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目的:调查北京地区艾滋病患者肝脂变的发生率,研究艾滋病患者肝组织中瘦素与肝脂变的关系.方法:应用免疫组织化学法检测18例国人艾滋病患者肝组织中瘦素、CD68及TNF-α的表达,评价这些患者肝脏的组织学改变及脂变状况,分析性别、年龄、肝功能、血脂水平、空腹血糖、HIV病毒载量、CD4+细胞计数和CD8+细胞计数与肝脂变的关系.结果:本组病例艾滋病患者肝脂变的发生率为61.1%(11/18),其中大泡脂变占72.7%(8/11),合并肝病相关性机会性感染者占22.2%(4/18).18例肝组织中瘦素检出率为44.4%,有肝脂变的肝组织其瘦素及CD68表达的阳性率高于无脂变组,但无统计学意义,脂变组TNF-α的阳性率显著高于无脂变组(100%vs42.9%P=0.012).除CD8+细胞计数(×106个/L)在脂变组显著低于无脂变组(142.0±93.0vs515.6±320.7,P=0.026)外,其余因素如年龄,体质量指数、肝功能、血脂水平、空腹血糖、HIV载量、CD4+细胞计数及是否合并丙型肝炎感染均与肝脂变的发生无显著相关.结论:艾滋病患者中肝脂变发生率较高,肝脂变的发生与瘦素的表达未见明显相关,可能与肝组织损伤修复机制有关.
Objective: To investigate the incidence of hepatic steatosis in AIDS patients in Beijing and to study the relationship between leptin and hepatic steatosis in AIDS patients.Methods: Immunohistochemical method was used to detect the levels of leptin, CD68 TNF-α expression, liver histological changes and lipid changes in these patients were evaluated, gender, age, liver function, blood lipid levels, fasting blood glucose, HIV viral load, CD4 + cell count and CD8 + cell count were compared with those of hepatic steatosis The incidence of hepatic steatosis in patients with AIDS was 61.1% (11/18), of which 72.7% (8/11) were large foaming fat, 22.2% were associated with opportunistic liver disease 4/18). The detection rate of leptin in 18 cases was 44.4%. The positive rate of leptin and CD68 expression in liver tissues with hepatic steatosis was higher than that in non-fat group, but there was no statistical significance The positive rate of TNF-αwas significantly higher than that of the non-adipose group (100% vs42.9%, P = 0.012). Except CD8 + cell count (× 106cells / L) ± 93.0vs515.6 ± 320.7, P = 0.026), other factors such as age, body mass index, liver function, blood lipid levels, fasting blood glucose, HIV load There was no significant correlation between CD4 + cell count and hepatitis C infection and the incidence of hepatic steatosis.Conclusion: The prevalence of hepatic steatosis is high in patients with AIDS, and the incidence of hepatic steatosis has no significant correlation with the expression of leptin And liver tissue damage repair mechanism.