[A new concept of the etiopathogenesis and prevention of atopic dermatitis].
The hypothesis proposed for the pathogenesis of atopy links the well-known alterations in cell-mediated and humoral immunity, the disturbances of mediator metabolism and the increased disposition of atopic epidermis for inflammation to a common underlying deficiency in the production of prostaglandin E1. The PGE1 deficiency is explained as the result of reduced delta-6-desaturase activity in atopic patients. The development of depressed cell-mediated immunity is regarded as a PGE1-dependent T-cell-maturation defect of the newborn's immune system post partum. Our hypothesis offers a novel approach to the prevention of atopy by administration of gamma-linolenic acid to newborns with increased risk of atopy and to nursing atopic mothers. Furthermore, it provides an explanation for the beneficial therapeutic effects of dietary supplementation of gamma-linolenic acid in patients with atopic dermatitis.
Melnik
B
B
Hautklinik, Heinrich-Heine-Universität Düsseldorf.
Plewig
G
G
D000527:Alprostadil / Q000172:deficiency*; D003876:Dermatitis, Atopic / Q000276:immunology* / Q000517:prevention & control; D006801:Humans; D007111:Immunity, Cellular / Q000502:physiology*; D008042:Linolenic Acids / Q000008:administration & dosage; D017965:gamma-Linolenic Acid
D008042:Linolenic Acids; D017965:gamma-Linolenic Acid; D000527:Alprostadil
Ein neues Konzept zur Atiopathogenese und Prävention der Atopie.