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.