Claveau J, Lavoie A, Brunet C, Bédard P M, Hébert J
Division de dermatologie, Université Laval, Sainte-Foy, Québec, Canada.
Ann Allergy Asthma Immunol. 1996 Dec;77(6):475-9. doi: 10.1016/S1081-1206(10)63353-4.
The pathogenesis of chronic idiopathic urticaria is characterized by defective histamine release. Skin mast cells show an increased release of histamine while circulating basophils are less responsive to immunologic stimulus.
The purpose of the study was to examine and compare the production of the histamine-releasing factor in the skin and within the peripheral blood of patients with chronic idiopathic urticaria and normal control subjects, as a possible factor responsible for the difference observed in the releasability of both skin mast cells and basophils.
Using the skin chamber technique, histamine-releasing factor production and histamine concentration were assessed in normal-appearing skin of patients with chronic idiopathic urticaria (n = 12) and normal controls (n = 5) over a 2-hour observation period. In both groups, histamine-releasing factor production by peripheral blood mononuclear cells was also measured.
The weighted average of histamine-releasing factor production during the 2-hour observation period was higher in the non-lesional skin of patients with chronic idiopathic urticaria as compared with normal controls (5.6 +/- 1.4% versus 0.7 +/- 0.6%, P < .01). In contrast, less histamine-releasing factor was produced by peripheral blood mononuclear cells in chronic urticaria as opposed to normal controls (17.2 +/- 2.1% versus 25.7 +/- 2.8%, P < .03). Spontaneous histamine concentration was not significantly different in patients with chronic urticaria than in normal controls.
Histamine-releasing factor production is increased in the skin, and decreased in the peripheral blood of patients with chronic idiopathic urticaria when compared with nonatopic controls. The lower production of histamine releasing factor in the blood could be explained by the migration of activated T-lymphocytes in the skin.
慢性特发性荨麻疹的发病机制以组胺释放缺陷为特征。皮肤肥大细胞组胺释放增加,而循环嗜碱性粒细胞对免疫刺激的反应性较低。
本研究旨在检测并比较慢性特发性荨麻疹患者与正常对照者皮肤和外周血中组胺释放因子的产生情况,这可能是导致皮肤肥大细胞和嗜碱性粒细胞释放能力差异的一个因素。
采用皮肤小室技术,在2小时观察期内评估慢性特发性荨麻疹患者(n = 12)和正常对照者(n = 5)外观正常皮肤中组胺释放因子的产生及组胺浓度。两组均检测外周血单个核细胞产生组胺释放因子的情况。
与正常对照相比,慢性特发性荨麻疹患者非皮损皮肤在2小时观察期内组胺释放因子产生的加权平均值更高(5.6±1.4%对0.7±0.6%,P <.01)。相反,与正常对照相比,慢性荨麻疹患者外周血单个核细胞产生的组胺释放因子较少(17.2±2.1%对25.7±2.8%,P <.03)。慢性荨麻疹患者的自发性组胺浓度与正常对照无显著差异。
与非特应性对照相比,慢性特发性荨麻疹患者皮肤中组胺释放因子产生增加,外周血中组胺释放因子产生减少。血液中组胺释放因子产生较低可能是由于活化的T淋巴细胞迁移至皮肤所致。