Alopecia & Hair Disorders

Meet the patient

A 35-year-old man has watched his temples recede and his crown thin for five years; his father and maternal grandfather are both bald. He wants to know whether anything works. The next patient, a 58-year-old woman, has noticed her frontotemporal hairline quietly retreating for two years and her eyebrows thinning — and on close inspection the skin along the hairline is smooth and shiny, with no follicular openings.^[1]

The man has androgenetic alopecia (non-scarring, reversible only while treated); the woman has frontal fibrosing alopecia (scarring, irreversible once lost). The single skill that earns marks on both is the bedside branch-point — are the follicular openings preserved or gone? Everything below is built around that question.^[1][6]

The pivotal branch-point — scarring or non-scarring

Make this call at the bedside before any test. Non-scarring alopecia preserves the follicle: the follicular ostia (openings) remain visible and, if the cause is removed or treated, hair can regrow. Scarring (cicatricial) alopecia destroys the follicle — the stem cells at the bulge region and the sebaceous gland are obliterated and replaced by fibrosis, the openings vanish, the scalp becomes smooth and shiny, and the loss is permanent.^[1]

The clinical implication is direct: non-scarring disease can be reversed; scarring disease can only be halted. Every day of untreated active scarring inflammation destroys more follicles that will never return — hence the dictum "biopsy early in any scarring-looking alopecia."^[1][7]

^[1]

The hair cycle — the clock every alopecia breaks

Every follicle cycles continuously: anagen (active growth, 2 to 7 years, 85 to 90 percent of scalp hairs) → catagen (regression, about 2 weeks) → telogen (resting, about 3 months, 10 to 15 percent) → exogen (shedding). Normal daily loss is 50 to 100 hairs. Each alopecia disturbs this cycle in a characteristic way, and knowing how is half the viva.^[1]

• Anagen disorders — androgenetic (anagen progressively shortens → miniaturisation), alopecia areata (T cells attack anagen follicles), anagen effluvium (chemotherapy poisons the anagen matrix).
• Catagen/telogen shift — telogen effluvium (a trigger throws follicles prematurely into telogen).

^[1]

Androgenetic alopecia — DHT and miniaturisation

Testosterone is converted to dihydrotestosterone (DHT) by 5-alpha-reductase type II within the dermal papilla. DHT binds the intracellular androgen receptor, and on genetically susceptible scalp follicles the net effect is a shortening of anagen and a progressive decrease in hair-shaft diameter — the miniaturisation that turns thick terminal hairs into fine vellus hairs. Follicles over the bitemporal and vertex scalp are most androgen-sensitive, while the occipital scalp is androgen-independent — which is why the occiput is the donor site for hair transplantation.^[1][11]

This immediately explains the two pharmacological anchors of therapy: oral finasteride 1 mg daily — a type II 5-alpha-reductase inhibitor that lowers serum and scalp DHT and, over two years of randomised treatment in 1553 men with pattern hair loss, slowed progression and increased hair growth — and topical minoxidil (FDA-approved for AGA as 5 percent solution or foam and 2 percent solution), which may affect the length of the anagen and telogen phases. Both demand prolonged, continuous use: sustained benefit is a prerequisite of ongoing therapy, not a one-time course.^[13][2][14]

Men — the Hamilton-Norwood scale (types I to VII). The earliest definite change is type II (small bitemporal recession). Type III is the clinical threshold of baldness; type III vertex adds a balding vertex. Types IV to V show progressive recession and a growing vertex bald spot separated by a band of hair. Type VI merges the two areas; type VII leaves a narrow horseshoe over the occiput. The occipital donor area is preserved in every type.^[1]

Women — the Ludwig (Savin) scale (grades I to III). Diffuse thinning over the crown with widening of the central hair part, preservation of the frontal hairline, and a characteristic "Christmas-tree" anterior taper. A receding hairline does not occur in classical Ludwig — if a woman has one, suspect frontal fibrosing alopecia, traction, or virilisation.^[1][6]

^{[1] [13] [15] [2]}

AGA is the commonest cause of hair loss in both sexes — roughly 50 percent of Caucasian men by age 50, rising to 80 percent by 70, and around 50 percent of women by age 80. It is polygenic (the androgen receptor gene lies on the X chromosome, explaining the strong maternal-line influence), and associates with smoking, insulin resistance and metabolic syndrome.^[1][11]

Alopecia areata — collapse of immune privilege

AA is a T-cell-mediated autoimmune attack on anagen follicles. The anagen bulb normally enjoys immune privilege — low MHC class I/II expression shields it from autoimmune attack. In AA that privilege collapses: follicles upregulate MHC and present autoantigens (notably melanocyte-derived peptides, which is why AA targets pigmented hairs and may spare grey ones). Autoreactive CD8+/NKG2D+ T cells infiltrate the peribulbar region and attack the anagen follicle, sustained by an IFN-γ/IL-15 axis signalling through JAK-STAT.^[3][12]

The follicle is shocked into catagen but not destroyed, which is why regrowth is always possible — and why JAK inhibitors, which block the central amplification loop, work so dramatically. The lifetime prevalence is about 2 percent; onset peaks in childhood and young adulthood, sex incidence is roughly equal, and AA travels with autoimmune thyroid disease, vitiligo, atopy, type 1 diabetes, IBD and Down syndrome.^[1][5]

The signature is a well-circumscribed, perfectly smooth, hairless patch with preserved follicular ostia. At the advancing margin sits the exclamation-mark (cadaverised) hair — broken 3 to 4 mm above the scalp, tapered proximally, broader distally. Nail involvement (fine geometric pitting, trachyonychia, onycholysis) occurs in 10 to 30 percent and flags more severe disease.^[1][12]

The severity spectrum carries the prognosis. Patchy AA regrows spontaneously in 30 to 50 percent within 6 to 12 months. Ophiasis (band-like occipitotemporal loss, from Greek ophis, snake) is more refractory. Alopecia totalis is loss of the entire scalp; alopecia universalis is loss of all body hair, the most refractory form (under 5 percent spontaneous regrowth). The rare Marie Antoinette syndrome — overnight greying — reflects selective loss of pigmented anagen hairs.^[1][12]

Telogen and anagen effluvium — the shedders

Telogen effluvium (TE) is diffuse shedding two to three months after a systemic trigger. Pregnancy (post-partum is classic), severe illness, surgery, febrile illness (including dengue, malaria, COVID-19), crash dieting or rapid weight loss, iron deficiency, thyroid dysfunction, severe emotional stress, and drugs (retinoids, anticoagulants, anticonvulsants, beta-blockers, ACE inhibitors) all shift an abnormally large cohort of follicles simultaneously into telogen. Two to three months later — the duration of telogen — they synchronously shed.^[8]

The patient describes hair "coming out in handfuls" — in the shower, on the pillow, in the brush — but there are no patches and the hairline is preserved. The pull test is positive in active shedding. TE is self-limiting within six months of removing the trigger; chronic TE (more than six months, middle-aged women, described by Whiting) is treated supportively with a minoxidil trial.^[8]

Anagen effluvium is overwhelmingly iatrogenic — cytotoxic chemotherapy arrests the rapidly dividing matrix cells, the shaft narrows to a fragile Pohl-Pinkus constriction, and it fractures within one to two weeks of the dose. Scalp cooling (cold cap) during chemotherapy reduces the cytotoxic effect by vasoconstriction; begun before and continued through and after infusion. Hair recovers one to three months after cessation, sometimes with a change in texture ("chemo curl").^[1]

Traction, trichotillomania, tinea — the patterned non-scarring

Traction alopecia produces frontotemporal and vertex-margin loss along the line of tension of tight braids, ponytails, buns, extensions, weaves and rollers; perifollicular erythema along the hairline is a "traction sign." Early traction is reversible; chronic traction scars permanently. Trichotillomania (an obsessive-compulsive-spectrum disorder) produces bizarre, irregular patches with hairs broken at varying lengths on an otherwise normal scalp; perifollicular pitting and haemorrhage may be seen, and psychiatric comorbidity is common.^[1]

In children, tinea capitis is the commonest cause of patchy hair loss — and it is the one you must not mistake for AA. Look for black-dot tinea (broken shafts flush with the scalp), grey-patch scaling, cervical lymphadenopathy, and kerion: a boggy, tender, pustular, inflammatory mass that is a hypersensitivity reaction to the dermatophyte, not a bacterial abscess — treated with oral antifungal plus corticosteroid, not antibiotics alone. KOH and fungal culture are positive.^[1]

Scarring alopecia — the goal is to halt, not reverse

Across all scarring alopecias, look for the trio: perifollicular erythema and hyperkeratosis (the activity marker), loss of follicular ostia (smooth, shiny scalp — the irreversibility marker), and patches of complete baldness. The inciting inflammation differs by subtype, but the shared end-point is destruction of follicular stem cells replaced by fibrosis — so lost follicles never regrow.^[6][7]

^{[6] [7] [9] [10] [11]}

The classic trap: any smooth, shiny, ostia-free patch must be biopsied — treating scarring as non-scarring loses follicles irreversibly. The single most important distinction in all of hair loss is this one.^[7]

The bedside exam — three tests and the trichoscope

Diagnosis is overwhelmingly clinical, supported by trichoscopy. Take a meticulous history — onset and rate (sudden TE versus gradual AGA), pattern, recent triggers in the last three months (illness, surgery, pregnancy, weight loss, drugs, stress), hairstyle practices, family history, autoimmune and thyroid history, drug history, and the psychological impact (use a DLQI or HADS).^[1]

Trichoscopy is first-line and often diagnostic. Androgenetic shows hair diameter diversity over 20 percent (the key threshold) and more than four yellow dots per cm². Alopecia areata shows yellow dots, black dots, exclamation-mark hairs and short vellus regrowth. Telogen effluvium shows upright regrowing hairs but uniform diameter — the contrast with AGA. Tinea shows comma and corkscrew hairs. Scarring shows loss of follicular openings, perifollicular scaling and white fibrosis.^[1]

Investigations — when to test and when to biopsy

Most non-scarring alopecia needs no investigation beyond clinical exam and trichoscopy. Tests are reserved for diffuse, uncertain or scarring presentations. For diffuse loss (especially in women and TE): ferritin (target at least 70 ng/mL for optimal cycling), TSH (both hypo- and hyperthyroidism cause TE), vitamin D, zinc, B12 and folate, CBC and CRP; and in women with AGA plus hirsutism, acne or oligomenorrhoea, total and free testosterone, DHEAS, LH, FSH, prolactin and 17-OH-progesterone to exclude PCOS. ANA if lupus is suspected.^[1]

A 4 mm punch biopsy (ideally two samples from the active edge) is mandatory for any scarring alopecia, any uncertain diagnosis, and any non-response to therapy. Horizontal sectioning allows follicular counts and the anagen-to-telogen ratio (normal at least 8 to 1) — the most informative single investigation for diffuse disease. KOH preparation and fungal culture is indicated for any child with patchy hair loss, black-dot, scaling or kerion.^[7]

The SALT (Severity of Alopecia Tool) score — percentage scalp hair loss graded 0 to 100 — is the standard outcome measure in AA trials; SALT of 20 or less is the conventional treatment target in JAK inhibitor trials.^[3][4]

Management — the resuscitation moments

Alopecia is rarely a physiological emergency, but several situations demand prompt action. A kerion in a child — the boggy, pustular inflammatory mass of tinea capitis — needs systemic antifungal therapy without delay: griseofulvin 20 to 25 mg/kg/day (typically for around 8 weeks, as treatment failures rise at lower doses); a 2-to-4-week terbinafine course performs at least as well for Trichophyton infection, while griseofulvin remains preferable for Microsporum. Because corticosteroids for kerion are controversial, reserve a short oral burst for the most severe disease. Mismanagement scars.^[16][17]

Active scarring alopecia — every day of untreated inflammation destroys more follicles permanently. Start a high-potency topical or intralesional corticosteroid immediately and arrange an urgent biopsy and dermatology referral; do not wait weeks for clinic. Severe psychological distress or suicidal ideation (especially in young women with severe AA) — acknowledge the impact, screen with PHQ-9, offer psychological support, and expedite systemic therapy. Uncovered systemic disease in TE (severe iron-deficiency anaemia, hypothyroidism) — treat the cause.^[1][5]

Management — definitive and stepwise

^[1]

Therapy is entirely subtype-specific. There is no role for long-term systemic corticosteroids in most alopecias — they work short-term, relapse on taper, and accumulate toxicity.^[1]

Androgenetic alopecia — men

^{[1] [2] [13] [20] [21]}

Androgenetic alopecia — women

Topical minoxidil is first-line — in pooled randomised trials, women on minoxidil reported moderate-to-marked hair regrowth more often than on placebo, with no clear efficacy advantage of 5 percent over 2 percent. Oral finasteride is avoided in women of childbearing potential because of antiandrogenic fetal risk; antiandrogens such as spironolactone (always with reliable contraception) are options for women with hyperandrogenism, though randomised evidence remains limited. Always rule out PCOS if hirsutism, acne or oligomenorrhoea coexist.^[15][2][11]

Alopecia areata — the stepwise ladder

^{[1] [3] [4]}

Relapse after stopping JAK inhibitors is the rule, not the exception — in real-life cohorts even patients with complete regrowth relapsed after discontinuation, so these are chronic maintenance therapies, not cures.^[22][5]

Telogen and anagen effluvium

Identify and remove the trigger. Correct iron deficiency (oral ferrous sulphate until ferritin is at least 70 ng/mL), treat hypothyroidism with levothyroxine, review drugs, and reassure — TE is self-limiting, regrowing within six months. For anagen effluvium, scalp cooling pre-, intra- and post-infusion; reassure that regrowth occurs within one to three months, and provide wig or prosthesis and psychological support.^[1][8]

Traction, trichotillomania, tinea

Traction — stop the offending hairstyle early: recognising traction alopecia at its reversible stage and counselling on looser styles prevents permanent scarring loss. Trichotillomania — cognitive-behavioural therapy is first-line, with the strongest support for habit-reversal training; among drugs, clomipramine has been the most effective in trials (SSRIs are commonly prescribed despite weaker evidence). Tinea capitis is always oral — griseofulvin 20 to 25 mg/kg/day (around 6 to 8 weeks) remains the reference standard, while a 2-to-4-week terbinafine course is at least as effective for Trichophyton infection; adjunctive sporicidal shampoo such as selenium sulphide helps reduce shedding and spread.^{[19][18][16][17]}

Special populations

Children: weight-based dosing for all systemic therapy; oral antifungal is mandatory for tinea capitis; minoxidil is generally avoided prepubertally; intralesional corticosteroid is safe in small doses; address the psychological impact of visible AA. Pregnancy and breastfeeding: avoid finasteride, dutasteride and systemic retinoids; topical minoxidil is not recommended; topical and intralesional corticosteroids are safe; post-partum TE is common and self-limiting — reassure.^[1]

Menopause: FFA and female pattern loss predominate; 5-alpha-reductase inhibitors are now widely used in postmenopausal FFA and CCCA; check bone density with long-term systemic corticosteroid. Immunosuppressed (HIV, transplant, chemotherapy): rule out infection (tinea, atypical mycobacteria, syphilis) and biopsy early; JAK inhibitors are relatively contraindicated in significant immunosuppression. Black patients: CCCA, traction alopecia and acne keloidalis nuchae predominate; take a culturally sensitive history of hair practices (braids, weaves, extensions, relaxers, heat).^[6][9]

Complications and pitfalls

The psychological burden is substantial across all types — depression, anxiety, low self-esteem, social withdrawal, and in severe AA, suicidal ideation. DLQI scores in AA parallel those of severe psoriasis; always screen and offer psychological support.^[5][12]

Permanent irreversible loss is the dominant complication of scarring alopecia and of late-stage traction or late-diagnosed CCCA. Squamous cell carcinoma may arise in chronic discoid lupus scars (Marjolin-type) — biopsy any non-healing ulcer. Minoxidil causes initial shedding in the first 2 to 8 weeks (reassure; do not stop), facial hypertrichosis in women on 5 percent, and contact dermatitis from the propylene glycol vehicle (switch to foam). Finasteride drops PSA by about 50 percent — multiply measured PSA by 2 for the prostate-cancer threshold — and is strictly contraindicated in pregnancy.^[2][11]

^[1]

Evidence and regional differences

The JAK inhibitor class is the modern landmark. BRAVE-AA1 and BRAVE-AA2 (NEJM 2022) established baricitinib as the first FDA-approved systemic therapy for severe AA; ALLEGRO (Lancet 2023) showed ritlecitinib is the first JAK inhibitor approved for adolescents aged 12 and over; a 2023 JAAD review summarises the class. Cochrane and comprehensive reviews confirm modest efficacy of finasteride and minoxidil, with combination superior to either alone and dutasteride more potent than finasteride. The EADV 2026 task force published a stepwise consensus for LPP; the Miguel-Gómez multicentre series underpins the rifampicin-plus-clindamycin regimen for folliculitis decalvans; and Whiting's classic descriptions of chronic TE remain definitive.^{[2][3][5][7][8][10]}

^[1]

Ward-round test

^[1]

1. A 40-year-old man has bitemporal recession and vertex thinning. Name the grading scale, the mechanism, and the two first-line drugs with doses.^[1][2]

AnswerShowHide

Hamilton-Norwood (types I to VII). The mechanism is DHT-driven miniaturisation via 5-alpha-reductase type II, shortening anagen and converting terminal to vellus hairs. First-line is topical minoxidil plus oral finasteride 1 mg daily — the finasteride trial data span two years of continuous treatment, and prolonged use is required for maintained benefit.^[13][14][2]

2. A 58-year-old postmenopausal woman has a receding frontotemporal hairline and eyebrow loss; the hairline skin is smooth and shiny with no follicular ostia. Diagnosis, and the irreversible implication?^[6]

AnswerShowHide

Frontal fibrosing alopecia (FFA) — a lymphocytic scarring alopecia. The implication is that once the hairline has receded it will not return — so treat early: stop facial sunscreens or moisturisers on the forehead, add a 5-alpha-reductase inhibitor and intralesional corticosteroid. The do-not-miss action is biopsy early in any scarring-looking alopecia.^[6]

3. A 6-year-old has a boggy, tender, pustular scalp mass with cervical lymphadenopathy. What is it, and what must you NOT do?^[1]

AnswerShowHide

Kerion — the boggy inflammatory mass of tinea capitis: a hypersensitivity reaction to a dermatophyte, not a bacterial abscess. Treat with an oral antifungal — griseofulvin 20 to 25 mg/kg/day (around 8 weeks), or a shorter 2-to-4-week terbinafine course for Trichophyton infection. Corticosteroids are controversial; reserve a short oral burst for the most severe disease. Mismanagement scars.^[16][17]

4. Diffuse shedding three months after a febrile illness, positive pull test, uniform trichoscopy. Diagnosis, prognosis, and the two blood tests to check?^[1][8]

AnswerShowHide

Telogen effluvium — self-limiting within six months of removing the trigger. Check ferritin (target at least 70 ng/mL) and TSH (both hypo- and hyperthyroidism cause TE). Reassure — no active treatment is usually needed.^[1][8]

5. A 30-year-old with alopecia totalis wants to know about JAK inhibitors. Name two drugs with doses, the trial that supports baricitinib, and the one counselling point on stopping.^[3][5]

AnswerShowHide

Baricitinib (JAK1/2) 2 or 4 mg daily and ritlecitinib (JAK3/TEC) 50 mg daily (studied in adults and adolescents aged 12 and over). Baricitinib is supported by BRAVE-AA1 and BRAVE-AA2 (NEJM 2022): roughly a third of patients on 4 mg reached a SALT score of 20 or less at 36 weeks (38.8 percent versus 6.2 percent on placebo in BRAVE-AA1; 35.9 percent versus 3.3 percent in BRAVE-AA2). The counselling point: relapse after stopping is expected even after complete regrowth — these are chronic maintenance therapies, not cures.^[3][4][22]

References23ShowHide

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17. [17]Fleece D, Gaughan JP, Aronoff SC. Griseofulvin versus terbinafine in the treatment of tinea capitis: a meta-analysis of randomized, clinical trials Pediatrics, 2004.PMID 15520113
18. [18]Huynh M, Gavino AC, Magid M. Trichotillomania Semin Cutan Med Surg, 2013.PMID 24049966
19. [19]Afifi L, Oparaugo NC, Hogeling M. Review of traction alopecia in the pediatric patient: Diagnosis, prevention, and management Pediatr Dermatol, 2021.PMID 34467569
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