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End Of Day Scalp Symptoms: EODSS

EODSS

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Scalp symptoms are common in everyday life. In addition to itching, a variety of symptoms are possible including burning, tenderness, pain, pins and needles, etc. Some patients find that symptoms seem to correlate with hair loss whereas some patients have concerns only about the symptoms and are not experiencing hair loss.

For some patients, symptoms are rare and occur every few months. For others, symptoms are present each and every day. Some patients wake up with symptoms whereas others ding their scalp feels fairly normal in the morning but worsens towards the end of the day. I refer to the second situation as “end of day scalp symptoms” (i.e. EODSS). There are millions of nerves on the scalp and these nerves all secrete chemical and respond to chemicals that come into the scalp from the blood stream and chemicals that are produced within the scalp itself. Some of these chemicals are part of the normal physiology of the scalp and some of these chemical are increased during states of inflammation, stress, or infection. All of these chemical have the potential to worsen scalp symptoms.

The exact reasons for EODSS is not clear but there are likely many reasons. The concentrations of dozens and dozens of different hormones, neurotransmitters and cytokines change from morning to bedtime. These all have the potential to impact the way our scalp feels. Cortisol and testosterone levels are high in the morning and drop in the afternoon. Melatonin levels increase in the evening. Even ‘core’ body temperature changes through the day - being lowest at 6 am and then peaking at round 6 pm to 9 pm. These changes all affect the events in the scalp.

EODSS are poorly researched and poorly studied. EODSS are not specific but may be more likely associated with certain conditions than others. A proportion of patients with inflammatory scalp disease in particular report EODSS. These include seborrheic dermatitis, psoriasis, scarring alopecia, scalp rosacea, burning scalp syndrome, and sensitive scalp syndrome. Some patients with depression and anxiety and some with shedding disorders also report EODSS.


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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PRP, Concentration and Volume: Analogy of Coffee vs Expresso

Analogy of Coffee vs Expresso

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I came across an interesting question today whereby a patient wanted to know specifically how much volume (in millilitres) of PRP various clinics used. As I’ll point out here, the question fails to take into account some of the finer details of the PRP procedure. To the hair follicle, volume does not matter as much as CONCENTRATION. What probably matters the most is the number of mL of HIGHLY CONCENTRATED PRP the clinic uses.

To explain the concepts of PRP volume and PRP concentration to patients and physicians, I generally use the analogy of Harry and Sam. 
Meet Sam. Sam works a busy job. Sam is feeling tired and thinks that some caffeine might help him feel more energized and so visits his local coffee shop. Sam is presented with two options for his beverage- a strong 60 mL (2 oz) espresso or a 350 mL (12 oz) large volume coffee/Americano. While making his decision Sam is advised that whichever beverage he chooses he is only allowed one sip and only one sip. This one sip rule is a strange rule but that’s how the coffee shop operates. Sam decides on the espresso. He estimates that one sip of espresso might have 30 mg of caffeine compared to one sip of the large volume coffee/Americano might have only 5 mg of caffeine. Sam considers the espresso as a better choice to wake him up!

Now meet Harry. Harry is a hair follicle. Harry is feeling tired and thinks that some PRP might help the follicle feel more energized and so Harry visits a local PRP clinic. Harry is presented with two options for PRP- 8 mL of PRP at 5 times above baseline volume or 15 mL of PRP at 2-3 times above baseline blood levels. 
While making his decision the PRP doctor advises hair follicle Harry that whichever PRP concentration he chooses his little hair follicle is only allowed to bathe in one tiny injection from the injecting needle.

Harry ultimately chooses the higher concentration of PRP estimates that one little injection of PRP at 5 times above baseline has a much higher concentration of growth factors than PRP at 2-3 times above baseline.

Hair follicle Harry considers the high concentration PRP as a better choice to wake up his hair follicle.


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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Placebo Effect: Pill Color Actually Matters

Pill Color Actually Matters

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The mind is powerful. It can make us feel better or make us feel worse. The way we think has the potential to eradicate symptoms in certain diseases. The mind can also cause symptoms to occur and make us feel worse. 

The science of placebo pills or "sugar pills" is fascinating and reminded us of just how powerful the mind really is. Study after study has shown just how powerful placebo effects are in humans. Placebo pills have been shown to help a wide range of health conditions - which points to the powerful effect of the mind to heal disease. Nowadays, placebo pills can even be purchased from the internet.

One systematic review published in 1996 examined the importance of pill color. Blue and green colored pills were shown to be associated with a tranquilizing effect when yellow, red, orange were seen as having a stimulant effect. White colored pills have been shown to perform well as pain pills. 

The color of pills is important and something we often take for granted. Pharmaceutical companies put a great deal of time and effort into choosing the precise color of pills we buy.
A recent report in the International Journal of Biotechnology suggested that red and pink pills are increasingly popular. Pink pills in particular are seen as sweeter and prompt patients to take them in order to achieve the intended effects. In some studies, data suggests that middle-aged people preferred red tablets compared to younger adults and more women prefer red tablets than men. 

References 

AJ de Craen et al. Effect of color of drugs: systematic review of the perceived effect of drugs and their effectiveness. BMJ 1996. 

RK Srivastava, Aarti T. More. Some aesthetic considerations for over the counter (OTC) pharmaceutical products. International Journal of Biotechnology, 2010; 11 (3/4): 267


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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Dutasteride in Young Women: Not Usually.

Dutasteride Prescribing for Pre-menopausal Women Requires Caution

If any drug is to be prescribed, the prescriber needs to know everything about the drug. So does the pharmacist who is dispensing the drug. The prescriber also needs to figure out what information is important to convey to the patient. If there are 10,000 things that the patient ‘could’ be told, which of these 10,000 things really should be relayed to the patient? The answer is mainly those pieces of information that are important to know about and the side effects that are common.

Dutasteride is a 5 alpha reductase inhibitor that is not formally approved for use in women. It is FDA approved for treated prostate problems in men and approved in South Korea for treating male balding. Dutasteride is sometimes used off label in many countries for treating androgenetic alopecia in men. In fact, studies have shown that dutasteride is more effective than finasteride in treating male pattern balding. It may or may not be associated with a higher risk of side effects such as sexual dysfunction.

The question often arises - if it’s used off label in treating male balding, can dutasteride be used off label in treating female genetic hair loss (i.e. female pattern hair loss)?

That answer is maybe - but maybe not.

Dutasteride for Female Hair Loss: Top 10 things to know

The following are my professional opinions and recommendations about the use of dutasteride for treating hair loss in women.

1 . Dutasteride is not FDA approved for women. That doesn’t it can’t be used for women it just means that it was formally approved for another use. Anyone using it needs to understand that. Many hair loss treatments we use are off label, so that fact alone is not alarming in any way.

2. Dutasteride is an oral medication that can be used to treat several types of hair loss in women, including post-menopausal female androgneetic alopecia and post menopausal frontal fibrosing alopecia. There’s evidence to back up the claim that it helps these conditions, albeit not everyone with these conditions.

3. Side effects of dutasteride in women include mood changes (depression), fatigue, weight gain, decreased sex drive, breast tenderness, breast enlargement, muscle soreness and rarely changes in blood counts.

4. Dutasteride has a long half life of 4-5 weeks. This simply means it stays around in the body a long time. In fact, dutasteride can even be detected in the body 6 months after stopping the drug.

5. Because of the long half-life, some women benefit from use once, twice or three times weekly. Daily use may not be required for all patients.

6. Because of the long half-life, women with pre-existing depression should not start dutasteride without careful discussion with their physician. It may worsen depression and if the drug is stopped it may take months to fully get out of the system. Other treatment options should be considered first.

7. Because of the long half-life, women with pre-existing sexual dysfunction should not start dutasteride without careful discussion with their physician. It may worsen sexual dysfunction and if the drug is stopped it may take months to fully get out of the system. Other treatment options should be considered first.

8. Because of the long half-life, pre-menopausal women who are planning to become pregnant at any time in the future should not use dutasteirde. My personal view is that dutasteride is medication that can be considered in post menopausal women and can be considered in pre-menopausal women over 40 who do not plan to have additional children or do not plan to have children provided it is used with contraception. Dutasteride, like finasteride, blocks conversion of testosterone to dihydrotestosterone (DHT) and by reducing levels of DHT may cause abnormalities in the external genitalia of the male fetus. The importance of using contraception and preventing pregnancy while using a 5 alpha reductase inhibitory drug can not be overemphasized. Unfortunately, this message may not be getting out to the public appropriately as some studies (i.e. Teirchert et al, 2017) have suggested that an extremely large proportion of women using finsateride and dutasteride may not using appoprirate contraception.

9. Given the limited number of studies in women, I do not recommend dutasteride for women with previous history of breast cancer or for women who have an elevated high risk for breast cancer. I particularly find the NIH Breast Cancer Risk Assessment Tool helpful in that regard and use it to help patients understand their baseline risk of breast cancer. Although there is no evidence that anti-androgens like spironolactone or finasteride increase the risk of breast cancer in women at low risk for developing breast cancer, we do not know whether women at very high risk for developing breast cancer place themselves at increased risk by using these drugs. It is unlikely but these studies have simply not been done.

10. Pre-menopausal women considering anti-androgen therapy may wish to discuss the use of other anti-androgens with their physician as well as other treatments. This would include spironolactone (Aldactone) and finasteride. Both of these drugs are also off label and both of these mediations are not to be used during pregnancy or by women who are trying to become pregnant. However, the shorter half life means that the drug is cleared rapidly from the body if side effects develop and if pregnancy is being considered in the near future.

REFERENCES

Teirchert M et al. Contraindicated use of 5‐alpha‐reductase inhibitors in women. Br J Clin Pharmacol. 2017 Feb; 83(2): 429–431. 



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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Does Using Spironolactone Increase Breast Cancer Risk?

Spironolactone and Breast Cancer: No evidence of Increased Risk

I just posted a new answer to our “Question of the Week.” I was asked to outline what is known at present about the risk of developing breast cancer in women who use spironolactone. Fortunately, there is no evidence that spironolactone use increases the risk of developing breast cancer.

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

Does Using Spironolactone Increase the Risk of Breast Cancer?

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


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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Hormonal Changes in Late Onset Congenital Adrenal Hyperplasia

Hormonal Changed in Late Onset CAH Resemble PCOS

Late onset on “non-classic” congenital adrenal hyperplasia (LOCAH) is an uncommon genetic disorder that is most often (95 % of the time) caused by mutations in 21-hydroxylase gene. This mutation leads to reduced levels of the 21 hydroxylase enzyme.  Late onset CAH from deficiencies or mutations in other genes such as  11β-hydroxylase (CYP11B1) and 3β-hydroxysteroid dehydrogenase (HSD3B2) are extremely rare.

Patients with LOCAH have CYP21A2 mutations that lead to reduced levels on the 21 hydroxylase enzyme but not a complete absence.  The amount of functional 21-hydroxylase enzyme determines the severity of the disorder. Low levels of the enzyme result in low levels of hormones such as cortisol and/or aldosterone and high levels of androgens (male hormones such as testosterone and androstenedione).

As a result of low cortisol, patients may experience changes in energy levels, blood pressure, blood sugar levels, as well as impaired ability of the body to respond to stress, illness, and injury. Aldosterone plays a key role in helping the body maintain the proper level of sodium and water and helps maintain blood pressure.  

 

Diagnosis of LOCAH

The patient's signs and symptoms may point to a possible diagnosis.  Even though LOCAH has several endocrine issues (high androgens and low cortisol), generally speaking, the clinical features of LOCAH are due to the excess of the androgens. Taking a careful medical history from the patient may reveal premature pubarche (i.e. the development of pubic hair, axillary hair, and/or increased apocrine odor prior to age 8 years in girls and age 9 years in boys). Affected children may be tall and have accelerated linear growth velocity, and advanced skeletal maturation.

Although LOCAH is estimated to occur in less than 1:1000 individuals, overall about 2-9 % of all women with hyperandrogenism may have late onset CAH. It has been estimate that 5 % of all women with hirsutism have LOCAH. Other symptoms can closely resemble the constellation of symptoms seen in women with polycystic ovarian syndrome. For example, women with late onset CAH may develop a variety of symptoms including frontal baldness, hirsutism, acne,  and irregular periods. Other symptoms include a delay in the timing of the very first period, early onset of pubic hair, accelerated growth, reduced final height and infertility.  

In a 2000 study by Moran and colleagues, the three most common symptoms among adolescent and adult women with LOCAH were hirsutism (59%), oligomenorrhea (54%), and acne (33%). Studies in 2009 by Bidet and colleagues suggested that the initial presenting symptoms in 161 women with late onset CAH were hirsutism (78%), menstrual dysfunction (54.7%), and decreased fertility (12%).

 

Testing for LOCAH

Blood tests. Generally, additional testing is ordered to help confirm the diagnosis.  These tests may include a blood test to measure the concentration of 17-hydroxyprogesterone (17-OHP) on day 3-5 of the menstrual cycle. Levels of 170–300  ng/dL have been found to be an excellent screening tool. These should be obtained in the morning and during the follicular (preovulatory) phase of the menstrual cycle.

The clinical features of late onset CAH in postpubertal adults may be difficult to differentiate from those of the polycystic ovary syndrome (PCOS). The following table shows some of the key differences in women with PCOS vs LOCAH. Note that even 17 OHP concentrations may be within the normal range for individuals with late onset CAH.  LH levels can be elevated in LOCAH and the LH/FSH ratio above 3:1 can also sometimes be observed. Prolactin levels are sometimes modestly elevated and DHEAS, testosterone and androstenedione levels may or may not be elevated. Aldosterone and cortisol levels are often normal may be lower range . Low sodium or high potassium levels may be present in the blood and abnormalities in glucose levels might be present.

 Comparison of Testing in PCOS vs Late Onset CAH.   DOWNLOAD PDF VERSION

Comparison of Testing in PCOS vs Late Onset CAH. DOWNLOAD PDF VERSION

ACTH Stimulation Test. An adrenocorticotropic hormone (ACTH) stimulation test may also be ordered which involves measuring the concentration of 17-OHP in the blood before ACTH is administered to the patient and then again 60 min after ACTH is given. This test is typically conducted through an endocrinologist.  The acute ACTH stimulation test remains the gold standard to confirm decreased 21-hydroxylase activity.  

To perform the ACTH stimulation test, a blood sample is first collected to measure baseline hormone concentrations. Then, synthetic ACTH (Cortrosyn, 0.25 mg) is administered. A second blood sample is collected 30–60 minutes later.  When the ACTH-stimulated 17-OHP value exceeds 1500  ng/dL a mutation is likely.

Ultrasound of Ovaries. Ultrasounds of the ovaries may not necessarily help differentiate PCOS from LOCAH because ultrasounds in LOCAH may show an ovarian morphology similar to polycystic ovary syndrome (PCOS) in about 50 % of patients.


Other tests

In addition to performing blood tests for day 3-5 17 OHP, other tests may be recommended by the physician caring for the patient. They include cortisol, androstenedione, testosterone, free testosterone, DHEAS, progesterone, sodium, potassium, creatinine, glucose, hemoglobin A1C. LH and FSH may also be measured. Aldosterone may be tested. Blood pressure measurements will also be obtained.


REFERENCES


56. Azziz R, Dewailly D, Owerbach D. Nonclassic adrenal hyperplasia: current concepts. Journal of Clinical Endocrinology and Metabolism. 1994;78(4):810–815. 

Witchel et al. Nonclassic Congenital Adrenal Hyperplasia Int J Pediatr Endocrinol. 2010; 2010: 625105. 

Moran C, Azziz R, Carmina E, et al. 21-hydroxylase-deficient nonclassic adrenal hyperplasia is a progressive disorder: a multicenter study. American Journal of Obstetrics and Gynecology. 2000;183(6):1468–1474.

Bidet M, Bellanné-Chantelot C, Galand-Portier M-B, et al. Clinical and molecular characterization of a cohort of 161 unrelated women with nonclassical congenital adrenal hyperplasia due to 21-hydroxylase deficiency and 330 family members. Journal of Clinical Endocrinology and Metabolism. 2009;94(5):1570–1578.  

Scaroni C et al. HLA and hormonal studies in 5 patients with late-onset 21-hydroxylase deficiency syndrome (21 OHDS). Journal of Endocrinological Investigation. February 1986, Volume 9, Issue 1, pp 65–70


Carmina E et al. The endocrine pattern of late onset adrenal hyperplasia (21-hydroxylase deficiency). J Endocrinol Invest. 1984 Apr;7(2):89-92.



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 of genetic hair loss: Can it ever make my hair worse?

Treating AGA: Will I be worse off with treatment?

Androgenetic hair loss is a type of hair loss that affects about 85 % of men and 50% of women in their lifetimes. In men, androgenetic alopecia is also known as male balding and male pattern balding. In women, this type of hair loss is known as female pattern balding and female pattern hair loss.

I’m often asked if using treatment for genetic hair loss can ever make one worse off than not using it at all. Overall, this is rare although not impossible. There are two scenarios that one needs to consider: short term and long term.

When can treatment make things worse?

Generally speaking, a treatment has the potential to make someone’s hair loss worse if 1) the patient has rapidly progressive androgenetic alopecia to begin with AND 2) the patient is a non-responder to the given treatment AND 3) the treatment provokes significant shedding AND 4) the treatment provides prolonged shedding. Generally all 4 of these need to be present.

It’s the patients with more rapid forms of genetic hair loss that have the potential to be worse off if a treatment provokes shedding and does not work. This is because shedding can speed up the progression of genetic hair loss. I have referred to this phenomenon in the past as AFMPS - accelerated follicular miniaturization from prolonged shedding. Unfortunately it takes about 9 months of treatment to really get a sense if a patient is a non-responder to treatment.

Prolonged shedding itself in patients who don’t have a rapidly aggressive form of genetic hair loss (i.e. criteria 1) doesn’t necessarily make things worse. There are some patients who shed with minoxidil for example and don’t seem to benefit and simply stop. They are not harmed by trying.

Common Misconceptions and Myths

There are a number of errors in judgement that patients make when thinking about whether a treatment can make their hair worse. For example, a patient might ask

“If I use a treatment for 5 years, and decide to stop, will I be worse off than if I didn’t use the treatment at all?

It’s important to understand that this answer is typically “no.” If a patient stops after 5 years they will simply return to the density they were supposed to have. This may of course be much less than they started with - but that’s because they were genetically determined to have that amount of hair loss.

Let’s say for the sake of discussion that a person decides to startstreatment at age 35 with 70,000 hairs on the scalp. They use a treatment and after 5 years they are pleased because they have 70,000 hairs on the scalp at age 40. Now, they stop treatment and find that one year at age 41 later they have 50,000 hairs on the scalp. Did stopping treatment make things worse? Yes, stopping made the hair loss worse, but it wasn’t the fault of being on the drug that did it. The patient was genetically programmed to have 50,000 hairs on the scalp at age 41. They are also genetically programmed to have 30,000 hairs on the scalp at age 49 so if they chose to remain off treatment, this is likely the density they are headed towards.


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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Androgenetic Alopecia (AGA): AGA Under the Microscope

AGA Under the Microscope

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There is often some degree of confusion as to what constitutes a typical biopsy from a patient with androgenetic alopecia (AGA). Here, I will review some of they key features of both horizontal and vertical sections (i.e. the two main ways a biopsy can be done). AGA is a non-scarring alopecia. In both horizontal and vertical sections sebaceous glands typically appear quite prominent. A reduction in sebaceous gland density should prompt one to consider that another diagnosis, such as scarring alopecia, might be present. 
Miniaturized hairs are a feature of AGA. In vertical sections, the miniaturized and vellus hairs simply appear as hairs which root themselves in the mid dermis rather than deep down in the subcutaneous fat. In horizontal sections, miniaturization can be appreciated by a shift in the terminal to vellus hair ratio (“T:V” ratio) from above 6:1 to well below 4:1 and possibly well below this.

Inflammation is very much a part of AGA. The legendary dermatologist Dr David Whiting showed that 40% of biopsies from patients with AGA showed perifollicular inflammation. This inflammation sits in the lower infundibulum and isthmus. The cells that comprise the inflammation are largely T cells. Perifollicular inflammation occurs early in the course of AGA and likely drives the development of perifollicular fibrosis and drives the progressive miniaturization of hairs.

Perifolliuclar fibrosis is also part of AGA and the concentric fibrosis can best be appreciated in horizontal sections. Perifollicular fibrosis can often be mistaken and misdiagnosed as scarring leading to a misdiagnosis of lichen planopilaris (LPP) and other scarring alopecias. However, the retention of sebaceous glands and absence of lichenoid change in the outer root sheath favours a diagnosis of AGA over LPP.

Cell death of keratinocytes in the outer root sheath is not a typical feature of AGA. Apoptosis is present in a proportion of dermal papilla cells and lymphocytes in the perifollicular inflammatory infiltrate - but not in the actual outer root sheath. Lichenoid change in the outer root sheath might cause one to consider a diagnosis of LPP rather than AGA.


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 Extensions: The 2011 Spike

The 2011 Spike

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Hair extensions continue to be very popular. This interest started to increase significantly in the late 1990s but increased even further over the last 7-8 years. Hair extensions were once an extremely private practice among women. That has changed in part due to the ever increasing acceptance of hair extensions, especially among celebrities. There are many types of extensions. including clip in, micro link, fusion and tape-in and weave-in extensions.

The last decade has witnessed a marked increase in the sale of hair extensions. In the United States alone there has been a 30 % increase in the number of salons offering hair extensions.

As one can see in this “Google Trends” search, interest in hair extensions saw a major peak in 2011 and this interest still remains strong to the present day.

China continues to be the number one supplier of human hair for wigs and extensions followed by India. The 2011 spike was not only in Google trends but in a reality in the hair industry. Between 2009 and 2011, China reportedly tripled its imports of Indian hair. The market for hair extensions is greatest in the United Kingdom, United States, Australia and South Africa.


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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Perifollicular Fibrosis and Perifollicular Inflammation in Androgenetic Alopecia

Perifollicular Inflammation and Perifolliuclar Fibrosis are Part of Balding

It had long been though that male and female patterned hair loss (‘balding') is a relatively non-inflammatory process. The last decade has repeatedly shown that this is not the case and that inflammation is likely very much a part of the process and likely contributes in some way to the balding process itself.

The current model of AGA suggests that ‘micro inflammation’ in AGA might trigger apoptosis and perifollicular fibrosis which in turn causes hairs to miniaturize and shed.

Inflammation in AGA: How common is it anyways?

Inflammation is commonly seen in androgenetic alopecia and is likely part of the condition itself. Studies by Whiting showed that perifollicular inflammation was present in 40 % of AGA biopsies. The inflammation present in AGA is different than the inflammation seen in the destructive scarring alopecias like lichen planopilaris. In 2000, Mahe used the term “microinflammation” to describe this types of inflammatory process.

Inflammation in AGA: Where is it found?

Inflammation in AGA is mainly seen in the upper parts of the hair follicle. Inflammation is commonly found in both the isthmus and isthmus which are the upper portions of the hair follicle. Minor amounts of inflammation around hair follicles can be seen in the normal scalp as well in in androgenetic alopecia. However, more marked degrees of inflammation are not normally seen in the scalp but can be a feature of androgenetic alopecia. Ramos in 2016 showed that inflammation is more common around miniaturizing hairs and this inflammation seems to be associated with a form of cell death known as apoptosis. In 1992, Jaworsky and colleagues showed that biopsies of males and females with androgenetic alopecia showed the presence of activated T-cell infiltrates about the lower portions of follicular infundibula. Inflammatory cells infiltrated the region of the follicular bulge, the putative source of stem cells in cycling follicles. It was postulated that the progressive fibrosis of the perifollicular sheath might begin with T-cell infiltration of follicular stem cell epithelium and that the perifollicular fibrosis actually impairs hair growth.

Cell death (Apoptosis) is AGA: Where does it occur?

Cell death via programmed cell death or ‘apoptosis. is also very much a part of AGA. It is known that apoptosis is dermal papilla cells is important in AGA and is proposed to reduce the cell mass of the dermal papilla and in turn lead to miniaturization.

In 2010, El-Domyati and colleagues showed that apoptosis (by bcl-2 immunostaining) was present in both the dermal papilla and in perifollicular lymphocytes (i.e. the white blood cells that comprise the perifollicular inflammation). The authors showed that the apoptosis in dermal papilla cells was associated with reduced cell activity and cell division (as measured by proliferating cell nuclear antigen staining PCNA).

Can we detect how much inflammation is present in AGA without a biopsy?

To date, there is no better way to detect inflammation than a biopsy. Of course, biopsies are seldom done in AGA because the diagnosis is largely clinical. However, careful examination of the scalp with dermosocpy may help pinpoint inflammation occurring beneath the scalp. In 2004, Deloche showed that peripilar signs (PPS) by dermoscopy were correlated with the presence of inflammation beneath the scalp.

Does inflammation and fibrosis really matter?

The inflammation and fibrosis seen in androgenetic alopecia probably does matter. The inflammation likely triggers abnormalities in how hair cycles (i.e. telogen effluvium) and likely contributes to the progressive ‘miniaturization’ of hairs over time.

Perifollicular inflammation in AGA appears to occur very early in the condition. In 2009, El-Domyati showed the perifollicular inflammation was present early the condition long before perifollicular fibrosis started to be seen. Over time, as perifollicular fibrosis became more commonly seen as perifollicular inflammation started to decrease. In other words, the two phenomena seemed to have an inverse correlation. Gonzalez showed in 2010 that perifollicular fibrosis was even a common findings in androgenetic alopecia occurring in teenagers.

Perfifollicular inflammation and fibrous probably affect how hairs grow. In 1993, Whiting performed some classic studies that have shaped how we think about inflammation in AGA. He showed that patients with perifollicular inflammation and fibrosis have poorer responses to minoxidil. Individuals with moderate or dense lymphocytic inflammation and perifollicular fibrosis may have poorer responses to minoxidil.

What causes the perifollicular fibrosis anyways?

It’s not entirely clear what causes the perifollicular fibrosis to occur. In 2006, Yoo and colleagues proposed that TGF-beta (transforming growth factor beta) seemed to play a role. They showed that testosterone treatment increased the expression of type I procollagen at mRNA and protein level and this was associated with a rise in TGF-beta protein levels by 81.9 % in dermal fibroblasts. Conversely, pretreatment of finasteride inhibited the ability of testosterone to make pro collagen RNA and protein and decreased the expression of TGF-bet by 30 %. Interestingly, pretreatment of follicles with a TGF-beta antibody inhibited pro collagen expression leading the authors of the study to conclude that testosterone triggers TGF-beta expression and perfiollciular fibrosis in AGA. They also postulate that one mechanisms of finasteride may be to reduce TGF-beta and therefore pro collagen expression.

Conclusion

Androgenetic alopecia is no longer viewed as a “non-inflammatory” condition. Inflammation is very much a part of AGA and this inflammation likely drives the development of perifollicular fibrosis and an inflammatory millieu that drives the apoptosis of dermal papilla cells and therefore the progression miniaturization of hair follicles.

So, do we need to treat the inflammation? That answer is ‘probably’ - it’s just we don’t quite know how to best do this yet. There are many different types of anti-inflammatory treatment including corticosteroids, doxycycline, tacrolimus, TNF-inhibitors, immunomodulatory and immunosuppressants. It’s a bit of a guess as to how best to address the inflammation in AGA and more research is needed. It’s extremely likely this will play a beneficial role, particularly the earlier such anti-inflammatory treatment is started. Treatment will likely be needed over an extended period rather than for a few days or weeks.

REFERENCES

Deloche C, et al. Histological features of peripilar signs associated with androgenetic alopecia. Arch Dermatol Res. 2004.

El-Domyati M, et al. Androgenetic alopecia in males: a histopathological and ultrastructural study.. J Cosmet Dermatol. 2009.

El-Domyati M, et al. Evaluation of apoptosis regulatory markers in androgenetic alopecia. J Cosmet Dermatol. 2010.

Gonzalez ME, et al. Androgenetic alopecia in the paediatric population: a retrospective review of 57 patients. Br J Dermatol. 2010.

Jaworsky C, et al. Characterization of inflammatory infiltrates in male pattern alopecia: implications for pathogenesis. Br J Dermatol. 1992.

Mahé YF, et al. Androgenetic alopecia and microinflammation. Int J Dermatol. 2000.

Nirmal B, et al. Evaluation of Perifollicular Inflammation of Donor Area during Hair Transplantation in Androgenetic Alopecia and its Comparison with Controls. Int J Trichology. 2013.

Ramos PM, et al. Apoptosis in follicles of individuals with female pattern hair loss is associated with perifollicular microinflammation. Int J Cosmet Sci. 2016.

Whiting DA. Diagnostic and predictive value of horizontal sections of scalp biopsy specimens in male pattern androgenetic alopecia. J Am Acad Dermatol. 1993.

Yoo HG, et al. Perifollicular fibrosis: pathogenetic role in androgenetic alopecia. Biol Pharm Bull. 2006.


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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Coffee, Caffeine and Immunity: Caffeine is an Immunomodulator

Caffeine is an Immunomodulator

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Caffeine appears to have an anti-inflammatory effect in some situations and helps calm down an “overactive” immune system. In animal (rodent) models, it’s quite clear that caffeine can affect a variety of different types of inflammation. The effects on humans appear similar, with caffeine having an effect on multiple parts of the immune system - particularly immune cells known as lymphocytes.

To date, there is good evidence to suggest a suppressive effect of caffeine on the proliferation of “stimulated” lymphocytes. In other words, immune cells that have become too active can be quieted down with caffeine. Other immune cells such as natural killer cells and macrophages also exhibited a reduced activity in the presence of high doses of caffeine.

Caffeine may also be truly Immunosuppressive in some situations given the reduced levels of anti-inflammatory cytokines such as TNF-α, IL-2 and IL-6. Moreover, certain receptors, such as TLR1, TLR2, TLR4, and MHC class I-related chain B molecules are also decreased by caffeine.A recent study showed that caffeine inhibits STAT1 signaling and downregulates inflammatory pathways involved in autoimmunity.
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In actual human epidemiologic studies, coffee has mixed effects. Caffeine (coffee) consumption appeared to increase the risk of developing type 1 diabetes and rheumatoid arthritis. In contrast, coffee may help somewhat to prevent ulcerative colitis and multiple sclerosis. There does not appear to be an association ether way for other autoimmune diseases such as systemic lupus erythematosus, psoriasis and Crohn's disease.

In the world of hair loss, there are very few studies which have objectively examined the benefits of caffeine. Some studies have suggested a minor benefit for caffeine containing shampoos but these studies are small and have not yet been independently replicated to any significant degree.

It is fascinating to consider that caffeine has the potential to effect so many parts of our immune system. More studies are needed to understand whether or not caffeine can integrate into the treatment of various types of hair loss.


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: Dermatoscopic (Trichoscopic) Features

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Dermatoscopic (Trichoscopic) Features

Up close examination of the scalp via dermoscopy allows the physician the opportunity to confirm the suspected type of hair loss and also evaluate how active the condition is at the present time. There are many known “dermatoscopic” features of alopecia areata and I will review five common ones here:

Yellow dots (red arrow) represent empty hair follicle openings (pores) and are very common. The more severe of a disease a patient has, the more yellow dots are seen all over the scalp.

Vellus hairs (white arrow) are short and thin regrowing hairs and are also common in patients with alopecia areata.

Black dots (black arrow) represent hair follicles broken at the surface and indicate an active disease state.

Tapered hairs (blue arrow) are long hairs that become quite thin as the are about to enter the scalp. They too represent active disease.

Exclamation mark hairs (green arrow) are short 4 mm hairs that are actually broken hairs. They are wider at the top compared to the bottom and are found in patients with active disease.


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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Donovan Hair Clinic Recipient of 2019 Consumer Choice Award

We’re honoured to be chosen as the recipient of the 2019 Consumer Choice Award in the category of Hair Restoration. Consumer Choice Awards are based on independent market research.

DONOVAN HAIR CLINIC TO RECEIVE 2019 CONSUMER CHOICE AWARD


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 and The Use of Relaxers

Relaxers May be Associated with Many Kinds of Hair Loss

I just posted a new answer to our “Question of the Week.” I was asked to outline how best to treat hair loss from relaxers.

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

Hair Loss from Use of Relaxers

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


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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TNF inhibitor induced AA: Adalimumab Infliximab Etanercept

Adalimumab Infliximab Etanercept

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Recent research in the past decade has shown the TNF inhibitors can rarely contribute to the development of alopecia areata as well as other types of hair loss as well (ie psoriatic alopecia and scarring alopecias). Alopecia areata has been reported with all three anti-TNF agents including adalimumab, etanercept and infliximab. To date, the most common TNF-inhibitor implicated is adalimumab followed by infliximab and etanercept.

In affected patients, hair loss can occurs with a matter of months to many years after the TNF agent is started. Of all the reports in the medical literature to date, onset in affected patients may occur fastest with adalimumab (6.8 months average) compared to over 1 year with the other 2 agents. The degree of hair loss varies greatly from patchy type AA to alopecia totalis and universalis.

Optimal treatment for TNF inhibitor induced AA is not clear. Some patients have improved their hair by stopping the TNF inhibitor although a smaller proportion may improve even with continued use of the TNF inhibitor. The option with the highest chance of success in terms of stopping hair loss and regrowing hair appears to be stopping the anti-TNF agent.


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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Sebhorrheic Dermatitis in LPP: Is it more common than we think?

Is it more common than we think?

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Current evidence would suggest that a greater proportion of patients with lichen planopilaris (LPP) have seborrheic dermatitis compared to people in the general population. For example, about 5% of people in the general population have seborrheic dermatitis compared to about 50% of patients with LPP.

In 2016, Berfeld’s group at the Cleveland clinic studied the incidence of seborrheic dermatitis in patients with lichen planopilaris. This study is important to understand as it was one of the few studies to date which really documented the increased incidence of seborrheic dermatitis in patients with LPP.

The study was a retrospective review of 246 patients seen over the period 2004-2015. Interestingly seborrheic dermatitis (SD) was present in 46.2 % of LPP cases. In 27.4 % of cases the SD was found outside the area affected by the LPP. On average the SD was diagnosed 7.8 months prior to the LPP diagnosis.

Having SD seemed to delay an actual diagnosis of LPP. Patients with both SD and LPP diagnosis (LPP-SD) received their diagnosis with significantly more delay than patients with LPP who did not have SD (ie LPP). For example, patients with LPP-SD received their diagnosis in 7.6 months on average compared to 2.3 months for LPP alone.

Whether SD actually plays a role in the scarring process as well remains to be determined. It is interesting that there was a greater prevalence of late stage scarring alopecia in ptient with LPP-SD than LPP alone (41.5 % vs 15.7%). On account of seborrheic dermatitis being so common in LPP, it makes sense that many people with LPP will feel better and gain at least some relief of their itching with use of antidandruff shampoos.

Reference


Ratnaparkhi et al. Association of lichen planopilaris with seborrheic dermatitis l: A retrospective case-control study. Poster 3727. JAAD May 2016.


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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Early Alopecia Areata: Subtle Findings

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Subtle Findings

Alopecia areata is an autoimmune disease that affects 2 % of the world. Most people develop small round or oval patches of hair loss when the disease first occurs. In the very earliest stages however, the clinical findings may be more subtle until sufficient time has elapsed for the actual circles of hair loss to form.

The earliest stages of alopecia areata may be associated with increased shedding of hair compared to the normal rate of shedding. Some shed hairs may be broken as well. Many patients with alopecia areata are asymptomatic although a proportion will note the presence of burning or itching prior to the hair loss.

Up close dermatoscopic examination, as shown here, may reveal reduced density as well as exclamation mark hairs (blue arrows), tapered hairs or black dots. Over time, the more classic findings typically emerge making the diagnosis much easier. 


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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Scarring (Cicatricial) Alopecia: Signs of Follicular Injury

Signs of Follicular Injury

Scarring alopecias are a group of hair conditions associated with the formation of scar tissue beneath the scalp. This scar tissue damages the hair follicle and affects how it emerges from the scalp. Minor degrees of follicular injury can give twisting of hairs known as pili torti. Severe injury to hairs such as shown here leads to highly curled hairs. This type of coiling is seen in scarring alopecias as well as in some post op hair transplants in which hairs were subjected to extreme injury during the procedure (especially FUE procedures).

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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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Scarring Alopecia: Ingrown hair

Ingrown hair

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Ingrown hairs occur when the distal or end portion of a hair follicle curves back into the scalp. Ingrown hairs can occur for a variety of reasons the most common being seen in individuals with coarser and curlier hair. Ingriwn hairs are seen in some individuals after shaving, and may also be seen in the context of some localized infections and folliculitis. Scarring alopecias such as dissecting cellulitis are more commonly associated with ingrown hairs than other scarring alopecias. Here an ingrown hair is seen in a patient with lichen planopilaris (LPP). Treatment includes removal of the hair from under the skin and treament of the associated inflammation or infection.


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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MTHFR Polymorphisms (677T allele, etc) and Hair Loss

MTHFR Mutations, Polymorphisms and Hair Loss

I just posted a new answer to our “Question of the Week.” I was asked to explain what is currently understood about MTHFR gene mutations and hair loss.

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

MTHFR Gene Mutations and Hair Loss: Is there a link?

To submit a question, simply visit complete our online form


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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