Mechanism of anthralin inflammation. I. Dissociation of response to clobetasol and indomethacin.
The effect of topical clobetasol propionate and a 1% topical indomethacin gel which could inhibit UV erythema was measured on anthralin inflammation by change in skin-fold thickness and erythema. The time course of the inflammatory oedema and erythema were different, as was their response to the drugs studied. The oedema of anthralin inflammation was completely inhibited by clobetasol propionate but the erythemal response showed a small and non-significant reduction. Indomethacin had no effect on anthralin oedema but produced a small but significant reduction in erythema in the first 24 h after anthralin application. These results suggest that either anthralin inflammation is not due to production of prostenoids, or that if it is, it occurs by other than the classical enzymic pathway.
D000328:Adult; D000368:Aged; D000873:Anthracenes / Q000633:toxicity*; D000875:Anthralin / Q000633:toxicity*; D001623:Betamethasone / Q000031:analogs & derivatives*; D002990:Clobetasol / Q000031:analogs & derivatives* / Q000627:therapeutic use; D003877:Dermatitis, Contact / Q000209:etiology*; D004487:Edema / Q000139:chemically induced / Q000188:drug therapy; D004890:Erythema / Q000139:chemically induced / Q000188:drug therapy; D005260:Female; D006801:Humans; D007213:Indomethacin / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D012871:Skin Diseases / Q000139:chemically induced / Q000188:drug therapy; D014466:Ultraviolet Rays
D000873:Anthracenes; D001623:Betamethasone; D002990:Clobetasol; D000875:Anthralin; D007213:Indomethacin