[Acne. Current pathophysiologic considerations]

Seborrhea, follicular hyperkeratosis, propionibacteria, and inflammatory reactions are the most important factors leading to acne. The combination of increased sebum producation and follicular hyperkeratosis facilitates an increased growth of Propionibacterium acnes. Its metabolic products lead to follicular inflammation and, in extreme cases, even to perifollicular abscesses. Sebum production is influenced by androgens, so that abnormalities in androgen levels can produce seborrhea and acne. Follicular hyperkeratosis may be triggered by a relative deficiency in linoleic acid, peroxides from sebum components, and especially by inflammatory mediators such as interleukin-1. Bacterial metabolic products such as lipases, proteases, or chemotactic factors lead to the perifollicular inflammation. This inflammation is not only a response to other pathogenetic factors, but also a cause of acne. An initial mild perifollicular inflammation can induce comedogenesis via a variety of mediators. The influence of dietary factors on the initiation and course of acne has recently received increased recognition. A connection has been postulated between acne and a high nutrients with glycemic index, as well as with milk products.