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Clinical, pharmacological and immunological aspects of delayed pressure urticaria
Author(s) -
CZARNETZKI B.M.,
MEENTKEN J.,
ROSENBACH T.,
POKROPP A.
Publication year - 1984
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.1984.tb04729.x
Subject(s) - histamine , leukocytosis , medicine , chemotaxis , immunology , pathogenesis , concanavalin a , leukotriene b4 , endocrinology , inflammation , chemistry , in vitro , biochemistry , receptor
Summary We studied the clinical features of thirty‐two patients with delayed pressure urticaria, and special laboratory tests were performed in seven patients. Striking clinical features included a long duration of the disease (mean 6 years) and an elevated erythrocyte sedimentation rate in 71%, dermographism in 63% and a leukocytosis in 33% of the patients. There was prolongation of weals in response to histamine, compound 48/80, concanavalin A and NaCl. In some patients, histamine and chemotactic factor levels were increased in suction blisters over skin test and delayed pressure sites. In extracts from pressure weals, chemotactic activity was found for leukotriene B 4 , its 20‐ω‐oxidation products and mono‐HETEs. Studies of peripheral blood leukocytes revealed significantly increased intracellular histamine levels and increased release of histamine, and a trend to increased release of chemotactic activity from stimulated patient cells. The response of leukocytes to mitogens was normal. We conclude that histamine plays a major role in the pathogenesis of PU. Arachidonate‐derived chemotactic factors might account for the variably observed leukocytosis and the cellular infiltrate in lesions of pressure urticaria. Additional mediators must be involved in PU in order to explain the unique prolonged wealing response.