Cutaneous IgE-mediated inflammatory lesion size is inhibited by an H1 antagonist (terfenadine) while mediator release is unaffected in vivo and in vitro.
Cutaneous IgE-mediated inflammatory lesion size is inhibited by an H1 antagonist (terfenadine) while mediator release is unaffected in vivo and in vitro.
复制标题
H1 拮抗剂（特非那定）可抑制皮肤 IgE 介导的炎症病变大小，而体内和体外介质释放不受影响。
DOI：
10.1111/j.1365-2222.1993.tb00345.x
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Lichtenstein,LM
中科院分区：
文献类型：
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作者：
Massey,WA;Charlesworth,EN;Freidhoff,L;Cooper,P;Kagey-Sobotka,A;Lichtenstein,LM
我们对了解皮肤IgE介导的晚期反应的发病机制很感兴趣。对10名受试者进行了一项双盲、安慰剂对照、随机交叉研究，研究非镇静性抗组胺药特非那定（Selddane）对皮肤对抗原（豚草或混合草）反应的影响。体外研究了特非那定对皮肤肥大细胞、肺肥大细胞和嗜碱性粒细胞释放抗IgE诱导介质的抑制作用。特非那定在第1 ~ 9小时显著抑制皮肤反应的大小（第9小时，对照组2250±500 mm2vs药物1250±250 mm2，P< 0.01,n=10），在第10 ~ 12小时有一定的抑制作用。而特非那定阻断组胺释放后鼻腔抗原挑战，释放介质在皮肤水泡部位不受影响。特非那定不影响白细胞向水疱上清的浸润，尽管先前的研究表明另一种抗组胺药西替利嗪具有显著的抑制作用。体外，特非那定。与其他抗组胺药一样，在肺和皮肤肥大细胞和嗜碱性细胞中，在浓度为10−4‐10−5M时，发现对抗IgE诱导的介质释放具有抑制活性。我们得出结论，新型抗组胺药对细胞进入皮肤的影响可能是多种多样的，特非那定可能在体内表现出器官特异性，特非那定显著降低了皮肤对抗原的早期和晚期总体炎症反应。到目前为止，我们还不能。解释发生这种情况的机制。
We are interested in understanding the pathogenesis of the cutaneous IgE‐mediated late phase reaction. A double‐blind, placebo‐controlled, randomized cross‐over study with 10 subjects of the effect of the non‐sedating antihistamine, terfenadine (Selddane), on the cutaneous reaction to antigen (ragweed or mixed grass) administered intradermally and over denuded blister bases was performed. The activity of terfenadine on anti‐IgE‐induced mediator release from the skin mast cell, lung mast cell and basophil was also examinedin vitro. Terfenadine significantly inhibited the size of the cutaneous reaction at every hour between hours 1 and 9 (hr 9, control 2250 ± 500 mm2vsdrug 1250 ± 250 mm2,P< 0.01,n=10) and showed some inhibitory effect at hours 10–12. While terfenadine blocks histamine release after nasal antigen challenge the release of mediators at skin blister sites was unaffected. The infiltration of leucocytes into the blister supernatant was unaffected by terfenadine although previous studies have shown significant inhibition with another antihistamine, cetirizine.In vitro, terfenadine. like other antihistamines, was found to have inhibitory activity on anti‐IgE‐induced mediator release at concentrations of 10−4‐10−5M in lung and skin mast cells and basophils. We conclude that the effects of the newer antihistamines on cellular movement into the skin may be diverse, that terfenadine may show organ specificityin vivoand that terfenadine significantly decreases both the early and late gross inflammatory response of the skin to antigen. We cannot, as yet. explain the mechanism(s) by which this occurs.