concanavalin-a and Urticaria

In seven patients with delayed pressure urticaria, the dermal inflammatory infiltrate was analyzed in early (4-6 hours) and late (20-24 hours) wheals by light and electron microscopy and by histomorphometric and immunohistologic methods. Results were compared with findings in normal skin of patients and in wheals induced with concanavalin A and compound 48/80 injections in patients and five healthy volunteers. Pressure wheals were characterized by a mild mononuclear perivascular infiltrate and by patchy dermal infiltrates of eosinophils. Neutrophils were almost completely absent. The number of dermal mast cells was markedly increased in early wheals, whereas their number was decreased in late wheals. Numerous mast cells were degranulated in late wheals, as shown by electron microscopy. On immunohistologic analysis, the perivascular infiltrate consisted primarily of lymphocytes with the helper phenotype. Epidermal OKT6 Ia-positive Langerhans cells were of normal number. The local increase of mast cells, eosinophils, and helper T lymphocytes suggests that pressure wheals result from a cellular immune response to as-yet-unknown antigens that are generated at pressure sites.

Topics: Biopsy; Concanavalin A; Eosinophils; Female; Humans; Lymphocyte Activation; Male; Mast Cells; Microscopy, Electron; p-Methoxy-N-methylphenethylamine; Pressure; Skin; Skin Tests; T-Lymphocytes, Helper-Inducer; Urticaria

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 B4, its 20-omega-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 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.

Topics: Adult; Blood Sedimentation; Chemotaxis; Concanavalin A; Female; Histamine; Humans; Male; Middle Aged; p-Methoxy-N-methylphenethylamine; Pressure; Skin Tests; Sodium Chloride; Time Factors; Urticaria

Concanavalin A (Con A)-induced histamine release from cells of subjects with extrinsic asthma, intrinsic asthma or urticaria and normal individuals was examined utilizing a single isotopic enzymatic assay for histamine. Maximum histamine release by Con A occurred with 0.9 to 4.5 microgram/ml. The mean percentage of maximum histamine release by Con A from cells of donors with extrinsic asthma was 36(+/- 19.3)% while that from cells of normal individuals was 21.4(+/- 23.7)%. However, there was no significant difference between the two groups. The higher reactivity to Con A of cells from individuals with intrinsic asthma or urticaria was not observed compared to that of the normal group. The histamine release by Con A was not correlated with IgE level in the plasma (r = 0.35). It was observed that compound 48/80 inhibited the enzymatic reaction in the isotopic, enzymatic assay.

Topics: Asthma; Concanavalin A; Histamine N-Methyltransferase; Histamine Release; Humans; Immunoglobulin E; Urticaria