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ACNE vulgaris is a common inflammatory disorder of the skin involving pilosebaceous structures; its pathogenesis is imperfectly understood. Earliest lesions demonstrate a partial rupture of the follicle wall, with surrounding dermal inflammation.1 The latter apparently results from the intrusion of material from the follicle into the dermis. Sebum, the lipid mixture secreted by sebaceous glands, has been implicated in this sequence. Injection of sebum into the human skin provokes a lymphocytic response. When various fractions of sebum are injected intradermally it is the free fatty acids, comprising up to 23 per cent of secreted lipids,2 that are primarily responsible for . . .
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Freinkel et al. (1965) studied this question.
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