在银屑病患者中进行的双盲对照研究中,西替利嗪调节粘附分子表达。

E Pestelli, I Floriani, P Fabbri, M Caproni
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引用次数: 0

摘要

银屑病是一种慢性炎症性t细胞介导的免疫性皮肤病,其特征是皮肤表达属于beta1和beta2整合素亚家族的粘附分子,如细胞内粘附分子(ICAM)-1、ICAM-3、淋巴细胞功能相关抗原(LFA)-1、血管细胞粘附分子(VCAM)-1和内皮粘附分子(ELAM)-1。西替利嗪是一种非镇静性、选择性的h1受体拮抗剂,其治疗效果可能是其对即时过敏反应和晚期过敏反应都有作用的结果。本研究采用免疫磷酸酶碱性(apap)双盲对照技术研究黏附分子(ICAM-1、ICAM-3、VCAM-1、LFA-1和ELAM-1)的表达。将19例活动性轻度寻常型银屑病患者随机分为两组:A组(2名男性和6名女性,年龄22-59岁)给予西替利嗪治疗(30 mg /天,每天3次,持续15天),B组(3名男性和8名女性,年龄24-72岁)给予安慰剂。阳性细胞由两名独立的盲眼观察者计数,并分析至少三个相邻的高倍视场(250倍)。A组经西替利嗪处理后,icam -1阳性细胞由75.8 (SE +/- 15.12)降至38.8 (SE +/- 7.57), icam -3阳性细胞由61.7 (SE +/- 12.72)降至45.2 (SE +/- 9.44), LFA-1由103.9 (SE +/- 17.34)降至66.5 (SE +/- 8.63) (p = 0.02)。在B组中,除ELAM-1外,其他粘附分子的表达在服用安慰剂后均无显著降低,其表达略有变化,从23.4 (SE +/- 3.56)降至21.5 (SE +/- 3.26)。西替利嗪治疗后银屑病中粘附分子表达的减少表明该药物可能对某些细胞表面蛋白产生抑制作用,从而抑制银屑病皮损中炎症细胞的迁移。我们的研究结果支持它的抗炎作用以及它的h1阻断活性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Cetirizine modulates adhesion molecule expression in a double-blind controlled study conducted in psoriatic patients.

Psoriasis is a chronic inflammatory T-cell-mediated immune dermatosis, characterized by the cutaneous expression of adhesion molecules belonging to the beta1 and beta2 integrin subfamilies, such as intracellular adhesion molecule (ICAM)-1, ICAM-3, lymphocyte function associated antigen (LFA)-1, vascular cell adhesion molecule (VCAM)-1 and endothelial adhesion molecule (ELAM)-1. Cetirizine is a nonsedating, selective H1-receptor antagonist, whose therapeutic efficacy is probably the result of its effect on both the immediate allergic reaction and the late-phase allergic response. The aim of this study was to investigate adhesion molecule expression (ICAM-1, ICAM-3, VCAM-1, LFA-1 and ELAM-1) by using an immunophosphatase alkaline (APAAP) technique in a double-blind controlled study. Nineteen patients with active psoriasis vulgaris minima were randomized into two groups: group A (two men and six women, aged 22-59 years) was treated with cetirizine (30 mg a day, 3 times a day for 15 days) and group B (three men and eight women, aged 24-72 years) were administered placebo. Positive cells were counted by two independent and blinded observers and at least three adjacent high-power fields (250 X) were analyzed. In group A, ICAM-1-positive cells decreased from 75.8 (SE +/- 15.12) to 38.8 (SE +/- 7.57) ICAM-3-positive cells decreased from 61.7 (SE +/- 12.72) to 45.2 (SE +/- 9.44) and LFA-1 decreased from 103.9 (SE +/- 17.34) to 66.5 (SE +/- 8.63) after cetirizine treatment (p = 0.02). In group B, a nonsignificant reduction was found after placebo administration in the expression of adhesion molecules except for ELAM-1, which showed a slight variation, from 23.4 (SE +/- 3.56) to 21.5 (SE +/- 3.26). The reduction in the expression of adhesion molecules in psoriasis after cetirizine treatment suggests a possible inhibitory effect of this drug on some cell surface proteins and subsequently on the migration of inflammatory cells in psoriatic skin lesions. Our findings support its antiinflammatory effect in addition to its H1-blocking activity.

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