Decreased epidermal aryl hydrocarbon hydroxylase and localized pustular psoriasis

Abstract

It was recently suggested that the underlying genetic defect in psoriasis may be related to an abnormality in aryl hydrocarbon hydroxylase (AHH) activity (the cytochrome P-450 mixed function oxidase system) since its concentration and capacity for induction are decreased in the clinically normal skin as well as in the lesions of psoriasis. Microsomal AHH activity was measured in suction separated epidermis from forearm skin of 13 patients with localized palmo-plantar pustular psoriasis and 13 normal subjects before and after induction by benzanthracene. AHH activity had a mean value of 2.32 .mu.m 3OH-BP[3-hydroxybenz(a)pyrene]/mg microsomal protein per h .+-. 0.23 (S.E. [standard error]) in the patients and 3.41 .+-. 0.23 in the normal subjects. AHH induction was also decreased with a mean value of 1.15 .+-. 0.1 (S.E.) compared with 1.98 .+-. 0.14 for the normal subjects. Since in 12 of the patients the psoriasis had always been localized to the palms and soles, the decreased basal and induced AHH activity appears to be a primary characteristic of psoriatic skin; AHH activity might initiate an increase in epidermal cell turnover through modulation of prostaglandin and adenylate cyclase activity.