Hair Disorders and Alopecia — Alopecia Areata, Telogen Effluvium and Androgenetic Alopecia

Every hair cycles through anagen (growth), catagen (involution), telogen (rest) and exogen (shedding). About 80 to 90% of scalp hair is in anagen, which lasts 2 to 6 years and sets hair length; less than 5% is in catagen and the rest in telogen. About 100 hairs a day are shed. Telogen hair is called club hair because of its root shape; it has a white bulb and no gelatinous sheath.

Alopecia is classified first as nonscarring (the follicle survives and hair can regrow) or scarring (cicatricial). In alopecia areata, StatPearls notes that absence of follicles points to cicatricial alopecia. Alopecia areata, telogen effluvium and androgenetic alopecia are the three nonscarring conditions examiners ask about most.

Alopecia areata (AA) is a chronic, immune-mediated disorder affecting hair follicles, nails and occasionally the retinal pigment epithelium. It targets anagen follicles and causes hair loss without permanent follicle damage. The classic picture is isolated, smooth, sudden, nonscarring, patchy hair loss on the scalp or any hair-bearing area.

• Lifetime risk about 2%; prevalence about 1 in 1,000.
• No sex predilection; more often seen in Asian, Black and Hispanic patients.
• Mean age at onset is 32 years in males and 36 in females.
• Associations: vitiligo, lupus erythematosus, psoriasis, atopic dermatitis, thyroid disease, allergic rhinitis, Down syndrome and polyglandular autoimmune syndrome type 1.

The hair follicle is normally an immune-privileged site, like the eye, CNS, testis, fetus and placenta. Loss of immune privilege is central to AA. Triggers — emotional or physical stress, vaccination, viral infection, medications — are thought to switch it off by lowering the anti-inflammatory signals TGF-beta and alpha-MSH, and by raising MICA expression on follicles.

1. MICA on follicle cells activates NK cells, which release interferon-gamma and IL-15.
2. IFN-gamma raises MHC class I on follicle cells, exposing hidden antigens to T cells; IL-15 suppresses regulatory T cells.
3. IFN-gamma and IL-15 signal through the JAK-STAT pathway.
4. Inflammatory cells attack the matrix epithelium of anagen follicles, pushing them into catagen or telogen.

The JAK-STAT pathway is why JAK inhibitors work in AA. Histology of active disease shows the 'bee-swarm' (swarm of bees) pattern: dense lymphocytes around the bulb of anagen follicles, CD8+ T cells inside the follicular epithelium and CD4+ T cells around it. Long-standing disease shows follicular miniaturisation.

Patches develop over a few weeks and may also involve the beard, eyebrows, eyelashes and limbs. In active disease exclamation-mark hairs — hairs narrower at the proximal end than the distal end — are seen at the periphery of lesions and are called pathognomonic. White hair is often spared, which can give the appearance of rapid greying.

Diagnosis is clinical: history and examination, with rapidly developing patches and minimal erythema. Dermoscopy helps, showing broken hairs, yellow dots, black dots, exclamation-mark hairs and short vellus hairs (the last indicating early regrowth). A hair pull test confirms active shedding, the nails should be examined, and a biopsy from the edge of an active patch is done only if the diagnosis stays uncertain.

About 50% of patients regrow hair naturally within a year, so some choose no treatment. For patchy AA the initial therapy is usually intralesional or topical corticosteroid.

Telogen effluvium (TE) is diffuse, usually acute, nonscarring shedding of resting hair after metabolic stress, hormonal change or medication. Normally about 85% of scalp hairs are in anagen and 15% in telogen; under significant stress about 70% of anagen hairs drop into telogen. Telogen lasts 1 to 6 months (average 3), so shedding begins about 3 months after the trigger, by which time the patient may have forgotten the event. Acute TE lasts under 6 months.

• Triggers: acute febrile illness, severe infection, major surgery or trauma, postpartum oestrogen fall, hypothyroidism, stopping oestrogen-containing drugs, crash dieting, low protein intake, heavy metal ingestion, iron deficiency.
• Drugs: beta-blockers, retinoids (including excess vitamin A), anticoagulants, propylthiouracil, carbamazepine, immunisations.
• Diagnosis: gentle pull test removes at least 4 hairs per pull during acute shedding; 100 or more hairs in 24 hours suggests TE; biopsy shows 25 to 50% of follicles in telogen.
• Work-up: TSH, and CBC, serum iron, iron saturation and ferritin where indicated; VDRL if syphilis is suspected.
• Treatment: self-limited; correct the cause (iron, thyroid, drug withdrawal) and hair returns.

Androgenetic (pattern) alopecia is a genetically determined excessive response to androgens affecting about 50% of males and females, usually starting after puberty. Androgen receptor activation shortens anagen, so follicles become progressively thinner and shorter (miniaturisation). Affected scalp has raised DHT, more 5-alpha-reductase and more androgen receptors; the type 2 isoform in the outer root sheath matters most. Prepubertal castration and androgen insensitivity syndrome do not develop pattern baldness.