[Dehydroepiandrosterone deficiency in psoriasis. Hypothesis on the etiopathogenesis of this disease].
In patients with psoriasis in extra- and intracellular deficiency of dehydroepiandrosterone can be demonstrated which leads to an activation of the pentose-phosphate cycle. This dehydroepiandrosterone deficiency is caused by an increased intracellular activity of 17 beta-hydroxysteroid-dehydrogenase. This results in an increased formation of the reduction product androstendiol, which is unable to inhibit the glucose-6-phosphate dehydrogenase, the keye enzyme of the pentose-phosphate cycle. In addition, a decreased penetration of the steroid through the membrane of erythrocytes is demonstrable, by which the intracellular deficiency of dehydroepiandrosterone is still augmented. The effects of this dehydroepiandrosterone deficiency are changes in the humoral regulation of events in growth and proliferation in patients with psoriasis.
D015067:17-Hydroxysteroid Dehydrogenases / Q000378:metabolism; D000734:Androstenediols / Q000378:metabolism; D003687:Dehydroepiandrosterone / Q000172:deficiency* / Q000378:metabolism; D005043:Etiocholanolone / Q000378:metabolism; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D006801:Humans; D009249:NADP / Q000378:metabolism; D010428:Pentosephosphates / Q000378:metabolism; D011565:Psoriasis / Q000209:etiology* / Q000378:metabolism
D000734:Androstenediols; D010428:Pentosephosphates; D003687:Dehydroepiandrosterone; D009249:NADP; D005043:Etiocholanolone; D015067:17-Hydroxysteroid Dehydrogenases; D005954:Glucosephosphate Dehydrogenase
Dehydroepiandrosteronmangel bei Psoriasis. Eine Hypothese zur Atiopathogenese diester Krankheit.