15-keto-13-14-dihydroprostaglandin-e2 and Dermatitis--Atopic

Immunological and biochemical alterations in atopic dermatitis have been attributed to a deficient conversion of omega-6 fatty acids (i.e. linoleic acid, gamma-linolenic acid, and dihomo-gamma-linolenic acid) to prostaglandin (PG) E1. In patients with atopic dermatitis, however, the formation of PGE1 has not been evaluated so far. We therefore measured plasma concentrations of 15-keto-13,14-dihydro-PGE1, which reflects endogenous PGE1 release, by gas chromatography-mass spectrometry in 31 patients with atopic dermatitis (aged 18-41 years, median 26 years) and in 31 healthy, age- and sex-matched control subjects. In order to exclude a metabolic shift from PGE1 to PGE2, we also measured the plasma levels of 15-keto-13,14-dihydro-PGE2. There was no difference between patients and control subjects with respect to plasma concentrations of 15-keto-13,14-dihydro-PGE1 (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-PGE2 (11.6-201.0, median 24.8 pg/ml vs. 8.6-201.0, median 19.6 pg/ml, P = 0.10), and the ratio of 15-keto-13,14-dihydro-PGE1 to 15-keto-13,14-dihydro-PGE2 (0.17-1.39, median 0.41 vs. 0.2-1.17, median 0.45, P = 0.29). These results indicate that the endogenous formation of both PGE1 and PGE2 is normal in our patients. The results do not confirm the pivotal role that other authors have attributed to a deficient PGE1 formation in the pathogenesis of atopic dermatitis.

Topics: Adolescent; Adult; Alprostadil; Dermatitis, Atopic; Dinoprostone; Female; Gas Chromatography-Mass Spectrometry; Humans; Male; Skin