de Larrañaga G F, Wingeyer S D A Perés, Puga L M, Alonso B S, Benetucci J A
Hemostasis and Thrombosis Laboratory, Hospital of Infectious Diseases F.J. Muñiz, Uspallata 2272, C1282AEN, Buenos Aires, Argentina.
Eur J Clin Microbiol Infect Dis. 2006 Feb;25(2):98-103. doi: 10.1007/s10096-006-0090-6.
Insulin resistance is associated with highly active antiretroviral therapy in HIV-infected patients, and the risk of developing insulin resistance is increased in hepatitis C virus (HCV)-infected patients. The aim of the present study was to determine whether hepatitis C virus infection constitutes an additional risk factor for insulin resistance or other prothrombotic conditions in HIV-HCV coinfected patients under highly active antiretroviral therapy. One hundred eighteen HIV-infected patients were studied: 50 who had no history of anti-HIV treatment and 68 who were receiving therapy with highly active antiretroviral treatment. The treatment-naive group consisted of 35 HCV-negative subjects and 15 HCV-positive ones. Within the treated group, 50 patients were HCV negative and 18 were HCV positive. For each patient, the lipid profile was determined and the following values measured: glucose, soluble P-selectin (as a marker of platelet activation), soluble thrombomodulin, von Willebrand factor and soluble vascular cell adhesion molecule-1 (as endothelial markers), and insulin resistance. No significant difference (p>0.05) for any variable was found among subjects with or without HCV coinfection in the treatment-naïve group. Among patients under highly active antiretroviral therapy, however, those with HCV coinfection showed higher values (p<0.05) for insulin resistance (homeostasis model assessment value: 2.65 vs. 1.79), glucose (93 vs. 86 mg/dl), endothelial markers (von Willebrand factor, 204 vs. 123%; soluble vascular cell adhesion molecule-1, 650 vs. 482 ng/ml), and platelet activation marker (soluble P-selectin, 78 vs. 51 ng/ml) in parallel with lower CD4+ cells counts (289 vs. 402 cells/mm3) and higher HIV-1 viral loads (305 vs. 50 copies/ml) compared to patients without HCV coinfection. Glucose, soluble P-selectin, and von Willebrand factor were independently related to HCV infection. The presence of HCV coinfection during HIV treatment was closely related to higher values of insulin resistance, to activated platelets, and to endothelial perturbation in parallel with lower CD4+ cell counts and higher HIV-1 viral loads compared to patients without HCV coinfection. On the basis of these results, it may be preferable to treat HCV infection prior to initiating treatment for HIV infection in HIV-HCV-coinfected patients.
胰岛素抵抗与HIV感染患者的高效抗逆转录病毒治疗相关，而丙型肝炎病毒（HCV）感染患者发生胰岛素抵抗的风险增加。本研究的目的是确定在接受高效抗逆转录病毒治疗的HIV-HCV合并感染患者中，丙型肝炎病毒感染是否构成胰岛素抵抗或其他血栓前状态的额外危险因素。对118例HIV感染患者进行了研究：50例无抗HIV治疗史，68例接受高效抗逆转录病毒治疗。未接受过治疗的组包括35例HCV阴性受试者和15例HCV阳性受试者。在接受治疗的组中，50例患者HCV阴性，18例患者HCV阳性。对每位患者测定血脂谱并测量以下数值：血糖、可溶性P选择素（作为血小板活化的标志物）、可溶性血栓调节蛋白、血管性血友病因子和可溶性血管细胞黏附分子-1（作为内皮标志物）以及胰岛素抵抗。在未接受过治疗的组中，HCV合并感染或未合并感染的受试者之间在任何变量上均未发现显著差异（p>0.05）。然而，在接受高效抗逆转录病毒治疗的患者中，与未合并HCV感染的患者相比，合并HCV感染的患者在胰岛素抵抗（稳态模型评估值：2.65对1.79）、血糖（93对86mg/dl）、内皮标志物（血管性血友病因子，204对123%；可溶性血管细胞黏附分子-1，650对482ng/ml）和血小板活化标志物（可溶性P选择素，78对51ng/ml）方面显示出更高的值（p<0.05），同时CD4+细胞计数更低（289对402个细胞/mm3），HIV-1病毒载量更高（305对50拷贝/ml）。血糖、可溶性P选择素和血管性血友病因子与HCV感染独立相关。与未合并HCV感染的患者相比，HIV治疗期间合并HCV感染与更高的胰岛素抵抗值、活化血小板以及内皮紊乱密切相关，同时CD4+细胞计数更低，HIV-1病毒载量更高。基于这些结果，对于HIV-HCV合并感染的患者，在开始HIV感染治疗之前先治疗HCV感染可能更为可取。
