IN-VIVO FORMATION OF PROSTAGLANDIN E(1) AND PROSTAGLANDIN E(2) IN ATOPIC-DERMATITIS

Immunological and biochemical alterations in atopic dermatitis have be en attributed to a deficient conversion of omega-6 fatty acids (i.e. l inoleic acid, gamma-linolenic acid, and dihomo-gammalinolenic acid) to prostaglandin (PG) E(1). In patients with atopic dermatitis, however, the formation of PGE, has not been evaluated so far. We therefore mea sured plasma concentrations of 15-keto-13,14-dihydro-PGE(1), which ref lects endogenous PGE(1) release, by gas chromatography-mass spectromet ry in 31 patients with atopic dermatitis (aged 18-41 years, median 26 years) and in 31 healthy, age- and sex-matched control subjects. In or der to exclude a metabolic shift from PGE(1) to PGE(2), we also measur ed the plasma levels of 15-keto-13, 14-dihydro-PGE(2). There was no di fference between patients and control subjects with respect to plasma concentrations of 15-keto-13,14-dihydro-PGE(1) (3.9-49.6, median 10.3 pg/ml vs. 3.2-80.4, median 8.3 pg/ml, P = 0.22), 15-keto-13,14-dihydro -PGE(2) (11.6-201.0, median 24.8 pg/ml vs. 8.6-201.0, median 19.6 pg/m l, P = 0.10), and the ratio of 15-keto-13,14-dihydro-PGE(1) to 15-keto -13,14-dihydro-PGE(2) (0.17-1.39, median 0.41 vs. 0.2-1.17, median 0.4 5, P = 0.29). These results indicate that the endogenous formation of both PGE(1) and PGE(2) is normal in our patients. The results do not c onfirm the pivotal role that other authors have attributed to a defici ent PGE(1) formation in the pathogenesis of atopic dermatitis.