occur from changes in blood pressure. The ankle edema occurs from fluid retention and rarely also manifests with swelling around the eyes. Of course other side effects are also possible, and one needs to understand the range of side effects that can occur. Shortness of breath, increased heart rate and weight gain from fluid retention are all possible.

6. Topical minoxidil does not often change heart rate and blood pressure in most users - but oral minoxidil can.

Studies of topical minoxidil showed that blood pressure and heart rate don’t change significantly in healthy users who use minoxidil at the appropriate dose. That said, there is an occasional patient who does find that their heart rate goes up in the firsts hours after applying minoxidil or that they feel dizzy.

Oral minoxidil can affect heart rate and blood pressure. 0.625 mg doses and 1 mg doses rarely cause changes in blood pressure and heart rate. As we increase the dose, the more and more likely it is for the patient to experience changes. For example, the 5 mg dose is much more likely to cause changes in blood pressure and heart rate than the 2.5 mg dose. We advise our patients to monitor heart rate and blood pressure after starting. (See ORAL MINOXIDIL MONITORING FORM).

7. Although the oral minoxidil reaches peak levels in the blood about 1 hour after a single dose of the pills, the main effect on blood pressure occurs at the 2-3 hour mark and then blood pressure rises again slowly after that. For those using minoxidil daily long term, the maximal effect on blood pressure occurs at the 10-14 day mark.

We generally advise patients to monitor their heart rate and blood pressure weekly after starting. We compare this to baseline measurements to get a sense of the hemodynamic changes (if any) that occur with oral minoxidil use.


It’s helpful to know what is happening to the blood pressure in the first few days but especially 10-14 days after any change in dose. It’s a good idea for users of oral minoxidil to get a baseline blood pressure reading before they start using the pills because one will refer back to this number in future days, weeks and months ahead. Previous studies have taught us that patients using oral minoxidil at doses 0.625 mg and 1 mg rarely have changes in their heart rate or blood pressure after using minoxidil. Changes in blood pressure and heart rate are not that common with 2.5 mg but certainly more common with 5 mg doses. I always advise measuring blood pressure and heart rate initially and then again at the end of the first week and then again at the end of the second and third week. Patients can do this at home themselves if they own a blood pressure cuff or in any local pharmacy (many pharmacies in North America have blood pressure machines that patients can use for free). For most people, there are no changes on the really low doses or oral minoxidil we use for hair growth. Blood pressure should be measured at any time a patient using oral minoxidil experiences dizziness. Fortunately, this is are.

Most studies in the past have shown that it’s once a patient starts using 5-10 mg doses of oral minoxidil that effects on heart rate and blood pressure can be seen. The early studies of oral minoxidil showed that serum concentrations of 21.7 ng/mL was the lowest concentration that resulted in significant blood pressure and heart rate changes in patients. About 1:200 to 1:300 patients using topical minoxidil will achieve this concentration but it’s a bit more common of course in users of 2.5 and 5 mg oral minoxidil.

8. Serum concentrations with oral minoxidil are about 20-30 times higher than topical minoxidil.

It is not surprising that blood levels of minoxidil are higher when you take it orally, but the key question is how much higher? First, it’s important to understand the there is some systemic absorption of minoxidil even in users of topical minoxidil. It’s just that it’s very low. About 99 % of users of topical minoxidil have blood levels less than 2-5 ng/mL. However, some patients using topical minoxidil occassionally do acheive much higher levels or minoxidil in the blood - even levels up to 21 ng/mL. Fortunately that is uncommon. Concentrations of minoxidil higher than 5 % may increase absorption. Topical medications like topical retinoids and topical cortisones can increase absorption of minoxidil for example. The serum concentration of minoxidil is about 20-30 times higher with use of oral minoxidil than topical minoxidil.

9. The higher the dose of oral minoxidil, the higher the levels in the blood.

It may seem obvious but bears mentioning that higher doses of minoxidil lead to greater levels in the blood and the potential for greater side effects. One needs to simply monitor side effects with any dose increase. The potential for side effects for those using 1 mg is greater than 0.5 mg. The chance of side effects for those using 5 mg is greater than 2.5 mg.

10. In addition to the scalp, hair growth on the body occurs in fairly predictable areas if it is to occur.

The eyebrows, hairline, temples, areas under the eyes (malar areas), back of the arms and shoulders are areas outside of the scalp which are most likely to be affected by oral minoxidil use.

About 15-20 % of women using oral minoxidil will experience an increase in body hair including hair on the face. Many users will chose to still continue the minoxidil because they are pleased with its effects on the scalp and remove the excess hair with various means (laser, electrolysis).


Oral minoxidil can be a very helpful second line treatment for many conditions. One must be aware to risks and benefits of this medication and how the risks and potential for side effects change with different doses. IN addition, one needs to be aware to how to monitor patients using oral minoxidil.



[2] Novak et al. Topically applied minoxidil in baldness. Int J Dermatol. 1985 Mar;24(2):82-7.

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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Frontal Fibrosing Alopecia: What are the treatments?

What are the treatments for frontal fibrosing alopecia?

Frontal fibrosing alopecia (FFA) is scarring alopecia that mainly affects women. Hair loss often begins in the eyebrows or in the frontal hairline - or both. The precise cause is unknown although hormone-related and immune-related mechanisms are felt to be involved. A variety of treatments are available to stop the disease although treatments are not effective in everyone. Sometimes regrowth to a slight degree of even marked degree can occur. However, the main goal of treatment of all scarring alopecias is to stop them from getting worse.


The Early Stages of FFA

Do I have Frontal Fibrosing Alopecia?

Inflammation in Frontal Fibrosing Alopecia

Baby Hairs in Frontal Fibrosing Alopecia

Frontal Fibrosing Alopecia: How long until treatments start helping?

FFA vs LPP: Which is often quieter in its appearance?

Scaling around Hairs in Frontal Fibrosing Alopecia

What treatments have good evidence of helping?

The treatments with the best evidence for helping FFA are the antiandrogens (finasteride/dutasteride) and the retinoids (isotretinoin). Other oral agents like doxycycline, hydroxychloroquine (Plaquenil) and methotrexate also are helpful although likely not quite to the same degree as the retinoids and antiandrogens.

Topical calcineurin inhibitors (tacrolimus, pimecrolimus) do appear more helpful than topical steroids based on a limited number of published studies. Topical antiandrogens likely help somewhat as well but require more study. Low level laser also needs more study but may have a role too. Steroid injections with triamcinolone acetonide help some patients (not all) and are typically performed every 2-3 months.


What treatments must we be very careful of?

Treatments like platelet rich plasma (PRP) are popular but have absolutely no solid evidence of being helpful in FFA. Hair transplants are an option if the disease has been completely quiet for 2 years (without medication) and the patient has proven that no hair loss has occurred in that 2 year waiting period. Otherwise hair transplants are not a good idea and can be a disaster leading to more hair loss.

Donovan Criteria for Hair Transplantation in FFA

Most hair supplements have limited benefit for FFA and can not be routinely recommended at this time.

The exact treatment I recommend depends on many patient factors. In general, I often start with a combination of topical steroids+ topical calcineurin inhibitors (pimecrolimus) + steroid injections + one systemic agent (pills). There is no standard template as it depends on patient factors. For example, a patient with a history of severe depression or personal history of breast cancer might not be started on finasteride.

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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How rare are scarring alopecias?

Scarring Alopecias: More Common than Realized

Five leaf clovers, like scarring alopecias, are probably alot more common than people realize.

Five leaf clovers, like scarring alopecias, are probably alot more common than people realize.

Five leaf clovers are much more common than people realize. It’s just that people don’t always think about it when looking in a patch of clovers or if they are on the lookout for it, they don’t quite have the skills that allow them to be spotted.

Scarring alopecias are also much more common than clinicians realize. It’s just that clinicians don’t always think about it when looking at the scalp or .... if they are on the lookout for it, they don’t quite have the skills that allow these conditions to be spotted.

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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Some Hair Loss Conditions Look Alike - but that not mean they can not be distinguished

Look-alike does not mean alike

I’m often asked how it’s possible to distinguish different hair loss conditions if sometimes they can look so similar. How can we distinguish a challenging case of seborrheic dermatitis from lichen planopilaris? How can we be sure that a patient who is concerned about hair shedding has early androgenetic alopecia not telogen effluvium?

The answer is to dig deeper and get more clues if one is not sure. Few detectives solve a complex mystery by sitting at the coffee shop. They get out on the scene and gather necessary clues. If the detective is not sure, they ask more questions, examine things closer or in more detail …. or perform more tests.

The same is true with hair medicine. We need to ask good questions that direct us in the right direction. We need to perform a careful scalp examination (including trichoscopy). We also have available a plethora of tests that we can use if we need to. These include blood tests, biopsies, swabs, pull tests, trichograms, and hair collections. When put to use at the right time and interpretted correctly - these tests also provide important information. A good doctor puts all the pieces together.

It’s true that some hair loss conditions can look similar. But that is far from needing to express frustration that we simply can’t tell them apart. In cases of frustration, I tell my trainees “Be an expert!” A golden retriever dog can look like a yellow lab dog but an expert can easily tell them apart. A wine expert can easily distinguish a Chardonnay from a Riesling, Pinot Grigio or Pinot Blanc. There are lots of things that seem alike but people who understand the subject can tell them apart. A knowledgeable hair expert can sort through challenging hair loss diagnoses.

Many hair loss conditions can look similar. Yes, this is true! If one is not sure, they ask more questions, examine things closer or in more detail …. or perform more tests. Few detectives solve a complex mystery by sitting at the coffee shop and few hair specialists can solve complex cases by sitting back in the office chair.

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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Inflammation and Scarring Alopecia: If I get rid of my inflammation, will hair loss stop?

Do scarring alopecias halt once inflammation disappears?

Many of the so called ‘primary scarring alopecias’ are associated with inflammation under the scalp. Conditions like lichen planopilaris, frontal fibrosing alopecia, discoid lupus, central centrifugal cicatricial alopecia, pseudopelade, folliculitis decalvans are all associated with inflammation.

This inflammation is present both histologically (under the microscope) and clinically (we see it on the surface of the scalp). The clinical disappearance of inflammation is always a good sign. The disappearance or reduction of redness, scaling, pustules, are all good signs that inflammation is going away and that treatments are helping.

Reduction of inflammation in necessary but not always sufficient to stop the disease.

The first step in treating scarring alopecia is to get rid of these signs of inflammation. It’s where we start as goal number 1. We try to get rid of the inflammation and see if the hair loss will stop. However, we need to keep in mind that sometimes even when the scalp returns back to quite a normal in appearance (minus the permanent scarring), it’s possible for the disease to still continue.

Fortunately for everyone - this is not the normal scenario.

The normal and typical scenario is for the disease to halt once inflammation disappears. However, there are situations where we stop the inflammation quite well but the hair loss grumbles onwards. There are several things that must be considered when this happens.

Consideration 1: Inflammation is still present under the scalp

Sometimes in situations where clinically the disease seems pretty quiet or inactive, the patient still experiences hair loss. Granted hair loss in this scenario is usually quite slow if it occurs at all. But sometimes there is inflammation going on under the scalp at varying degrees that could, at least theoretically, be driving further hair loss. We don’t in the present day and age have a way of picking out an inflammatory cell from the scalp and asking it whether it is responsible for hair loss or not. That’s simply not possible. But we do have situations where there is a tiny bit of inflammation present and the patient has not lost a strand of hair in years and another situation where the same amount of tiny bits of inflammation are present in the scalp and the patient is still losing hair. Why these differences occur is still a mystery.

Consideration 2: Other non-inflammation based mechanisms are operative

Inflammation seems to be at the center of the mechanisms that operate in scarring alopecia. However, we need to be humble to the fact that that we really understand very little about these diseases (despite our feeling that we are getting closer). There are likely a variety of mechanisms that contribute to the progressive depletion of stem cells in scarring alopecias. Some of these may be dependent on inflammation and some others might not be.


In the present day, clinicians treating scarring alopecia must have as their goal number 1 the removal of inflammation from the scalp. We need to help the patient stop their itching. We need to help them stop their burning and tenderness. We need to get rid of redness from the scalp and get rid of scaling and pustules. Fortunately when we achieve all this - we stop the scarring alopecia disease. But we don’t always. Tiny bits of inflammation under the scalp can still drive progression of scarring alopecias in some cases. In addition, there may be a variety of cytokine, chemokine, and endocrine changes that drive stem cell depletion even in the absence of gross inflammation.

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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Are Sunscreen Chemicals absorbed into the Blood?

Sunscreens, Sunscreen Chemical and Systemic Absorption

If you work in the field of hair loss, particularly in the field of scarring alopecia, you have been required to learn a thing or two about sunscreens in the last few years. This is because a few studies have suggested (but not definitively proven by any means) that sunscreen use may have some type of link to the scarring alopecia known as frontal fibrosing alopecia. The precise link is still not really known but a few research groups have suggested that women with FFA wear more sunscreens and facial moisturizers “on average” than women in the general population. Some have even proposed that it could be tiny so called “nano particles” of physical blocking ingredients like zinc or titanium dioxide that plug up the hair follicle and incite and immune reaction. The reality is that we really don’t know if there is a link or what the mechanism would be if there was a link. A recent study suggested that women with severe FFA use sunscreens just as frequently as women with mild FFA which raises some doubt about the whole connection. What I’m referring to here is a study by Moreno-Arrones et al which showed that 70-80 % of patients with FFA used facial sunscreens. However, there was no difference between those with severe disease and those with mild disease in terms of use of these products.


Sunscreens and FFA: What do we know so far?

Is sunscreen use more common in women with FFA?

Sunscreen use in males with FFA: What do we know?

New study on sunscreen absorption into the blood

A new 2019 study has not only provided us all with a good reminder that things that we put on our skin have the potential to get absorbed into the blood but have also triggered the US Food and Drug Agency to demand further toxicology testing of sunscreen ingredient from manufacturers.

The study was a randomized study of 24 patients (12 men and 12 women) who applied sunscreens 4 times a day to 75 % of their body surface area for four days. 6 patients use a lotion, 6 used a cream, 6 used a spray and 6 used a second type of sunscreen spray. These sunscreens contained ingredients avobezone, oxybenzone, octocrylene, and ecamsule. The sunscreen was applied at the current recommend amount - namely 2 mg per cm2. The study researchers collected 30 blood samples from study subjects not only for the 4 days that the sunscreen was applied but also 3 additional days as well. The study was conducted indoors in a somewhat artificial setting without exposure to heat, sunlight, or moisture.

What were the main results of the study?

Matta and colleagues found that after 4 applications on day 1, 23 of 24  subjects had systemic concentrations greater than 0.5 ng/mL for all active ingredients in the formulation applied. This concentration is important because 0.5 ng/mL is the so called “Threshold of Toxicological Concern (TTC)” that the FDA adopted to approximate the highest plasma level below which the carcinogenic risk of any unknown compound would be less than 1 in 100,000 after a single dose. The average levels of avobenzone was 4.0 and 3.4 ng/mL in the 2 sunscreen sprays studied, 4.3 ng/mL in the lotion. Interestingly, the avobenzone concentration in the blood in those using the cream was lower at 1.8 ng/mL.

The numbers for the other sunscreen ingredients were also higher than the 0.5 ng/mL cut off. For oxybenzone, the corresponding values were 209.6 ng/mL for spray 1, 194.9 ng/mL for spray 2, and 169.3 ng/mL for lotion. The the ingredient octocrylene, the concentrations were 2.9 ng/mL for spray 1, 7.8 ng/mL for spray 2, 5.7 ng/mL for lotion, and 5.7 ng/mL for the cream cream. Finally for ecamsule, the systemic concentration was 1.5 ng/mL for the one product that contained it (cream).

The researched showed that the blood levels above this “0.5 ng/mL” level were reached quickly: within 6 hours after the first application of avobenzone, 2 hours after application of oxybenzone, and 6 hours after application of octocrylene. In addition, there was evidence that these drugs accumulated in the blood after more and more exposure.


I actively follow the sunscreen research field because it may (or may not) be related to at least some of the hair conditions I treat. The links to the hair loss are still not clear and so this makes it even more important to dive in an understand what these products do and don’t do in the body and to the body. What was really interesting to me about this study was that it was actually created because the FDA could not get sunscreen manufacturing companies to provide good toxicology data. Some have even suggested that the fact the the FDA did the testing indicates that the FDA has some amount of concern for the paucity of good data on safety. One should be aware that the FDA does not normally do testing - it is mainly a regulatory agency.

The authors of the present study did not conclude that we should not be using sunscreen - only that more safety type studies are needed. Sunscreen clearly reduce the risk of us developing certain types of skin cancers and reduce our risk of photoaging and burns.

There are many important questions that need to be considered when thinking about the role of sunscreens in hair loss medicine. First, sunscreen block ultraviolet radiation which is naturally immunosuppressive to the skin. When this in turn affects inflammation in the skin and hair in patients with inflammatory hair loss disorders is not known. In addition, we must keep in mind that animal studies have raised concerns that chemicals like oxybenzone might disrupt normal hormone patterns in humans. More study is needed to understand the effects in humans. It’s important to emphasize again and again that the precise link (or lack of a link) of sunscreens to hair loss issues (like frontal fibrosing alopecia) is still not known.

We’ll be hearing a whole lot more about safety and toxicology data of sunscreens as the FDA has given sunscreen manufacturers a deadline of November 2019 to provide them with safety data. This includes data on how they are absorbed, the risk of cancers, risks to reproductive health. This is a reminder to us that really solid human safety data on sunscreen use by humans is lacking. Hopefully the new data coming soon will clarify things.


Matta et al. Effect of Sunscreen Application Under Maximal Use Conditions on Plasma Concentration of Sunscreen Active Ingredients. A Randomized Clinical Trial. JAMA. 2019;321(21):2082-2091. doi:10.1001/jama.2019.5586

Moreno-Arrones OM et al. Factors influencing frontal fibrosing alopecia severity: a multicentre cross-sectional study.J Eur Acad Dermatol Venereol. 2019 Mar 21. doi: 10.1111/jdv.15590.

Califf RM, Shinkai K. Filling in the Evidence About Sunscreen. JAMA. 2019 May 6. doi: 10.1001/jama.2019.5528.

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 get my hair back?

Can I grow my hair back or not?

Many patients want to know if they can grow back their hair if they decide to start a treatment plan. Certainly patients can grow back hair sometimes but growing back hair may or may not be the goal of treatment. I’ve given examples here of three hair loss conditions with very different treatment goals. It’s absolutely essential that patients understand whether they are realistically aiming for compete regrowth or not.

1. Scarring Alopecia - What are the goals of treatment?

For patients with scarring alopecia, the goal of successful treatment is mainly to STOP further loss. While we can occasionally get regrowth when treating scarring alopecia, the main goal is to stop the disease. If the patient has the same hair density after one year of treatment, it means some aspect of the treatment is helping.

Hair regrowth may not be a goal of treatment of scarring alopecia.

Hair regrowth may not be a goal of treatment of scarring alopecia.

2. Androgenetic Alopecia - What are the goals of treatment?

For androgenetic alopecia (AGA), we certainly want to try to get back some amount of regrowth. But it’s important for patients to understand that we rarely reverse the condition fully. It’s wonderful when we can get significant improvement but sometimes we need to accept that we can only stop it from getting worse. While there is a much higher chance of getting regrowth in AGA than scarring alopecia, there are many patients that don’t achieve regrowth but do find that treatment is preventing the hair density from getting any worse.


3. Alopecia areata - What are the goals of treatment?

For alopecia areata, our hope is to get regrowth and often the goal is complete regrowth. From the very beginning, we are trying to design a treatment plan that we regrow the hair completely. In fact, if the patient does not experience regrowth, the clinician usually considers changing the treatment plan.


4. Telogen Effluvium - What are the goals of treatment?

Telogen effluvium refers to excessive hair shedding. A variety of triggers can cause hair shedding including low iron, thyroid disease, weight loss, surgery, medications and diets. For patients with telogen effluvium, the goal of successful treatment is to figure out exactly what caused the shedding (ie determine the trigger) and then fix or remedy things to correct whatever it was that set off the shedding in the first place. If the telogen effluvium was due to weigth loss, the only real way to correct the telogen effluvium is to maintain a steady healthy . The goal of treating a telogen effluvium is to get the density back.



In summary, patients with hair loss should ideally know if their hair loss condition is associated with high chances for regrowth or whether the main goal is to simply stop it from getting worse. Hair loss conditions like alopecia areata and telogen effluvium are associated with high changes of regrowth, conditions like androgenetic alopecia are associated with moderate chances. For those with scarring alopecia, chances of regrowth are much lower and the main goal is to stop the condition from getting worse.

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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Burnt out vs Stable/Inactive LPP: Not Quite the Same

What’s the difference between stable or inactive LPP and burnt out disease?

Lichen planopilaris is a type of scarring alopecia that is associated with redness, itching and burning in the scalp as well as ongoing hair loss. Treatments can help stop symptoms and signs of the disease and may help stop ongoing hair loss as well. Once the disease comes under control, physicians often use terms such as “inactive” and “burnt out.” Let’s take a closer look at these terms and what exactly they mean. They are often used incorrectly - so it’s important to get a good sense of what they really mean. The following table helps clarify some of these points.


What is inactive or stable LPP?

Inactive LPP and stable LPP refer to LPP that is not removing hair from the scalp. In my clinic, stable and inactive LPP are quite similar - although what constitutes inactive LPP is much stricter in definition than what constitutes stable LPP. As shown in the table, a patient with stable LPP or inactive LPP both have had no change in density over a fairly long period of observation. However, patients with stable LPP still may have a bit of redness or scaling in the scalp and may even have occassional symptoms. For patients with inactive LPP, redness and scaling and symptoms are uncommon.

Inactive LPP can potentially become active (although chances are low) and stable can potentially becomes unstable but for now they are not. LPP may be rendered inactive or stable from treatment or on it’s own. It is absolutely possible for inflammation to be present clinically and/or histologically and yet the patient’s density remain the same. Of course, that would not be the norm but it’s an important point that one would be making a mistake if they prescribe more and more drugs simply based on seeing inflammation on the scalp or under the microscope. The most important finding is whether hair density is changing and what sort of symptoms are remaining. There are occasional patients who maintain redness and even a bit of scale but yet do not have any significant loss of density over 5-10 years of follow up. Granted this is not the norm but it’s a good point to keep in mind that we really ought to be making decisions on LPP treatment based on changes in density first followed by clinical features second. They are both important but nothing more important than a photo.

What is burnt out LPP?

Now we come to the important point regarding what truly constitutes “burnt out” LPP. For this, we do need a much stricter definition. First and foremost, a patient with burnt out LPP is not on treatment. Absence of clinical features of inflammation must also be noted in order to say LPP is burnt out including absence of symptoms of itching and burning and absence of clinical signs of redness and scaling.

I think alot of patients and physicians go wrong with definitions of inactive vs burnt out. LPP can be stable or inactive with the patient having no change in hair density but not be burnt out. Burnt out means 1) no signs of inflammation and 2) no change in density a long period of follow up. LPP that is stable, even after 10 years of follow up, but not truly burnt out has a much much higher chance of flaring in the future. This is especially true when it comes to discussing issues such as hair transplant surgery. Inactive and stable LPP has a much higher likelihood of flaring and reactivating with hair transplant surgery compared to LPP that is truly burnt out.

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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Increased Shedding of Hair without Appreciable Loss of Density (ISHWALD PHENOMENON)

Can one have increased shedding without a change in pony tail diameter or density?

Hair loss is a normal part of being human. Everyday between 30-120 hairs are lost from the scalp. Hair shedding can certainly be much higher on a wash day. I’m often asked if it’s possible to have increased shedding without really having a change in the density of the hair. For example, the patient says “I’m losing more hair on a daily basis than I used to… but I feel my density looks just the same.” What could be going on?


Increased Shedding of Hair without Appreciable Loss of Density (ISHWALD Phenomenon)

Most people are experts in themselves. After all, few people really know a patient’s hair better than the patient themselves. When a patient notices that their rate of shedding is higher than normal, they are usually correct. Most people who have increased shedding feel that they’ve lost density too. They feel some part of the scalp is just not as thick as it once was. We see shedding PLUS a change in hair density in lots of different conditions such as telogen effluvium, androgenetic alopecia. lichen planopilaris, lupus, marked seborrheic dermatitis, and many others too.

But what about when someone has increased shedding but they are NOT seeing any change in their density. More hair is coming out but they hair looks just a good as it always did. This is an important exercise for hair experts to work through! When I teach doctors about hair loss, we often work through examples of why I have come to call the ISHWALD Phenomenon - or “Increased Shedding of Hair without Appreciable Loss of Density.”


1) A Very Mild Acute Telogen Effluvium

Some people can have a mild acute telogen effluvium (acute TE) that does not really lead to much in the way of a noticeable change in density. These are usually individuals that have NO OTHER hair loss condition going on - especially no evidence of androgenetic alopecia. They start out with 100,000-120,000 hairs on the scalp and shed out a bit but still have 90,000-100,000 hairs remaining. Usually one can’t tell the difference between 90,000 and 100,000 hairs especially if the hair is on the thicker side or curly (or both). Individuals with fine hair might be more apt to notice a change. But a patients with healthy hair with a bit of a seasonal shedding, or a bit of a shed from stress or low iron might notice increased shedding of hair without much in the way of a change in hair density.

2) Early and Slowly Progressive Androgenetic Alopecia

The very earliest stages of androgenetic alopecia may be associated with increased daily hair shedding. There may be months that go by where all the patient notices is increased shedding but the hair still looks quite dense. It’s only one day down the road that the patient comes out of the shower or stands under a bright light and says - “Oh my, I think my hair is getting thinner.” This type of phenomenon is more likely to occur in patients with a form of genetic hair loss that is very slow in progressive. Often this is a woman 35-50 with later onset AGA.

3) Mild Seborrheic Dermatitis (SD)

Dandruff and seborrheic dermatitis are closely related. They are inflammatory conditions that are common. 5-10 % of the world has seborrheic dermatitis and up to 50 % have dandruff at some point. Seborrheic dermatitis may give a bit more shedding in some people although it usually goes completely unnoticed. Seborrheic dermatitis may be associated with increased greasiness of hair. Some patients with mild SD find they are shedding more. If the SD is mild and there are no other conditions going on (like androgenetic alopecia or other forms of acute TE), they may find their density is maintained at quite a high level.

4) Chronic Telogen Effluvium (CTE)

Chronic telogen effluvium is a very special condition that typically happens in women 35-60. Affected patients with CTE often start out with extremely thick hair and then suddenly develop high rates of hair shedding. Surprisingly, the density may decrease a bit (or alot at first) but they remains the same for year after year after year. Patients are often shocked that they could possibly have any hair left on the scalp when they have so much shedding. This is CTE. Some patients just don’t appreciate the initial drop in density to realize that their density has in fact been reduced compared to the past. But the main point is that these patients maintain the same density year and year after years despite massive amounts of shedding. CTE is said to be a hair shedding condition not a hair loss condition per se.

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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Dr. Donovan - Interview with The Alopecia Project Podcast

Podcast Interview with The Alopecia Project

The Alopecia Project is an extremely informative podcast about what living with alopecia areata is all about. Started in 2018, the monthly podcast is headed towards finding a place among the podcasts of the world that truly make a difference for people.

Sarah and Sarah, the podcast hosts, do an absolutely amazing job navigating tough subjects and tough questions. What’s so unique about this podcast is how they get to the core of what alopecia is about. I’m so glad to know there’s people who care enough to create resources like this.

The podcasts of the first season dealt with many topics including how one navigates alopecia in both the workplace and personal spheres. Dating, friendships, family and the co-worker - the Alopecia Project takes on deep and meaningful discussions that you simply won’t find anywhere quite like this. The second season begins the many considerations that go into buying a wig. The season continues with topics that include having alopecia areata as a man and how patients with alopecia areata can best care for their mental health.

The Alopecia Project is a must listen to podcast for patients, families, spouses, partners hairdressers, trichologists, physicians and all those who are in any way affected by alopecia areata. Certainly, many of the topics that are discussed in the podcast are helpful for a variety of types of hair loss - but this podcast is focused on the autoimmune immune condition alopecia areata.

I was honoured to be a part of the July episode.

Interested listeners can listen to the podcast interview in apple podcasts or soundcloud - under “The Alopecia Project”


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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Health Canada and PRP Procedures:

Some PRP Procedures for Hair Loss Still Okay in Canada

It’s been a busy last two months as Health Canada cracks down on clinics offering unproven stem cell treatments. This unfortunately has lead to a great deal of confusion and we’ve received many emails and calls too.

I was happy to see Friday that Health Canada clarified position on platelet rich plasma treatment stating they are "not the same as cell therapies and, as a result, are not subject to Health Canada’s Policy Position Paper on Autologous Cell Therapy Products."

Health Canada Gives Canadian Physicians Green Light To Purse PRP

What’s not allowed?

I think it’s important for the public to be aware that not all PRP is allowed in Canada. For example, PRP with adipose derived stem cells is still banned - and no physician in Canada may perform liposuction to obtain stem cells and add these two the PRP for treatment of hair loss. Also, many other ‘stem cell’ sounding treatments for hair loss may be banned to. The public should check with Health Canada is any uncertainty exists. The goal of the Health Canada crackdown is to halt unproven therapies.

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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New Data in One of the Largest FFA Studies to Date

New Study of 490 Patients Shows Interesting Information about Frontal Fibrosing Alopecia (FFA)

Researchers from France and Germany performed an observational, cross-sectional study to identify demographic and health characteristics associated with the severity of FFA. In total they analyzed data from 490 patients with FFA, of which 95 % were female and 84 % were post menopausal. I was interested to read this paper as it represents one of the largest studies to date.

The main findings that intriqued me were the following

1. There was  a high incidence of thyroid disease in women with FFA. Specifically 35 % of women reported thyroid diasese which 9 times higher than the general population.

2. Cholesterol levels were the same as the general population. I’m continually wondering about the degree fo metabolic dysfunction in patients and this was interesting to see. 47 % of patients with FFA had lipid abnormalities but this was not really higher than the general population.

3. Nail lichen planus was rare. We know that for scalp lichen planopilaris (LPP), the incidence of nail disease is reported to be fairly high. It was interesting to note that frequency of nail disease in patients with FFA in this study was acutally quite low

4. Mucosal lichen planus was also uncommon in FFA patients. Similar to nail LP, mucosal LP (oral and vaginal) was quite low as well. In this study on 4 % of patients had mucocal LP.

5. The use of facial moisturizers did not seem to be associated with worse disease. In this study,  the majority of patients reported regular use of a facial moisturizer (98% of women and 73% of men) and a facial sunscreen (55% of men and 68% of women). In this study  the regular use of hair colorants and hairspray was asosicated with lower disease activity (LPPAI values). The jury is still out as to whether or not these cosmetic products really cause problems

 6. The hormonal status of most FFA patients was mostly normal. When abnormal estrogen levels were found it was associated with abnormal testosterone values suggesting these two go together somehow. Interestingly, the authors reported that abnormal estrogen and testosterone values were strongly associated with lesser disease activity.

7. In this particular study, the authors found that the incidence of rosacea in FFA patients was less common than the general population. This finding goes against previous studies.  It seems we don’t have a clear handle on this information quite yet.



Kanti et al. Frontal fibrosing alopecia: demographic and clinical characteristics of 490 cases.
J Eur Acad Dermatol Venereol. 2019 Jun 9. doi: 10.1111/jdv.15735. [Epub ahead of print]



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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Frontal Fibrosing Alopecia: Top Five Factors Associated with Severe Disease

Top Five Factors Associated with Severe Disease in FFA

A nice study was recently published by O.M. Moreno-Arrones and colleagues looking at the risk factors for severe disease in patients with frontal fibrosing alopecia (FFA). I found that this study had a number of interesting findings. 

First, the 2/3 of  patients in their study had mild disease and 1/3 had severe disease. This is a nice reminder for us all that it’s really not an insignicant number who present to the clinic with severe disease. Second, the authors did a really nice job comparing variables associated with having SEVERE disease with variables associated with having MILD disease. There were five main factors that stood out as being associated with severe disease:

1. Age of patient (older age associated with more severe disease)

2. Age when diagnosed (older age at diagnosis associated with more severe disease)

3. Years they have had the disease (longer duration associated with more severe disease)

4. BMI (higher body mass associated with more severe disease)

5. Lower academic level

Several factors are thought to be associated with more severe disease in patients with frontal fibrosing alopecia.

Several factors are thought to be associated with more severe disease in patients with frontal fibrosing alopecia.


Third, I was interested to see that 70-80 % of patients used facial sunscreens and about 90 % used facial moisturizers. However, there was no difference between those with severe disease and those with mild disease in terms of use of these products. One of the current hypotheses is that facial moisturizer and sunscreen ingredients are important triggers of FFA.

Fourth, it’s very clear that FFA is a hormonal disease and this study supports this notion as well. A proportion of women with FFA have early menopause and some have histories of hysterectomies. Body mass stands out as also being somewhat of a risk factor – women with higher body mass were found to have more severe disease. The significance of this is not clear but certainly one wonders what exactly the significance of this is given that higher body mass if often associated with higher estrogen levels (and lower estrogen is proposed to have some relevance).  Clearly we have more to learn!


Moreno-Arrones OM et al. Factors influencing frontal fibrosing alopecia severity: a multicentre cross-sectional study.J Eur Acad Dermatol Venereol. 2019 Mar 21. doi: 10.1111/jdv.15590.

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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Susncreens and FFA: What do we really know so far?

Sunscreens and Frontal Fibrosing Alopecia (FFA): What do we really know so far?

The 2016 publication by Dr Messenger’s group that the incidence of sunscreen use in FFA was greater than that of patient witouth FFA has lead to a marked increase in research in this area. Some studies have suggested that susncreens and facial moisturizers are somehow related to the disease. Other studies have suggested they are not. 

The interest in facial products as a culptrit in FFA is very much a part of active study. Allergy testing (Patch testing) in patients with FFA shows a high prevalence of sensitization to cosmetic ingredients but not to a specific culprit. This suggests that patient with FFA could potentially be using more cosmetic products than the general population. 

The 2019 Cranwell and Sinclair Study

Cranwell and Sinclair published an intriguing study in 2019 of a patient who reported improvement in her FFA after stopping sunscreen use. Many potential explanations can be given - and we do not know really which is correct.

At the preset time, titanium dioxide sits on the top of the list as ingredients that may be causing problems in FFA. The data is by no means crystal clear and more studies are needed. It is important to understand that titanium dioxide is often added to susncreens and facial products because it has very desirable properties such as being a thickening agent, being a a pigment and being a sunscreen.  

 What you may not be aware is that titanium dioxide has significant ‘photocatalytic activity’ when it is exposed to UV irradiation. It’s certainly possible, but not yet fully proven that when ultraviolet radiation hits the skin of someone wearing a titanium dioxide containing sunscreen that there is some sort of tissue damage. Whether patients with FFA are more predisposed to tissue damage compared to someone who does not have FFA is really not clear. Most of us don’t come home after a period of being out in the sun with concerns that we’ve had tissue damage from wearing our sunscreens. Clearly we’re in the earliest stages of understanding what this all means. In most modern cosmetics, these zinc and titanium dioxide particles are actually coated ot make them less reactive. The cosmetics industry is very much aware of these properties of titanium and zinc.

Nowadays, many cosmetic products consist of very tiny particles (called nanoparticles) of titanium and zinc dioxide. They are in fact so small some are only 40 nm in size. It has been proposed that with such as small size it is possible for these product to enter skin and hair cells.

Recent studies have shown that our hairs do have titanium dioxide in them. A recent study by Thompson and colleagues tested hair shafts from 16 women with biopsy-proven FFA using scanning electron microscopy with energy-dispesive X-ray spectroscopy (SEM/EDX). Each of the study subjects had a hair plucked form the hairline and the content was analyzed. Interestingly, titanium was identified in all 16 hair shafts. But three control patients who did NOT have FFA were also found to have hair shafts continaing titatium dioxicde. This data does not prove that titanium is involved and shows that the relationship is far more complex. 

Why would sunscreens be involved?

It’s not clear how sunscreens would be involved in FFA. One possibility that has been raised is that this tiny titaniusm dioxide penetrates down to the isthmus (upper part of the hair follicle) and then trigger a lichenoid reaction. Another possibility is that these sunscreens block out the anti-inflammatory benefits effects of sunlight (Yes, sunlight can be anti-inflammatory).



1) Aldoori N, Dobson K, Holden CR et al. Frontal fibrosing alopecia: possible association with leave-on facial skin care products and sun- screens; a questionnaire study. Br J Dermatol 2016; 175:762–7. 

2) Cranwell WC and Sinclair R. Frontal fibrosing alopecia: regrowth fol- lowing cessation of sunscreen on the forehead. Australas J Dermatol 2019; 60:60–1. 

3) Debroy Kidambi A, Dobson K, Holmes S et al. Frontal fibrosing alopecia in men: an association with facial moisturizers and sun- screens. Br J Dermatol 2017; 177:260–1. 

4) Moreno-Arrones OM, Saceda-Corralo D, Rodrigues-Barata AR et al. Risk factors associated with frontal fibrosing alopecia: a multicentre case–control study. Clin Exp Dermatol 2019; 1111/ced.13785. 

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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Buckwheat and Millet Groats: Could they have a role in Frontal Fibrosing Alopecia (FFA) ?

What’s the role of diet in Frontal Fibrosing Alopecia (FFA)?

The search is well underway to find triggers that might be responsible for the epidemic of frontal fibrosing alopecia (FFA). For those not aware of this condition, it is an inflammatory hair loss condition that largely affects women 45-60. Other age groups and men, are rarely affected as well. It causes hair loss along the frontal hairline, eyebrows, eyelashes and body hair. Facial papules (bumps on the face) are also a part of the condition.

Recent studies had suggested a few triggers that might be relevant. The most popular of these are sunscreens although more research is desperately needed. Not all studies have supported a clear role for sunscreens.

Buckwheat and Millet Groats: A Role in FFA?

Rudnika and Rakowska set out to examine the role of dietary factors in FFA. They performed a pilot study to identify the dietary practices in 59 consecutive women with FFA and 59 age‐matched healthy controls. There were no other statistically significant differences between patients and healthy individuals in regard to other dietary practices like eating meat, fish, vegetables, fruits and drinking coffee or alcohol.

Interestingly, 81 % of patients with FFA declared consumption of buckwheat at least twice weekly in the recent 3 months compared to 22 % of women who did not have FFA. Similarly , 81.4 % of patients with FFA reported consumption of millet groats compared to 8.4 % of indivdiuals who did not have FFA. The differences were statistically significant (P < 0.01).


This is an interesting study. These sorts of dietary studies are always open to scrutiny as there are methodological challenges in such small studies. Nevertheless, it’s an interesting study and no doubt will help fuel further studies of dietary practices in FFA and other scarring alopecia.


Rudnicka and Rakowska. The increasing incidence of frontal fibrosing alopecia. In search of triggering factors.J Eur Acad Dermatol Venereol. 2017 Oct;31(10):1579-1580. doi: 10.1111/jdv.14582.

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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Hydroxychloroquine (Plaquenil) and Cancer: Is there an increased risk?

No Clear Increased Risk of Cancer with Hydroxychloroquine

Hydroxychloroquine (Plaquenil and generics) is an immune modulating medication frequently used in treating a variety of immune-mediated diseases. In hair loss, we use this medication for treating lichen planopilaris, lupus, discoid lupus, frontal fibrosing alopecia and pseudopelade.

Concerns about cancer are always important with drugs that affect the immune system. Surprisingly, most larger scale epidemiologic studies of hydroxychloroquine have not shown an increased risk of cancer in patients using these drugs.

Current data would suggest there is no increased risk of cancer with hydroxychloroquine

Current data would suggest there is no increased risk of cancer with hydroxychloroquine

Studies by Fardet and colleagues in 2017 found that the use of hydroxychloroquine was not associated with an increased cancer risk. The authors even proposed the users of hydroxychloroquine may have a reduced risk of metastatic cancer. Other studies including recent studies by Mao and colleagues in 2018 did not show any increased cancer risk among hydroxychloroquine users.

Continued studies are needed - especially as they pertain to certain groups. For example the risk of cancer in a patient with systemic lupus or rheumatoid arthritis may be quite different than those with lichen planopilaris or frontal fibrosing aloepcia. Studies in animals have suggested that these drugs may have anti-cancer effects for some types of cancers. Although there is ongoing interest as to whether these drugs could actually reduce the risk of some cancers- to date, this has not been seen in bigger studies. Overall, compared to immunosuppressives like methotrexate, hydroxychloroquine seems to have a lower cancer risk and this fact is important to keep in mind when treating patients at high risk for cancer.


Fordet et al. Clin Epidemiol 2017
Mao et al. Ther Clin Risk Manag 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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