Hair & Nail Disorders

Approach to hair loss

The hair cycle. Scalp hairs spend 2–7 years in anagen (growth; about 85–90% of hairs), 2–3 weeks in catagen (involution), and about 3 months in telogen (rest; 10–15%) before the club hair is shed. Losing up to about 100 hairs a day is normal.

Scarring or nonscarring? Nonscarring alopecia preserves follicular openings and can recover; scarring (cicatricial) alopecia leaves smooth, shiny skin without them, and the loss is permanent.

Nonscarring alopecias

Androgenetic alopecia. The most common cause of hair loss. Dihydrotestosterone, produced by 5α-reductase type 2, miniaturizes genetically susceptible follicles so terminal hairs become fine vellus hairs. Topical minoxidil works in both sexes; finasteride 1 mg is used in men, lowers PSA by about 50% (double the value when screening), can cause sexual side effects, and is contraindicated in women who may become pregnant because it can undervirilize a male fetus. Benefit lasts only while treatment continues. A woman with pattern hair loss plus acne, hirsutism, irregular menses, or virilization needs total testosterone and DHEA-S: polycystic ovary syndrome is the usual cause, and rapid virilization suggests an androgen-secreting tumor.

Alopecia areata. A T-cell–mediated attack on anagen bulbs produces sharply demarcated, smooth patches over normal skin, with exclamation-point hairs (short hairs tapering toward the scalp) at the margins and fine, regular nail pits. It is associated with autoimmune thyroid disease (check TSH), vitiligo, atopy, and Down syndrome. Adults with limited patches receive intralesional triamcinolone every 4–6 weeks, children use potent topical steroids, and severe disease responds to oral JAK inhibitors such as baricitinib and ritlecitinib or to topical immunotherapy. Small patches often regrow within a year; extensive loss, the band-like ophiasis pattern, childhood onset, atopy, and nail changes predict progression to alopecia totalis or universalis.

Telogen effluvium. Childbirth, high fever or severe illness, surgery, crash dieting, emotional stress, or a new drug pushes many anagen hairs into telogen at once, and diffuse shedding of club hairs follows 2–4 months later. Check TSH, ferritin, and a CBC, then reassure: regrowth follows over about 6 months once the trigger resolves.

Anagen effluvium is different: chemotherapy or radiation halts dividing anagen hairs, and they break and fall within days to weeks rather than months.

Tinea capitis. A dermatophyte infection of school-age children, usually Trichophyton tonsurans in the United States. It causes scaly patches, black dots of broken hairs, posterior cervical or occipital lymphadenopathy, or a boggy, pustular kerion, which is an inflammatory reaction rather than an abscess and should not be drained. Confirm with KOH and fungal culture. Topical agents cannot penetrate the hair shaft, so treat with oral griseofulvin for 6–8 weeks or terbinafine for 2–4 weeks, adding selenium sulfide or ketoconazole shampoo to reduce spore shedding.

Trichotillomania and traction. Trichotillomania, an obsessive-compulsive–related disorder, leaves irregular patches with broken hairs of varying lengths, often on the side of the dominant hand, and may involve eyebrows and lashes; habit reversal therapy is first-line, and swallowed hair can form a trichobezoar (Rapunzel syndrome when it extends into the small bowel). Traction alopecia thins the frontotemporal hairline under tight braids or ponytails and becomes permanent if tension continues.

Scarring alopecia

Recognize and biopsy. Smooth, shiny skin without follicular ostia signals follicle destruction. Discoid lupus causes scaly plaques with follicular plugging and dyspigmentation; lichen planopilaris causes perifollicular erythema and scale at the advancing edge, and its frontal fibrosing variant recedes the frontal hairline and eyebrows in postmenopausal women; central centrifugal cicatricial alopecia spreads outward from the crown. A punch biopsy from the active border identifies the cause, and early treatment is needed because lost follicles do not return.

Nail infections and ingrown nails

Onychomycosis. Usually Trichophyton rubrum: thick, yellow, crumbling toenails with subungual debris and onycholysis. About half of dystrophic nails are not fungal (psoriasis and trauma mimic it), so confirm with KOH, culture, or a PAS-stained clipping before systemic therapy. Oral terbinafine is first-line (12 weeks for toenails, 6 weeks for fingernails) with baseline liver enzymes; topical efinaconazole or ciclopirox suits mild disease.

Paronychia. Acute paronychia is a painful, red, swollen fold after trauma, manicures, or nail biting, usually from S. aureus; warm soaks treat early cases, a fluctuant collection needs incision and drainage, and oral antibiotics are for spreading cellulitis. Chronic paronychia lasts 6 weeks or more and involves several folds with lost cuticles in people whose hands are often wet; it is an irritant dermatitis with secondary Candida, treated by keeping hands dry, gloves, and a topical steroid with or without an azole.

Grouped vesicles on a fingertip are herpetic whitlow; treat with antivirals and do not incise.

Ingrown toenail. The lateral edge of the great toenail embeds in the fold after short, curved trimming or tight shoes. Mild cases respond to warm soaks, a cotton wisp or floss under the edge, and straight-across trimming; moderate, severe, or recurrent cases need partial nail avulsion with phenol matrixectomy.

Nail signs of systemic disease

Longitudinal melanonychia. A pigmented band from the nail matrix is often benign: several nails in people with darker skin, a nevus, drugs such as zidovudine or hydroxyurea, or trauma (a subungual hematoma grows out distally). Features of subungual (acral lentiginous) melanoma are a single digit, usually the thumb or great toe; a band wider than 3 mm; irregular, dark, or widening pigment; nail dystrophy; and Hutchinson sign, pigment extending onto the proximal or lateral nail fold. These findings call for a nail matrix biopsy.