Association of Platelet-Activating Factor with Primary Acquired Cold Urticaria

We investigated the possibility that the inflammatory reaction in primary acquired cold urticaria might be associated with the release of platelet-activating factor. Six patients with the disease and five normal controls were subjected to cold-water challenges during which blood samples were obtained for measurement of the release of possible mediators: i.e., histamine, neutrophilic chemotactic activity, and platelet-activating factor-like lipid (PAFLL). Four of the patients had pronounced experimentally induced cold urticaria with angioedema and release of mediators. Levels of the three mediators were not elevated in five normal controls or in two patients in whom cold challenges induced only mild urticaria and angioedema. The effective suppression of cold-induced urticaria in three patients treated with doxepin correlated with inhibition of PAF-LL release but not inhibition of histamine or neutrophilic chemotactic activity release. These data suggest a positive correlation between PAF-LL release and cold urticaria, although the exact relation between PAF-LL and cutaneous lesions of primary acquired cold urticaria has not yet been established. (N Engl J Med 1985; 313: 405–9.) Platelet-activating factor has been chemically characterized as a unique ether phospholipid, acetyl-glyceryl-ether-phosphorylcholine (AGEPC). 1 2 3 Platelet-activating factor derived its name from its capacity to induce platelet aggregation and the release of granule constituents in rabbits. 4 It was subsequently learned that platelet-activating factor has a variety of other potent biologic properties, such as the induction of aggregation, chemotaxis, and enzyme secretion by polymorphonuclear leukocytes; stimulation of monocytes, hypotension, and contraction of bronchial and visceral smooth muscles; and induction of increased vascular permeability. 5 Pinckard et al. have described the in vivo release of platelet-activating factor in rabbits during antigen-induced, IgE-mediated anaphylaxis. 6 The injection of . . .