Sebaceous and sweat glands—acne

Aetiopathogenesis

In acne, the androgen-sensitive pilosebaceous unit (p. 4) shows a hyper-responsiveness that results in increased sebum excretion. Colonization with the bacterium P. acnes initiates inflammation through chemical mediators inducing enzymes (e.g. lipase), cytokines and prostaglandins ( Fig. 36.1 ). These and possibly other factors in sebum induce microanatomical changes in the pilosebaceous unit such as ductal hyperkeratosis, with comedone formation and a cascade of other manifestations.

Clinical presentation

Comedones are either open (blackheads: dilated pores with black plugs of melanin-containing keratin) or closed (whiteheads: small cream-coloured, dome-shaped papules). They appear at about the age of 12 years and evolve into inflammatory papules ( Fig. 36.2 ), pustules or cysts ( Figs 36.3 and 36.4 ). The sites of predilection—the face, shoulders, back and upper chest—have many sebaceous glands. The severity of acne depends on its extent and the type of lesion, with cysts being the most destructive.

Acne usually persists until the early twenties, although in a few patients, particularly women, the disease continues into the fifth decade. Scars may follow healing, especially of cysts or abscesses. Scars may be ‘ice-pick’, atrophic ( Fig. 36.5 ) or keloidal.

Some variants of acne are seen:

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  Acne excoriée : due to squeezing and picking, often affects depressed or obsessional young women

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  Chloracne : caused by systemic toxicity of certain aromatic halogenated industrial chemicals (p. 160)

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  Conglobate : a mass of burrowing abscesses and sinuses with scarring

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  Cosmetic : pomade and cosmetic-induced comedonal and papular acne (mainly seen in the United States)

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  Drug-induced : by systemic steroids, androgens and topical steroids

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  Infantile : mostly found on the faces of male infants; cause unknown

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  Physical : occlusion by the back of a wheelchair or on a violinist’s chin.