On the mechanism of thrombocytopenic purpura in sexually active homosexual men.
On the mechanism of thrombocytopenic purpura in sexually active homosexual men.
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性活跃的同性恋男性血小板减少性紫癜的机制。
DOI：
10.1056/nejm198409063111004
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发表时间：
1984
期刊：
影响因子：
--
通讯作者：
Karpatkin,S
中科院分区：
文献类型：
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作者：
Walsh,CM;Nardi,MA;Karpatkin,S
最近在性活跃的同性恋男性中发现了血小板减少性紫癜。为了阐明这一人群中血小板减少性紫癜的发病机制，我们将33名同性恋男性患者与23名被认为患有典型自身免疫性血小板减少性紫癜的患者（15名女性和8名男性）进行了比较。与自身免疫性血小板减少性紫癜患者相比，同性恋组血小板结合IgG水平高3.8倍，血小板结合补体水平高4.2倍。10名同性恋患者中只有1名的血小板洗脱液在体外与正常血小板反应，而15名自身免疫性血小板减少性紫癜患者中有12名的血小板洗脱液。24名同性恋患者中有21名（88%）血清中能够与血小板结合的免疫复合物水平升高，而5名自身免疫性血小板减少性紫癜患者中没有循环免疫复合物。来自三名同性恋患者的阳性血清样本的IgG部分不与正常血小板结合，而来自两名自身免疫性血小板减少性紫癜患者和一名在怀孕期间产生等免疫抗血小板抗体的妇女（作为阳性对照研究）的阳性血清样本的IgG部分与正常血小板结合。我们得出结论，尽管典型的自身免疫性血小板减少性紫癜涉及针对血小板抗原决定因子的抗血小板IgG，但发生在性活跃的同性恋男性中的血小板减少性紫癜通常不是由抗血小板IgG引起的，而可能是补体和免疫复合物在血小板上的非特异性沉积引起的。[中华医学杂志1984；31:635-9]
Thrombocytopenic purpura has recently been noted in sexually active homosexual men. To elucidate the pathogenesis of thrombocytopenic purpura in this population, we compared the disorder in 33 homosexual men with that in 23 patients (15 women and 8 men) thought to have classic autoimmune thrombocytopenic purpura. The homosexual group had 3.8-fold higher levels of platelet-bound IgG and 4.2-fold higher levels of platelet-bound complement than the patients with autoimmune thrombocytopenic purpura. Eluates from the platelets of only 1 of 10 homosexual patients reacted in vitro with normal platelets, as compared with those from the platelets of 12 of 15 patients with autoimmune thrombocytopenic purpura. Twenty-one of 24 homosexual patients (88 per cent) had elevated serum levels of immune complexes that were capable of binding to platelets, whereas none of 5 patients with autoimmune thrombocytopenic purpura had circulating immune complexes. The IgG fraction of positive serum samples from three homosexual patients did not bind to normal platelets, whereas that from the positive serum of two patients with autoimmune thrombocytopenic purpura and one woman in whom isoimmune antiplatelet antibody developed during pregnancy (studied as a positive control) did bind to normal platelets.We conclude that, whereas classic autoimmune thrombocytopenic purpura involves antiplatelet IgG directed against platelet antigenic determinants, the thrombocytopenic purpura that occurs in sexually active homosexual men is usually caused not by antiplatelet IgG but probably by the nonspecific deposition of complement and immune complexes on platelets. (N Engl J Med 1984; 311: 635–9.)