Female pattern loss

Linda Chan, David K Cook APPROXIMATELY 49% of women will be host of underlying or contributing medical affected by throughout their and psychiatric conditions. All causes , with female of , such as ovarian Background (FPHL) being the most common cause of or adrenal tumours, polycystic ovarian Female pattern hair loss (FPHL) is female alopecia.1 The incidence steadily syndrome and adrenal hyperplasia, can a commonly encountered clinical increases with age in all ethnicities, and induce rapid hair loss in women. The presentation in primary care. Patterned hair loss in women is characterised the age-adjusted prevalence among adult diagnosis of FPHL is associated with by diffuse hair thinning and often Australian women of European descent underlying hypertension in women aged becomes an ongoing cause of is >32%.1–4 This translates to 800,000 ≤35 years and psychosocial distress. women who suffer from moderate-to- in women aged ≤50 years.7 One study severe FPHL.4 Alopecia is associated with found that patterned hair loss was an Objectives significant psychological distress and independent predictor of mortality from The aim of this article is to present a practical approach for the clinical reduced quality of . In one survey, 40% mellitus and heart disease in assessment of female hair loss and of women experienced marital problems both females and males.7–9 Screening to review the up-to-date treatment and 64% had career difficulties that they for metabolic cardiovascular risk factors modalities. ascribed to their hair loss.5 Alopecia can is useful in patients presenting with also be the first symptom of underlying patterned hair loss.3,10 Discussion Alopecia can be the first symptom of systemic illness within the primary 1,6 systemic illness. It is therefore crucial care setting. Risk factors for the primary care to be FPHL is a non-scarring alopecia able to differentiate between FPHL characterised by progressive transformation The risk factors for FPHL include increasing and more concerning causes of hair of thick, pigmented into age, family history, smoking, elevated loss. Treatment options often involve short, thin, non-pigmented villous hair. fasting glucose levels and light a combination of non-androgenic This undesired process is known as hair exposure of >16 hours/week.8 and androgenic therapy. The use of 1,3,5,6 oral in combination with follicle miniaturisation. The trigger oral is a novel therapy for miniaturisation remains unclear Psychological morbidity with promising results. The role of but is postulated to be a combination the general practitioner is paramount of genetic predisposition, FPHL is less well understood and accepted in establishing the diagnosis, setting influence and other not yet elucidated by society than alopecia in males. This achievable therapeutic goals and factors. exert their effect on generates feelings of greater confusion navigating the psychosocial comorbidity hair via circulating levels of , and distress for female patients. A study associated with this . which is produced in females by the showed that 52% of women were very- ovaries and adrenal glands. The free to-extremely upset by their hair loss, testosterone either binds to intracellular compared with 28% of men.1 In another androgen receptors in the hair bulb, questionnaire, 70% of surveyed women causing follicular miniaturisation, or is with hair loss had a negative metabolised by 5-alpha reductase and poorer self-esteem, with poorer into (DHT). DHT sleep, feelings of guilt and restriction and testosterone both bind to the same of social activities.3 Clinicians should androgen receptors, but DHT does so also screen for maladaptive coping with more affinity, leading to increased mechanisms such as compulsive fixing miniaturisation.3,5,6 of one’s hair and underlying psychiatric .1,10,11 Female pattern hair loss and general health Assessment

As alopecia is highly visible, a patient may The diagnosis of FPHL is made on clinical note hair loss as the first symptom of a grounds.4,5

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History menopause has occured and, if so, at Treatment Classically, the pattern of alopecia which age; use of hormonal contraception; begins with hair density reduction on the fertility concerns and any previous Key points of counselling and non- mid‑frontal hairline. The anterior part gynaecological .1,3,5 A discussion pharmacological treatment options are width then widens, resulting in prominent of plans is necessary as some outlined in Figure 2. Pharmacological thinning in a Christmas tree pattern. treatments are teratogenic.1 Generalised and rapid shedding with global hair thinning is unusual and points Family history Table 1. Key features in history taking to other causes such as hyperadrenalism, Fifty-four per cent of patients have a first- and examination for detection of exposure, major stressors degree male relative of age >30 years with underlying systemic illnesses1,6,10 or change in practices.1,3,6,10,11 alopecia, and 21% have a first‑degree Hair loss over the temporal region is female relative aged >30 years with Underlying systemic diseases that may uncommon in FPHL, compared with male FPHL. An Australian gene-wide study present with alopecia pattern alopecia. If temporal thinning of Caucasian women suggested that • Virilising tumours was the first symptom, , aromatase gene CYP19A1 may contribute • Polycystic ovarian syndrome frontal fibrosing alopecia, tractional to FPHL.3 • Hyperandrogenism +/– associated alopecia and should be metabolic syndrome considered.6 Symptoms of pruritus, Examination • dysfunction burning and pain point to another General observations for body habitus, • Systemic erythematosus (SLE) • Dermatomyositis diagnosis (Table 1).6 , and acanthosis nigricans After diagnosing FPHL, concurrent should be made. Focused examination • +/– anaemia medical illnesses that exacerbate alopecia should identify the calibre of the and • Caloric restriction: anorexia/bulimia should be ruled out to improve overall the location of the affected areas. Findings • Psychiatric disorder: trichotillomania outcome. These include iron deficiency, consistent with FPHL include: • Medication/toxin exposure or ingestion , thyroid dysfunction and • loss of terminal hair in the mid-frontal • Infection: 3,11 nutritional deficiencies. Occupational scalp Red flags on history taking for history and exposure to, or ingestion of, • normal hair density in occiput regions underlying systemic illnesses toxic chemicals should be elicited.10 and preserved frontal hairline1,6 • Generalised and rapid hair shedding • miniaturised hairs: hair of various • Lateral hair loss/thinning Gynaecological history lengths and diameters in thinning • Menstrual irregularity, fertility difficulty A detailed gynaecological history is areas3,6 • Severe acne necessary to rule out hyperandrogenism, • widening of central part with diffuse • Marked hirsutism polycystic ovarian syndrome or a reduction in hair density in a Christmas • Associated cutaneous eruption virilising tumour as underlying diagnoses. tree pattern1,11 • New photosensitivity History should include age of menarche; • normal-appearing scalp • Severe fatigue details; whether • negative hair pull test: hold a bundle of • Weight changes: gain or loss 60 hairs close to the scalp between the • Fevers or chills , index and middle . The • Joint and muscle aches test is positive when more than three • Severe psychological stressors hairs can be pulled away.12 Non-classic symptoms and signs that Examination findings suggestive of underlying disorders suggest other types of alopecia are • SLE: isolated parietal alopecia, scarring outlined in Tables 1 and 2. alopecia (violaceous , follicular ), associated cutaneous malar Laboratory investigations , arthralgia Laboratory testing should be considered • Thyroid dysfunction: temporal region in patients with diffuse alopecia, signs of alopecia, lateral eyebrow hair-loss androgen excess and early-onset FPHL. • Trichotillomania: broken hair shafts Recommended tests and rationale are of variable length, diffuse and patchy outlined in Table 3. Note that testing of hair loss androgen levels needs to occur during the • Endocrinopathy: acanthosis nigricans, hirsutism, truncal acne (especially follicular phase, between the fourth and nodulocystic), high body mass index seventh days of the menstrual cycle, and Figure 1. Female pattern hair loss with • Nutritional deficiency: conjunctival Christmas tree pattern oral contraceptives should be discontinued pallor, glossitis, muscle wasting eight weeks prior to the test.1,3

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Table 2. History and examination findings of common non-scarring and scarring alopecia disorders6,10,11

Non-scarring alopecia Typical history Examination findings Hair pull (common)

Female/male pattern Age: or older No marked shedding Negative (usually) hair loss Onset: gradual Hair thinning, wider midline part of Commonly positive family history the , no bare patches, occipital region spared

Telogen effluvium Age: adults Prominent shedding Positive (if worse on Onset: abrupt – triggered by iron Global hair thinning – evenly frontal then occipital) deficiency, thyroid dysfunction, distributed throughout scalp general anaesthesia, and No bare patches

Alopecia areata Age: ≤20 years Prominent shedding Positive Onset: abrupt Well-defined bald patches – Personal or family autoimmune can be isolated or multifocal history Rarely with diffuse hair thinning (5% can have complete alopecia)

Tinea capitis Age: children Prominent shedding Positive (can have Onset: gradual/abrupt Bare patches of scalp broken hairs) Animal contact history (pets, zoos) Any area of scalp can be affected, isolated or multifocal – can have and scales

Trichotillomania Age: children/adolescents Minimal shedding Negative Onset: gradual/abrupt Fronto-temporal hair or frontal parietal Sensation of tension that is only areas affected relieved by pulling hair Irregularly shaped patches of reduced History of other psychiatric hair density with irregular borders disorders

Other common non-scarring alopecia differentials: Hypothyroidism, nutritional deficiencies, , , (syphilis)

Scarring alopecia Typical history Examination findings Hair pull

Lichen planopilaris Age: adults Variable shedding Positive Onset: gradual Bare patches and/or diffuse thinning Scalp and burning Begins in parietal scalp 50% of patients also have Perifollicular erythema and scales

Chronic cutaneous Age: young adults Variable shedding Onset: gradual/acute Parietal area with bare patches Positive (discoid lupus) Scalp itch and pain Scaly papules, erythematous and More prevalent in Caucasian women violaceous discolouration of scales, Associated systemic lupus follicular plugging and telangiectasia erythematosus 10%

Folliculitis decalvans Age: young and middle-aged adults Variable shedding Positive Onset: gradual Begins at the vertex with bald patches Scalp pain and itch Follicular papules, pustules and crusting Common in men

Other differentials for scarring alopecia: Dermatomyositis, dissecting , central centrifugal cicatricial alopecia

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management is categorised into androgen-independent (non–androgen dependent) and androgen-dependent • No current treatment will the condition – therefore, avoid paying expensive fees for unproven options. treatment • The goal of treatment is to prevent further loss of hair, Non–androgen dependent treatments although some individuals may have new hair growth Minoxidil is a piperidinopyrimidine • Clinical effect will take at least 3–6 months’ Counselling derivative and a vasodilator that is used treatment to be noticeable orally for hypertension. When applied • There may be increased shedding in the first few topically, minoxidil is effective in months of treatment as hairs transition into the arresting hair loss and producing some growth phase • Treatment needs to be continued daily, and if degree of regrowth.2 discontinued, the treatment effect will be lost Topical minoxidil is the first-line therapy for FPHL, with Food and Drug Administration approval since 1992. Non- • Shorter (generates greater volume and lift) It has been shown to stop hair loss and pharmacological • Zig-zagging part induce mild-to-moderate regrowth treatment: • Adding soft layers at the top in 60% of women.2,13 It is available hairstyling • Adding soft or light curls to add volume as a solution or foam in 2% and 5% concentrations, which show a 14% and • Using toothed /brushes to allow thin hair to 18 % increase respectively in non-vellus Non- flow through without breakage 2 hair after 48 weeks. Topical minoxidil pharmacological • Using a friction-free towel that blots moisture without has a well-established safety profile; local treatment: damaging hair irritation and are hair care • Using hair sprays that are light and non-drying to give the main side effects.2,14 Treatment needs volume and prevent breakage to be continued indefinitely. If treatment is stopped, clinical regression occurs within six months. The degree of alopecia • Camouflaging products are best suited for those with mild to moderate hair loss will return to the level that would have • Hair building fibres ( fibres in shaker bottle) occurred if there were no treatment.2 • Scalp spray thickeners (bond to hair fibres to create Non- Oral minoxidil 0.25 mg daily in density) pharmacological combination with spironolactone 25 mg • Alopecia masking (tinted lotion dabbed onto treatment: was shown to be effective in reducing thinning areas; one tube lasts 3–4 months) hair loss severity and hair shedding • Topical shading (tinted pressed powder that covers score at six months and 12 months in an thinning areas; apply with sponge tipped applicator) Australian prospective study with 100 • Oily to normal scalp – use pressed powder. women with mild-to-moderate FPHL. • Dry scalp – use cream to prevent further dryness Spironolactone was added to reduce the risk of fluid retention and augment • Topical minoxidil lotion/foam treatment response.2 Side effects in the • Spironolactone (50–200 mg/day) study were seen in eight patients: two had Pharmacological • acetate 100 mg/day (postmenopausal) or treatment postural hypotension that was controlled 50 mg/day for 10 days (premenopausal) with 50 mg sodium chloride; six patients • Oral minoxidil 0.25 mg/day + spironolactone 25 mg/day had hypertrichosis that was managed with . Two patients terminated oral minoxidil because of urticaria. There Figure 2. Summary of counselling points and treatment options1,2,10,15 were no reports of hyperkalaemia or laboratory function abnormality.2 prescribed as they have been shown to receptor activity in target tissues. It is Androgen-dependent treatments produce regrowth in 44% of patients.4 approved in Australia for the treatment blockers target Spironolactone is an aldosterone of female hirsutism. It has been used off- androgen conversion and subsequent antagonist and is used as a potassium- label for FPHL with a treatment regimen binding onto target receptors sparing diuretic. In alopecia, it acts by of 50–200 mg daily for at least six months in alopecia. Spironolactone and reducing the levels of total testosterone and shown to arrest progression in 90% of are most commonly and completely blocking androgen women and improve hair density in 30%.2

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Common side effects are lethargy and in premenopausal women who had Provenance and peer review: Not commissioned, externally peer reviewed. 14,15 menorrhagia, which improve after three associated hyperandrogenism. Conflicts of interest: None. months. This is a D medication.5,14 Conclusion Cyproterone acetate directly References blocks androgen receptor activity FPHL is a common, non-scarring 1. Dinh QQ, Sinclair R. Female pattern hair loss: and decreases testosterone levels by alopecia that affects women of all ages Current treatment concepts. Clin Interv Aging 2007;2(2):189–99. suppressing luteinising and and carries significant psychological 2. Sinclair RD. Female pattern hair loss: A pilot study follicle stimulating hormone release. morbidity. It may be the first presenting investigating with low-dose Effective dosages are 100 mg daily in complaint of hyperandrogenism, oral minoxidil and spironolactone. Int J Dermatol 2018;57(1):104–09. doi: 10.1111/ijd.13838. postmenopausal women, and 50 mg for thyroid dysfunction or chronic 3. Vujovic A, Del Marmol V. The female pattern hair 10 days in premenopausal women for deficient diet. A detailed history with loss: Review of etiopathogenesis and diagnosis. three months.4 In one study of 80 patients, appropriate laboratory testing to Biomed Res Int 2014;2014:767628. cyproterone produced similar results to screen for associated cardiovascular doi: 10.1155/2014/767628. 5 4. Rathnayake D, Sinclair R. Innovative use 200 mg daily of spironolactone. This is disease, hypertension and metabolic of spironolactone as an in a pregnancy category X medication as it syndrome is indicated. Sufficient time the treatment of female pattern hair loss. may cause feminisation of the male .14 should be dedicated to discussing Dermatol Clin 2010;28(3):611–18. doi: 10.1016/j. det.2010.03.011. Side effects include weight gain, psychological , treatment 5. Brough KR, Torgerson RR. Hormonal therapy in 5 tenderness and decreased . options and realistic treatment goals. female pattern hair loss. Int J Womens Dermatol The introduction of low-dose oral 2017;3(1):53–7. doi: 10.1016/j.ijwd.2017.01.001. 5-Alpha reductase inhibitors minoxidil is the key recent advancement 6. Levy LL, Emer JJ. Female pattern alopecia: Current perspectives. Int J Womens Health 2013;5:541–56. Although 5-alpha reductase inhibitors in the management of this challenging doi: 10.2147/IJWH.S49337. have revolutionised the treatment of condition. 7. Su LH, Chen LS, Lin SC, Chen HH. Association male pattern alopecia, their use in FPHL of androgenetic alopecia with mortality from is limited because of lack of and Authors diabetes mellitus and heart disease. JAMA Dermatol 2013;149(5):601–06. doi: 10.1001/ Linda Chan MBBS, Senior Medical Resident Officer, the teratogenic potential (pregnancy jamadermatol.2013.130. Concord Repatriation General Hospital, Sydney Local category X).5 A dose of Health District, NSW. [email protected] 8. Su LH, Chen LS, Chen HH. Factors associated 1 mg daily was no better than placebo David K Cook MBBS, FACD, Consultant with female pattern hair loss and its prevalence in Taiwanese women: A community-based survey. J in treating FPHL in postmenopausal Dermatologist at Concord Repatriation General Hospital, Clinical Senior Lecturer – The Sydney Am Acad Dermatol 2013;69(2):e69–77. women and was only mildly efficacious University Concord Clinical School, NSW doi: 10.1016/j.jaad.2012.09.046.

Table 3. Laboratory tests in hair loss evaluation1,3,10,11

Patient characteristics Underlying disorder Investigation

Menstrual irregularity, dysmenorrhea, (Endocrine screen) Androgen index test severe acne and marked hirsutism Hyperandrogenism level Ovarian hyperandrogenism sulfate (DHEA-S) Adrenal hyperandrogenism and 17-hydroprogesterone (17-OH)

Obesity, hirsutism, menstrual irregularity, Associated metabolic syndrome Fasting blood level severe acne and confirmed female pattern Fasting profile hair loss monitoring

Marked temporal region thinning and Thyroid dysfunction related hair loss Thyroid function test, thyroid antibodies lateral eyebrow loss

Arthralgia/myalgia Systemic lupus erythematosus, Erythrocyte sedimentation rate, rheumatoid autoimmune disorders factor, autoantibody tests

Rapid and diffuse hair shedding in a Alopecia syphilitica Non-treponemal and treponemal antigen sexually active individual testing

Lymphadenopathy Scalp fungal scrapings for culture and

Rapid and diffuse hair shedding, low body Nutritional deficiency Iron studies and full blood count mass index

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9. Arias-Santiago S, Gutiérrez-Salmerón MT, Buendía-Eisman A, Girón-Prieto MS, Naranjo- Sintes R. Hypertension and aldosterone levels in women with early-onset androgenetic alopecia. Br J Dermatol 2010;162(4):786–89. doi: 10.1111/j.1365- 2133.2009.09588.x. 10. Ahanogbe I, Gavino AC. Evaluation and management of the hair loss patient in the primary care setting. Prim Care 2015;42(4):569–89. doi: 10.1016/j.pop.2015.07.005. 11. Mubki T, Rudnicka L, Olszewska M, Shapiro J. Evaluation and diagnosis of the hair loss patient: Part I. History and clinical examination. J Am Acad Dermatol 2014;71(3):415.e1–e15. doi: 10.1016/j. jaad.2014.04.070. 12. McDonald KA, Shelley AJ, Colantonio S, Beecker J. Hair pull test: Evidence-based update and revision of guidelines. J Am Acad Dermatol 2017;76(3):472– 77. doi: 10.1016/j.jaad.2016.10.002. 13. van Zuuren EJ, Fedorowicz Z, Schoones J. Interventions for female pattern hair loss. Cochrane Database Syst Rev 2016;(5):CD007628. doi: 10.1002/14651858.CD007628.pub4. 14. Atanaskova Mesinkovska N, Bergfeld WF. Hair: What is new in diagnosis and management? Female pattern hair loss update: Diagnosis and treatment. Dermatol Clin 2013;31(1):119–27. doi: 10.1016/j.det.2012.08.005. 15. Rogers NE, Avram MR. Medical treatments for male and female pattern hair loss. J Am Acad Dermatol 2008;59(4):547–66; quiz 567–68. doi: 10.1016/j.jaad.2008.07.001.

correspondence [email protected]

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