Male and female patterns (androgenetic alopecia)

Male pattern baldness is inherited (the exact mode is unclear) and androgen dependent. Over several cycles, the androgen-sensitive follicles miniaturize from terminal to vellus hairs. Males are affected from the second decade and, by the seventh decade, 80% have involvement. Patterned balding also occurs in females, the majority of whom are hormonally normal. It becomes more pronounced after the menopause and is present in 70% of 80-year-old women. In men, bitemporal recession followed by a bald crown is the usual pattern (Fig. 1); women may show this but more commonly exhibit a diffuse thinning. Mostly, no treatment is required but, if indicated, topical minoxidil (Regaine) produces some response in a third of cases, and finasteride can help.

Fig. 1 Male pattern baldness.

Hair loss may progress from bitemporal recession (a) to vertex involvement (b) to the most severe form (c), where only a horseshoe of hair runs from the ears to the occiput.

Endocrine and nutrition related

Endocrine disorders often present with hair loss. Underactivity of the thyroid, pituitary or adrenals can cause diffuse alopecia, as may hyperthyroidism. Androgen-secreting tumours in women produce male pattern baldness with virilization. Malnutrition induces dry brittle hair that becomes pale or red in kwashiorkor (protein deficiency). Diffuse hair loss is also seen with iron or zinc deficiency.

Telogen effluvium

Hair follicles are not usually in phase but, if synchronized into the telogen-resting mode, they will be shed in unison about 3 months later. Such an effluvium can be a response to high fever, childbirth, surgery, drug reaction or other stress.

Drug induced

Abrupt cessation of growth (anagen effluvium) may follow ingestion of a poison such as thallium, but is more commonly drug induced, e.g. with cytotoxics (especially cyclophosphamide), heparin, warfarin, carbimazole, colchicine and vitamin A.

Alopecia areata

Alopecia areata is a common condition, associated with autoimmune disorders, in which anagen is prematurely arrested. It generally starts in the second or third decade and presents with sharply defined non-inflamed bald patches on the scalp. Pathognomonic exclamation mark hairs, which taper as they approach the scalp, are seen. The eyebrows and beard can also be affected, and nails may show pitting.

The course is unpredictable: bald patches may enlarge progressively but, for a first attack, regrowth (often initially with white hairs) is usual (Fig. 2). Prepubertal onset, extensive involvement (especially of the posterior scalp) and atopy signal a poor prognosis. Complete scalp alopecia (totalis) or loss of all bodily hair (universalis) is seen occasionally. Rarely, diffuse scalp alopecia occurs.

Fig. 2 Alopecia areata showing some exclamation mark (!) hairs and growth of white hair.

Treatment depends on the extent: if localized, spontaneous regrowth is probable, and intralesional steroid (e.g. triamcinolone acetonide) may accelerate this. If extensive, therapy is less successful. Contact immunotherapy by the application of the sensitizer diphencyprone is effective but not widely available. Wigs are often necessary.

Infections

Scalp ringworm infection can result in patchy hair loss and is described below. Secondary syphilis causes a patchy alopecia.

Trauma and traction

Constantly rubbing or pulling the hair can result in its loss. Traction from tight rollers or pulling hair into a bun causes alopecia at the scalp margins. Hair straightening, bleaching and permanent waving produces a damaged hair shaft that is easily broken.