dinoprost and Dermatitis--Contact

Ten nickel-allergic patients and 5 healthy control subjects participated in a study of the kinetics of the flux and concentration of migrated leukocytes and extracellular PGE1 and PGF2 alpha during a 48 h period, using a skin chamber technique. The patients were provided with two skin chambers, one with and one without nickel challenge. A higher flux of leukocytes, PGE1 and PGF2 alpha was observed during the second day of allergen exposure, while the concentrations probably due to dilution were unchanged or diminished, indicating an unspecific role of the prostaglandins during the contact allergic reaction. No correlations were found within the groups between the migration of leukocytes and the prostaglandin content.

Topics: Adult; Cell Movement; Dermatitis, Contact; Dinoprost; Dinoprostone; Exudates and Transudates; Female; Humans; Hypersensitivity, Delayed; Leukocytes; Male; Middle Aged; Nickel

To study the role played by prostaglandins (PGs) in contact urticaria, concentrations of 13,14-dihydro-15-keto-PGF2 alpha, 6-keto-PGF1 alpha, and thromboxane B2, the stable metabolites of PGF2 alpha, prostacycline and thromboxane A2 were measured by radio-immunoassay of the fluid taken from suction blisters in 11 patients. The blisters were raised on contact urticarial reactions induced by benzoic acid. The effect of peroral indomethacin on contact urticaria from benzoic acid was studied in a further 14 dermatological patients. The levels of these prostanoids in the blister fluid of urticarial skin did not differ from those derived from control blisters raised on apparently normal skin. Premedication with indomethacin, 50 mg t.i.d., completely prevented contact urticarial reactions to benzoic acid in all patients.

Topics: Adolescent; Adult; Benzoates; Benzoic Acid; Dermatitis, Contact; Dinoprost; Epoprostenol; Female; Humans; Indomethacin; Male; Middle Aged; Prostaglandins; Prostaglandins F; Thromboxane A2; Urticaria

The cutaneous metabolism of exogenous arachidonic acid and endoperoxide (PGH2) to prostaglandins and hydroxy-fatty acids was investigated in experimental contact dermatitis in guinea pigs and compared to normal skin, unsensitized animals treated with the allergen dinitrochlorobenzene, and Trafuril-induced irritant dermatitis. The main alterations of cutaneous arachidonate metabolism in contact dermatitis comprise: (1) an inhibition of PGD2 synthesis; (2) a switch from predominant PGD2 production to a predominance of PGE2 and (3) a marked inhibition of the lipoxygenase activity.

Topics: Animals; Arachidonic Acids; Chromatography, Thin Layer; Dermatitis, Contact; Dinitrochlorobenzene; Dinoprost; Dinoprostone; Female; Guinea Pigs; Lipoxygenase; Prostaglandins D; Prostaglandins E; Prostaglandins F; Skin