Platelet-activating factor (PAF) is considered to be one of the most potent
lipid mediators in allergic and inflammatory reactions. Suggestions that PAF is produced by cutaneous cells, and cells infiltrating the skin from the blood, have been reported. PAF has been identified in allergic cutaneous reactions and also in psoriatic lesions. The
biological activity of PAF is thought to be mediated by cell membrane receptors. Studies revealed that PAF-antagonists can be active in animal models of cutaneous
inflammation. In humans PAF-antagonists showed minimal therapeutic improvement in studies of
antigen-induced cutaneous responses in atopic subjects. No data are available on the effects of PAF-antagonists in
psoriasis. The objective of this study was to investigate the effect of a potent PAF-antagonist (
Ro 24-0238, 10%
solution in
diethylene glycol monoethyl ether) in 10 patients with chronic plaque
psoriasis, a placebo-controlled double-blind study. Clinical response was evaluated and markers of
inflammation, differentiation and proliferation were studied immunohistochemically on punch biopsies taken from actively treated and placebo-treated lesions, before and
after treatment. This study demonstrated that
a 10%
solution of the PAF-antagonist
Ro 24-0238 was not effective at the clinical or cell
biological level after a 4-week treatment period. The most likely explanation for these negative observations is that PAF is not a significant factor in the pathogenesis of
psoriasis.