External Medicine
DISCLAIMER: This website is a collection of primary literature and the opinions of the website creators on that literature. It is not intended to be used for the practice of medicine or the delivery of medical care in the absence of other appropriate credentials (like a medical degree). Discuss any information with your doctor before pursuing treatments mentioned on this site.
Alopecia
ALOPECIA AREATA
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Quality review articles incorporated here include:
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Alopecia areata: Disease characteristics, clinical evaluation, and new perspectives on pathogenesis. J Am Acad Dermatol. 2018. PMID: 29241771.
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Alopecia areata: An appraisal of new treatment approaches and overview of current therapies. J Am Acad Dermatol. 2018. PMID: 29241773.
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The Alopecia Areata Consensus of Experts (ACE) study: Results of an international expert opinion on treatments for alopecia areata. J Am Acad Dermatol. 2020. PMID: 32165196.
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What is it?
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A nonscarring alopecia most commonly presenting as well-demarcated patches of hair loss. It's thought to be caused by CD8+ autoreactive T cells. It can present as a solitary patch, multifocal, involve the beard only, the entire head (totalis), or the entire body (universalis). Special patterns include ophiasis (involving the inferior occipital and parietal scalp, named after greek word for snake, which is not strikingly apt), or in contrast may be confied to the crown (sisaipho, ophiasis spelled backwards...sort of). Other hair findings includes a depigmenting form of AA with sudden graying of hairs, and a perinevoid AA with loss of hairs around nevi.
Incidence
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Prevalence is ~30% higher in women. Notably higher prevalence in ages 30-50yo. Asians>multiracial>blacks=hispanics>white. 36857044
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AA incidence is highest in female adults aged 18-44y, and in female children and adolescents aged 12-17y. It's more common in adults than children, and the female predilection is also stronger in adults. It's rare in children <6yo. 36857069
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Alopecia totalis and universalis follows similar trends especially with respect female predilection, but age predominance favors those >44yo. 36857069
Diagnosis
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Disease activity can be indicated by exclamation point hairs, trichoscopic black dots, positive hair pull test, anagen effluvium. Clinical exam is all that is needed to establish diagnosis. Trichograms are not useful. Consider biopsy in the setting of a single patch not responding to therapy, diffuse hair loss, or signs of scarring. One biopsy is usually sufficient. Obtain biopsy from edge of lesion (not center) and from a location typically not affected by androgenetic alopecia. (ACE consensus, 32926985).
Differential
Trichotillosis (trichotillomania)
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Hairloss usually incomplete, and broken hairs more prominent. Although, AA can also display incomplete hairloss, especially early.
Temporal triangular alopecia
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Triangular shape of non-scarring alopecia which is usually unilateral in the frontotemporal area. Unresponsive to treatment. Biopsy lacks inflammation (chronic AA can also lack inflammation).
Telogen effluvium
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Diffuse AA can resemble telogen effluivium, but lacks the accompanying stressor and inflammation on biopsy; an increase in telogen hairs is seen in TE.
Prognosis
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Severity of initial hairloss and age are the most predictive indicators, with younger patients having less favorable prognosis.
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Risk of progression from AA to totalis or unverisalis is about 1 in 20.
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Ophiasis subtype has a poor prognosis. The exception to the severity rule is acute diffuse AA and alopecia totalis, which have more favorable prognoses. Eyebrow, eyelash, nonscalp hairloss, and nail pitting/trachyonychia portends poorer prognosis (ACE consensus, 32926985).
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AA Consesus of Experts (ACE) consensus is that race and ethnicity do not alter its natural history, and ethnicity and climate does not affect response to treatment. (32926985)
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ACE consensus is that systemic steroids and JAK inhibitors reduce the progression of multifocal AA to alopecia totalis/universalis. (32926985)
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Prognosis is worse when AA lasts beyond 5 years and can become irreversible if lasting >10yrs. (32926985)
Etiology/Pathogenesis
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The hair bulb is an immune privileged site, but in AA this immune privilege is lost leading to T cell attack of the hair bulb. This disrupts the anagen phase leading to abnormal hair growth.
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The cause of this autoimmunity is unknown, but hypothesized that the target is melanogenesis-associated antigens. This in part may explain why regrowth of non-pigmented hairs is typically first.
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Keratinocyte-derived antigens may also be involved.
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Over time, this inflammation leads not to follicle loss but to miniaturization.
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Overexpression of JAK (mainly 3 but also 1 and 2) is seen in AA. IFN-γ signals through JAK1/2 and IL-15 through JAK1/3.
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ACE consensus is that family and personal history autoimmunity, including atopy and atopic dermatitis, are correlated with increased risk of AA. Acute stress is thought to trigger disease. (32926985)
Treatment
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Spontaneous remissions occur, but are less likely with severe disease.
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One proposed treatment flow chart can be found here. Generally topical/intralesional therapies are considered first line, especially in pediatric patients. Consensus statements for topical therapies and for first line treatment in pediatric patients can be found at the links provided.
Topical corticosteroids
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Response rate may be adequate but usually inferior to ILTAC. Good for children in general and specifically those that don't tolerate injections
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Superpotent TCS BID for 12 weeks. Clobetasol foam preferred by some. In children, mometasone cream is often preferred.
Intralesional corticosteroids
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2.5 to 5mg/cc q6 weeks for 3-6mo. Best for <50% scalp involvement or as an adjunctive treatment.
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Some data suggests that 2.5mg/cc of ILTAC confers same benefit as 5 or 10mg/cc (26183987), but my clinical experience suggests otherwise, and a meta-analysis supports the notion that 5mg/cc may offer the greatest risk/benefit profile. (31843657)
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Some suggest limiting to 20mg total dose per session, which is 8cc. (26183987)
Oral corticosteroids
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Provides significant benefit for most clinical variants of AA, with reduced efficacy in ophiasis and universalis.
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Appropriate for severe AA in children >13, dosing 0.4-0.6mg/kg/day tapered over 12wks (longer than 12mo may be needed in adults). (ACE consensus, 32165196)
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Tapers starting at <0.8mg/kg for a 6-week course have been suggested. Despite good initial efficacy, relapse is common 1-2 months after cessation.
Minoxidil
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Useful only as an adjuvant (although spontaneous regrowth while treating with minoxidil monotherapy has been described), and for those who want to maximize hair regrowth. Benefits are marginal but for the motivated may be worth it. Topical or oral.
Methotrexate
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A reasonable option for refractory or severe AA, although JAK inhibitors may replace this for many. Doses of 15-25mg/wk, w/ or w/o prednisone at doses of 10-20mg daily.
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DBRCT: MTX alone rarely leads to complete or near complete hair regrowth of alopecia universalis or totalis. Patients receiving MTX plus low dose pred had a 20% complete or almost complete response rate. 36884234
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Topical immunotherapy
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Diphenylcyclopropenone (DPCP) - contact sensitizing agent thought to work by inducing allergic contact dermatitis which may cause antigen competition and change the inflammatory milieu (hands waving). Good for >50% scalp involvement.Sensitize the patient to 2% DPCP in acetone applied to a 4cm circle on the arm. 1 week later, 0.001% DPCP is applied unilaterally. Concentration is increased each subsequent week until mild pruritus and erythema is elicited lasting 36hrs. This concentration should then be used weekly. When hair regrowth is observed, bilateral treatment is initiated. With each application it should be left on for 48hrs and covered from light which degrades the molecule. There is a greater risk of relapse if the dose is not tapered, so treatment should not be interrupted. Combination therapy with anthralin 0.5-1.0%, which causes an irritant dermatitis, may enhance efficacy. Clinically evident dermatitis may not be necessary for efficacy. 29108907
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Squaric acid dibutylester (SADBE) - an alternate agent with similar efficacy that can be tried if DPCP fails. Unlike DPCP, an eczematous reaction is not required for efficacy.
JAK inhibitors
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Initial investigations were done with ruxolitinib (JAK1/2) and tofacitinib (JAK1/3). More targeted inhibitors have since been approved, baricitinib under trade name Olumiant, ritlecitinib under the name Lifulo.
Baricitinib
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Uptitration from 2mg to 4mg after lack of response does appear to be effective. However, when lack of response should be assessed and uptitration initiated is not defined. 37556146
Ivarmacitinib
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Currently being investigated, ivarmacitinib is a selective JAK1 inhibitor which showed efficacy in a phase II 94 patient RCT. 37019385
Others
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Simvastatin/ezetimibe 40mg/10mg has shown some efficacy. Apremilast and topical crisaborole are also being investigated.
Ancillary Workup
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Routine thyroid function screening should be restricted to AA patients with a medical history of Down syndrome, personal history of atopy, a family history of thyroid disease, or clinical findings (goiter) suggestive of potential thyroid dysfunction in the individual patient. (28973128)
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Lab testing for associated things like autoimmune conditions and for triggers is not indicated. (ACE consensus, 32926985).
ANDROGENETIC AND FEMALE PATTERN ALOPECIA
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Quality review articles incorporated here include:
Female pattern hair loss: A clinical, pathophysiologic, and therapeutic review. Int J Womens Dermatol. 2018. PMID: 30627618.
Interventions for Female Pattern Hair Loss. JAMA Dermatol. 2017. PMID: 28114675.
SUMMARY: Review of evidence on current treatments for female pattern alopecia. Concludes that there was low- to moderate-quality evidence that topical minoxidil (2% and 5%) was associated with improvements in FPHL; low-quality evidence that finasteride was no more effective than placebo. There were inconsistent results from studies that laser devices were effective, but total hair count increased compared with baseline (moderate- to low-quality evidence). Safety of all treatments examined was similar to placebo.
Background
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May occur in adolescent girls and respond to PO minoxidil and spironolactone. 33333154
Workup
Female Pattern
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Any physical, mental, or emotional stressors that may have occurred within the previous 3 to 6 months (ddx telogen effluvium).
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Signs of hyperandrogenism such as hirsutism, ovarian abnormalities, menstrual irregularities, acne, and infertility.
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Use of OCPs containing progesterone with a high androgenic potential (i.e. norethindrone) or recent discontinuation of long term use of an estrogenic OCP.
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Hair pull test: grab 50-60 hairs near base and firmly pull. >2 hairs is abnormal test. Prior brushing or washing has no bearing on results.
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Other lab tests of limited utility (30627618), but often times some basic labwork (CBC, TSH, iron studies) can be helpful to reassure patient.
Treatment
Overview
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There are currently only 3 FDA-approved treatments: topical minoxidil, oral finasteride (men only), and low-level laser light therapy (LLLLT). Most data exists for male patients. All FDA-approved treatments show statistically significant benefit over placebo: finasteride 1 mg daily (18.37 hairs/cm2), LLLLT (17.66 hairs/cm2), 5% minoxidil twice daily (14.94 hairs/cm2), and 2% minoxidil twice daily (8.11 hairs/cm2). 28396101
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Other treatments include: Minoxidil, see below. Prostaglandin analogs - latanoprost and bimatoprost small trial in men showed efficacy, no supportive data in women. Ketoconazole - acts as an androgen-receptor antagonist, and thus has shown some benefit in FPHL in those with hyperandrogenism. Melatonin topical solution shown effective in one study; ?data for oral use. Platelet rich plasma emerging data. Microneedling very promising with demonstration of possibly best results. often used in combo with other first line therapies for increased drug delivery. Low-level light therapy data is diminished by significant variability and bias, but regarded as a potentially effective treatment with low side effects. Therapy with 650 to 900 nm wavelength at 5mW recommended. Most studied device is Hair Max LaserComb. Finasteride not approved in women and 1mg/daily for 12 months was proven ineffective in postmenopausal women. Conversely, it may be effective in women with hyperandrogenism at slightly higher doses. Dutasteride not approved in men or women, but effective for FPHL at doses from 0.25-0.5mg/day. Cyproterone acetate may be effective in women with hyperandrogenism. Spironolactone not approved but very commonly used; data are mixed, similar to cyproterone acetate. Nutritional supplementation overall very mixed evidence. There seems to be a relationship to iron (low serum ferritin) and vitamin D but no great data supporting replacement as an effective treatment. Data limited for Viviscal. 28114675
Topical Minoxidil
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Mechanism: exact mechanism of minoxidil (Rogaine) is unknown, but it is a potent vasodilator (originally approved by FDA for HTN) via potassium channel opening. It stimulates hair growth by increasing the anagen phase, and also increases angiogenesis around the follicle. It may also activate prostaglandin synthase-1 which can be protective to hairs (and may be the mechanism for prolonged anagen phase). Sulfotransferase in outer root sheath of hair shaft coverts prodrug to active drug, and enzyme activity may predict response. 30627618, 28114675
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Dosing: available as 2% and 5% solutions and a 5% foam.
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For females: 5% foam daily and 2% solution twice daily are FDA approved. 5% foam daily is noninferior to 2% twice daily solution. 21700360 There does not appear to be a dramatic difference between 5% and 2% twice daily solutions. 15034503
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For males: 5% foam or solution and 2% solution are all FDA approved for twice daily application. 5% solution twice daily appears superior to 2% twice daily. 12196747
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40% show improvement within 6 mo but should use for 12mo minimum. Should continue indefinitely otherwise will experience TE w/in 4-6 mo of stopping. May experience transient increased hair loss in first few months. Most common SEs are irritation (usually 2/2 propylene glycol vehicle; 5% foam does not have this). Minoxidil, oral may have results similar to topical, but with possible SEs of fluid retention, postural hypotension, hypertrichosis. 28114675
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Efficacy:
The Efficacy of Topical Minoxidil for Non-Scarring Alopecia: A Systematic Review. J Drugs Dermatol. 2019. PMID: 30794366.
SUMMARY: Nice summary of minoxidil studies with charts broken down by type of alopecia, and male vs female subjects. They report that minoxidil has been studied in concentrations of 0.01% to 15% and responses in hair growth range from 17% to 70%.
A randomized, placebo-controlled trial of 5% and 2% topical minoxidil solutions in the treatment of female pattern hair loss. J Am Acad Dermatol. 2004. PMID: 15034503.
SUMMARY: Patients applied 1 mL of assigned solution (5% minox, 2% minox, or placebo) twice daily at approximately 12-hour intervals (total daily dose of 2 mL) for 48 weeks. There was no dramatic difference between 5% and 2% formulations, but side effects of irriation and hypertrichosis were higher in 5% group. CONCLUSION: In this 48-week study of 381 women with female pattern hair loss, 5% topical minoxidil was superior to placebo at increasing nonvellus hair count, and patient/investigator assessments of hair growth and scalp coverage. Application of 2% topical minoxidil was superior to placebo for assessments of nonvellus hair counts and investigator assessment of hair growth/scalp coverage at week 48; differences in patient assessment of hair growth at week 48 were not significantly different from placebo. At week 48, the 5% topical minoxidil group demonstrated statistical superiority over the 2% topical minoxidil group in the patient assessment of treatment benefit. Both concentrations of topical minoxidil were well tolerated by the women in this trial without evidence of systemic adverse effects.
Oral Minoxidil
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Low dose oral minoxidil, generally considered anything less than 5mg daily, has become increasingly utilized for alopecia of all types.
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Efficacy:
Minoxidil 1 mg oral versus minoxidil 5% topical solution for the treatment of female-pattern hair loss: A randomized clinical trial. J Am Acad Dermatol. 2020. PMID: 31473295.
SUMMARY: 52 Female patients mean age 40 for oral, 47 for topical. 1mg minoxidil vs once daily 5% topical minoxidil. At 24 weeks, 12% increased hair density in oral vs 7.2% topical, p=0.09. No HoTN events observed, no difference in BP. Hypertrichosis was higher in oral vs topical (27% vs 4%), but mild and well-tolerated.
Low-dose oral minoxidil for treating alopecia: A 3-year North American retrospective case series. J Am Acad Dermatol. 2021. PMID: 33098962.
SUMMARY: All forms of alopecia were treated (not just AGA). Patients were prescribed low oral minoxidil (LDOM) 1.25 mg nightly for 3 months. Most patients requested re-prescription of LDOM at reassessment (43/51; 84%). Reasons for stopping included: nausea, acne, lack of efficacy, facial hypertrichosis, lightheadedness, edema. Hypertrichosis was reported in almost half of patients but cited as a reason for stopping in only 1. At follow-up, escalated 2.5-mg dosing was adopted by 9 of 12 men (75%) and 7 of 39 women (18%) despite known risk of facial hypertrichosis. Results from this retrospective series indicate increased scalp hair growth (33/51; 65%) and decreased hair shedding (14/51; 27%) with LDOM.
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Safety/Side Effects:
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Although side effects are common, they are rarely a cause for discontinuation. Most common side effect is hypertrichosis affecting 15-55% of patients depending on the study. 32622136, 33639244, 33253848 (original data from the studies can be found here). Other side effects include: headache (<1%-9%), lightheadedness/dizziness (1.7%-5%), lower limb edema/periorbital edema/fluid retention (<1%-6%), palpitations/tachycardia/EKG changes (<1%-4%), insomnia/nightmares <1%-2%). Initial shedding of hair is also common (as it is with topical minoxidil) lasting for a month on average, occurring in up to 32% of patients, and even higher in women. 33253848 Side effects appear to occur according to the following timeline:
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Mean Time to Development (Range) | Adverse Effect | Management Options |
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1 day (0-3) | Tachycardia | Beta-blockers; if persistent, refer to cardiologist |
5 days (2-7) | Lightheadedness | Taking LDOM at bedtime, getting up slowly from a lying/sitting position,
increasing fluid intake, adjusting doses of antihypertensives (by general
practitioner) |
20 days (15-20) | Headache | Simple analgesics, eg, paracetamol, nonsteroidal anti-inflammatory drugs |
60 days (45-90) | Hypertrichosis | Hair removal methods (laser, shaving, plucking, bleaching, waxing) |
60 days (45-90) | Fluid Retention/Edema | Limiting salt intake; diuretics, eg, furosemide (in males and females) and
spironolactone (in females) |
90 days | Insomnia | Sleep strategies/relaxation, pharmacotherapy (by general practitioner) |
Modified from 33639244.
Oral minoxidil treatment for hair loss: A review of efficacy and safety. J Am Acad Dermatol. 2021. PMID: 32622136.
SUMMARY: summarizes efficacy over a number of studies but does not quote a range of percent efficacy which was disappointing. Looked at efficacy for a variety of types of hair loss. Cited concomitant use of spironolactone and sodium chloride supplementation to reduce edema as a side effect.
Safety of low-dose oral minoxidil for hair loss: A multicenter study of 1404 patients. J Am Acad Dermatol. 2021. PMID: 33639244.
SUMMARY: 1404 patients (67.2% women) treated for any type of alopecia. Adverse effects: hypertrichosis (15.1%), lightheadedness (1.7%), fluid retention (1.3%), tachycardia (0.9%), headache (0.4%), periorbital edema (0.3%), and insomnia (0.2%). No life-threatening adverse effects. 1.7% of patients discontinued treatment owing to adverse effects, most commonly hypertrichosis.
Adverse effects of low-dose oral minoxidil for androgenetic alopecia in 435 patients. J Am Acad Dermatol. 2021. PMID: 33253848.
SUMMARY: letter reviewing AEs in use of oral minoxidil in 435 patients. This study reported higher rates of AEs than other similar studies looking at AEs to oral minoxidil.
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In patients taking concurrent BP meds: it does not appear that the addition of low dose oral minoxidil (majority of doses at 2.5mg or less) in patients with hypertension taking other BP meds impacts BP or heart rate. (39069264)
Melatonin
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Topical:
Topical melatonin for treatment of androgenetic alopecia. Int J Trichology. 2012. PMID: 23766606.
METHODS: One pharmacodynamic study on topical application of melatonin (0.0033% solution) and four clinical pre-post studies were performed in patients with androgenetic alopecia or general hair loss and evaluated by standardised questionnaires, TrichoScan, 60-second hair count test and hair pull test.
RESULTS: Five clinical studies showed postiive effects of a topical melatonin solution in the treatment of AGA in men and women while showing good tolerability: (1) Pharmacodynamics under once-daily topical application in the evening showed no significant influence on endogenous serum melatonin levels. (2) An observational study involving 30 men and women showed a significant reduction in the degree of severity of alopecia after 30 and 90 days (P < 0.001) based on questionnaires completed by investigators and patients. (3) Using a digital software-supported epiluminescence technique (TrichoScan) in 35 men with AGA, after 3 and 6 months in 54.8% to 58.1% of the patients a significant increase of hair density of 29% and 41%, respectively was measured (M0: 123/cm(2); M3: 159/cm(2); M6: 173/cm(2);) (P < 0,001). (4) In 60 men and women with hair loss, a significant reduction in hair loss was observed in women, while hair loss in men remained constant (P < 0.001). (5) In a large, 3-month, multi-center study with more than 1800 volunteers at 200 centers, the percentage of patients with a 2- to 3-fold positive hair-pull test decreased from 61.6% to 7.8%, while the percentage of patients with a negative hair-pull test increased from 12.2.% to 61.5% (P < 0.001). In addition, a decrease in seborrhea and seborrheic dermatitis of the scalp was observed.
Melatonin increases anagen hair rate in women with androgenetic alopecia or diffuse alopecia: results of a pilot randomized controlled trial. Br J Dermatol. 2004. PMID: 14996107.
METHODS: A double-blind, randomized, placebo-controlled study was conducted in 40 women suffering from diffuse alopecia or androgenetic alopecia. A 0.1% melatonin or a placebo solution was applied on the scalp once daily for 6 months.
RESULTS: Melatonin led to a significantly increased anagen hair rate in occipital hair in women with androgenetic hair loss compared with placebo (n=12; P=0.012). For frontal hair, melatonin gave a significant increase in the group with diffuse alopecia (n=28; P=0.046). The occipital hair samples of patients with diffuse alopecia and the frontal hair counts of those with androgenetic alopecia also showed an increase of anagen hair, but differences were not significant. Plasma melatonin levels increased under treatment with melatonin, but did not exceed the physiological night peak.
Platelet Rich Plasma
Platelet-rich plasma lacks evidence of clinically significant improvement in androgenetic alopecia. J Am Acad Dermatol. 2021. PMID: 33253851.
SUMMARY: Viewpoint by the great Michael Bigby making a case that PRP does not lead to clinically meaningful results. Provides table of 9 RCTs.
The effect of platelet-rich plasma on female androgenetic alopecia: A randomized controlled trial. J Am Acad Dermatol. 2020. PMID: 32649961.
RESULTS: Blinded global photographic assessment indicated that 57% of patients receiving PRP versus 7% of patients receiving saline improved at week 24 from baseline (P < .01). Compared to baseline, there was improvement in mean density in the PRP group versus the placebo group at week 8 (+71.1 vs -26.7 hairs/cm2; P < .01) and week 24 (+105.9 vs -52.4 hairs/cm2; P < .01). Compared to baseline, there was improvement in mean caliber in the PRP group versus the placebo group at week 8 (+0.0043 vs -0.0034 mm; P < .01) and week 24 (+0.0053 vs -0.0060 mm; P < .01). Adverse effects included headache, scalp tightness, swelling, redness, and postinjection bleeding.
Finasteride
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There are some concerns that finasteride, particularly in younger patients (33175100), may increase rates of suicidality and other psychological adverse events. However, the association is not clear cut. Similar suicidality and psychological adverse event signals were not seen in patients using minoxidil for alopecia, finasteride for BPH, older patients (>45yo) using finasteride, or patients using tamsulosin for BPH. Nor was a signal seen for patients using dutasteride. One would expect given mechanistic similarities between finasteride and dutasteride that the same side effect would be observed. This raises the question of possible reporting bias. 33175100
Dutasteride
The importance of dual 5alpha-reductase inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride. J Am Acad Dermatol. 2006. PMID: 17110217.
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416 men randomized to dutasteride 0.05, 0.1, 0.5, and 2.5mg per day, finasteride 5mg per day, or placebo.
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Outcome measures were done at 12 and 24 weeks and were: hair counts, visual grading of photographs on a 7 point 2-sided scale (-3 to 3, 0 = no change), subject assessment on a 3 point scale, and assessment via Hamilton-Norwood scale. There were 2 visual grading assessments that were similar, but one by a "panel of experts" and one by "investigators". It is not clear to me the difference.
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RESULTS: majority of benefit of all treatments were seen at 12 weeks, with additional improvement at 24 weeks.
Hair Counts
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Increases in hair counts at 24 weeks: dutasteride 0.1/0.5/2.5mg = 78.5/94.6/109.6, finasteride 5mg = 75.6, placebo = -32.3. Importantly, average baseline hair counts were 938.5, so these changes only represent at best an ~12% increase.
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Hair count change was correlated with change in scalp DHT levels from baseline.
Self assessment
Table IV. Percentage of men with improvement in scalp hair after 24 weeks according to answers to a self-assessment questionnaire
Placebo Dutasteride Finasteride
0.05/0.1/0.5/2.5mg 5.0 mg
Size of vertex spot 31 58*/57*/52*/69* 61*
Hair loss on top of scalp 29 55*/52/40/63* 51*
Bitemporal recession 16 28/27/18/31* 39*
Hair shedding 47 67*/63/56/74* 64*
Hair quality 36 47/47/45/60* 57*
Overall satisfaction 42 58/57/56/72* 61*
*P < .05 compared with placebo, based on the overall distribution of answers (improved, no change, worse).
Scalp DHT and Testosterone Levels
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Scalp DHT Levels (decreases): Finasteride 5mg / dutasteride 0.5mg / dutasteride 2.5mg = 41% / 51% / 79%
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Scalp Testosterone Levels (increases): Finasteride 5mg / dutasteride 0.5mg / dutasteride 2.5mg = 23% / 99% / 222%
Serum DHT and Testosterone Levels
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Serum DHT Levels (decreases): Finasteride 5mg / dutasteride 0.5mg / dutasteride 2.5mg = 73% / 92% / 96%
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Levels returned to baseline or near baseline in all groups by 36wks except dutasteride 2.5mg
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Serum Testosterone Levels (increases): Finasteride 5mg / dutasteride 0.5mg / dutasteride 2.5mg = 10% / 24% / 27.5
Side Effects
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Decreased libido, ejaculation disorders, and impotence were assessed.
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No noticeable difference in impotence (most frequent in placebo group)
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Decreased libido was noticeably higher in dutasteride 2.5mg group (13%) vs 0.5mg or finasteride 5mg (1%, 4%, resp.)
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Ejaculation disorders were more common in most treatment groups than placebo, but there did not appear to be a dose depepndent of medication dependent effect.
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Safety and Tolerability of the Dual 5-Alpha Reductase Inhibitor Dutasteride in the Treatment of Androgenetic Alopecia. Ann Dermatol. 2016. PMID: 27489426.
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712 patients 18-41yo given dutasteride 0.5mg, average time of exposure 204.7 days. Side effects were infrequent: libido decrease 1.3%, dyspepsia 1.1%, fatigue 0.7%, sexual function abnormality 0.6%, gynecomastia 0.3%, ejaculation disorder 0.1%.
A randomized, active- and placebo-controlled study of the efficacy and safety of different doses of dutasteride versus placebo and finasteride in the treatment of male subjects with androgenetic alopecia. J Am Acad Dermatol. 2014. PMID: 24411083.
Marked suppression of dihydrotestosterone in men with benign prostatic hyperplasia by dutasteride, a dual 5alpha-reductase inhibitor. J Clin Endocrinol Metab. 2004. PMID: 15126539.
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1. Roberts JL, Whiting D, DeViUez R, et al. Clinical dose ranging studies with finasteride, a type 2 5cz-reductase inhibitor, in men with male pattern hair loss. Published online 1999:9.
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2. Clark RV, Hermann DJ, Cunningham GR, Wilson TH, Morrill BB, Hobbs S. Marked Suppression of Dihydrotestosterone in Men with Benign Prostatic Hyperplasia by Dutasteride, a Dual 5α-Reductase Inhibitor. The Journal of Clinical Endocrinology & Metabolism. 2004;89(5):2179-2184. doi:10.1210/jc.2003-030330
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4. Tsukamoto T, Endo Y, Narita M. [Assessment of recommended dose of dutasteride on Japanese men with benign prostatic hyperplasia: a randomized, double-blind, placebo-controlled, parallel-group, dose response study]. Hinyokika Kiyo. 2009;55(4):209-214.
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5. Bhasin S, Travison TG, Storer TW, et al. Effect of Testosterone Supplementation With and Without a Dual 5α-Reductase Inhibitor on Fat-Free Mass in Men With Suppressed Testosterone Production: A Randomized Controlled Trial. JAMA. 2012;307(9):931-939. doi:10.1001/jama.2012.227
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8. Almudaimeegh A, AlMutairi H, AlTassan F, AlQuraishi Y, Nagshabandi KN. Comparison between dutasteride and finasteride in hair regrowth and reversal of miniaturization in male and female androgenetic alopecia: a systematic review. Dermatol Reports. Published online April 12, 2024. doi:10.4081/dr.2024.9909
Botulinum Toxin
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Botulinum toxin does not appear effective for androgenic alopecia. (39047987)
SCARRING ALOPECIA
ETIOLOGY/PATHOGENESIS
Risk Factors
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Sunscreens: no data that sunscreen use leads to frontal fibrosing alopecia.
Sunscreen and frontal fibrosing alopecia: A review. J Am Acad Dermatol. 2020. PMID: 31654665.
CONCLUSION: There is insufficient evidence to establish a direct causal relationship between sunscreen and FFA.
Risk factors for frontal fibrosing alopecia: A case-control study in a multiracial population. J Am Acad Dermatol. 2021. PMID: 32835739.
RESULTS: When adjusted by sex, age, menopause, and skin color, FFA was associated with hair straightening with formalin (odds ratio [OR], 3.18), use of ordinary (nondermatologic) facial soap (OR, 2.09) and facial moisturizer (OR, 1.99), thyroid disorders (OR, 1.69), and rosacea (OR, 2.08). Smokers (OR, 0.33) and users of antiresidue/clarifying shampoo (OR, 0.35) presented a negative association with FFA. There was no association with the use of sunscreen.
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Contact Allergens
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A cohort of 42 patients with LPP or FFA were tested for relevant contact allergens (+1 reaction plus and the agent was present in the patient's personal care products). Gallates (dodecyl, octyl, propyl gallate), which are preservatives added to products to prevent microbial growth, were the most common reaction found (26.2%). Fragrance mixes (I and II) and linalool, a ubiquitous fragrance chemical, were also very common (both 19%). Other common contact allergens found were ammonium persulfate (14.3%), benzophenone 4 (14.3%), MI/MCI (11.9%), propolis (9.5%), benzoyl peroxide (9.5%), and balsam of peru (7.1%). 31962088, Table.
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TREATMENT
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An algorithmic approach to treating FFA can be found here.
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Delphi consensus for CCCA treatment can be found here.
Metformin
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500mg extended released metformin seemed to improve hair growth in 6 of 12 patients treated. This was a retrospective review, and patients were on multiple other treatments that could have contributed to this finding. (39230880)
TRACTION ALOPECIA
ETIOLOGY/PATHOGENESIS
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A variant of traction alopecia dubbed "acquired diffuse trichomalacia (ADT)" can be caused by the use of detangling brushes. They mention that corkscrew hairs, which are thought to be highly specific for tinea capitis, are observed in this condition. Given the tensile stress is relatively limited, resolution of alopecia may be slow as the hair follicle may remain in anagen phase and continue to produce corkscrew hairs. (36920357)