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Akne

Aktuelle pathophysiologische Aspekte

Acne

Current pathophysiologic considerations

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Zusammenfassung

Seborrhoe, follikuläre Hyperkeratose, Propionibakterien und entzündliche Vorgänge sind die wichtigsten Faktoren, die zu Akne führen. Das Zusammenwirken von verstärktem Talgfluss und follikulärer Hyperkeratose begünstigt ein starkes Wachstum von Propionibacterium acnes. Dessen Stoffwechselprodukte fördern follikuläre und im Extremfall abszedierende perifollikuläre Entzündungen. Die Talgproduktion wird von Androgenen gesteuert, und Störungen im Androgenhaushalt können Seborrhoe und Akne provozieren. Die follikuläre Hyperkeratose wird durch ein relatives Linolsäuredefizit, Peroxide von Talgkomponenten und insbesondere auch von Entzündungsmediatoren wie Interleukin-1 provoziert. Bakterielle Stoffwechselprodukte wie Lipasen, Proteasen oder chemotaktische Faktoren fördern die perifollikuläre Entzündung. Entzündung ist aber nicht nur Resultat anderer pathogenetischer Faktoren, sondern auch Wegbereiter der Akne: Eine initiale perifollikuläre Entzündungsbereitschaft fördert über Entzündungsmediatoren die Komedogenese und bereitet hierdurch Akne vor. Der Bedeutung von Ernährungsgewohnheiten für die Entstehung und den Verlauf der Akne wird seit Kurzem wieder mehr wahrgenommen. Vermutet werden insbesondere Zusammenhänge zwischen Akne und Nahrungsmitteln mit einem hohen glykämischen Index sowie mit Milchprodukten.

Abstract

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 infammation 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.

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Degitz, K., Ochsendorf, F. Akne. Hautarzt 59, 503–512 (2008). https://doi.org/10.1007/s00105-008-1497-z

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