[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.