Levels of vaginal secretory leukocyte protease inhibitor are decreased in women with lower reproductive tract infections

Levels of vaginal secretory leukocyte protease inhibitor are decreased in women with lower reproductive tract infections
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DOI:
10.1067/mob.2000.107383
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发表时间:
2000-11-01
影响因子:
9.8
通讯作者:
Heine, RP
Heine, RP
中科院分区:
医学1区
文献类型:
--
作者:
Draper, DL;Landers, DV;Heine, RP

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目的:分泌性白细胞蛋白酶抑制剂有助于抵抗口腔原发性人类免疫缺陷病毒感染。然而,这种抑制剂在患有性传播疾病或阴道炎的女性生殖道中的水平尚未得到很好的描述。目的是确定有症状和无症状生殖器感染妇女的阴道抑制剂水平。研究设计:我们用标准方法检测了207名未怀孕妇女的淋病奈瑟菌、阴道毛滴虫、沙眼衣原体、念珠菌和细菌性阴道病。第二组无症状孕妇(N = 231)也进行了研究。采用酶联免疫吸附法测定分泌性白细胞蛋白酶抑制剂,并采用非参数法比较结果。结果:两组有任何性传播疾病的女性阴道分泌性白细胞蛋白酶抑制剂水平均显著低于无感染的女性(P < 0.0001)。细菌性阴道病患者和细菌性阴道病合并酵母菌性阴道炎患者的水平也降低(P < 0.025)。结论:下生殖道感染的女性阴道分泌性白细胞蛋白酶抑制剂水平降低。这可能是人类免疫缺陷病毒感染易感性增加的共同机制。
OBJECTIVE: Secretory leukocyte protease inhibitor contributes resistance to primary human immunodeficiency virus infection in the oral cavity. However, the levels of this inhibitor in the genital tract of women with sexually transmitted diseases or vaginitis are not well described. The objective was to determine vaginal inhibitor levels in women with symptomatic and asymptomatic genital infections.STUDY DESIGN: We tested 207 nonpregnant women for Neisseria gonorrhoeae, Trichomonas vaginalis, Chlamydia trachomatis, Candida species, and bacterial vaginosis by standard methods. A second group of symptom-free pregnant women (N = 231) was also studied. Secretory leukocyte protease inhibitor was measured by enzyme-linked immunosorbent assay, and results were compared by nonparametric methods.RESULTS: Vaginal levels of secretory leukocyte protease inhibitor in both groups were significantly lower in women with any sexually transmitted disease than in those without infection (P < .0001). Patients with bacterial vaginosis and those with bacterial vaginosis with yeast vaginitis also had decreased levels (P < .025).CONCLUSIONS: Levels of secretory leukocyte protease inhibitor in vaginal fluid are decreased in women with lower genital tract infection. This may represent a common mechanism of increasing susceptibility to infection with human immunodeficiency virus.