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与 HCV 和 HIV 感染者或高危人群中白细胞介素-6 和 C 反应蛋白升高相关的因素。

Correlates of elevated interleukin-6 and C-reactive protein in persons with or at high risk for HCV and HIV infections.

机构信息

*Department of Epidemiology, Johns Hopkins University School of Public Health, Baltimore, MD; †Johns Hopkins University Center on Aging and Health, Baltimore, MD; Divisions of ‡Geriatric Medicine; and §Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, MD.

出版信息

J Acquir Immune Defic Syndr. 2013 Dec 15;64(5):488-95. doi: 10.1097/QAI.0b013e3182a7ee2e.

Abstract

BACKGROUND

HIV and hepatitis C virus (HCV) infections may increase interleukin-6 (IL-6) and C-reactive protein (CRP). However, relationships between inflammatory biomarkers, chronic viral infections, clinical factors, and behavioral factors remain poorly understood.

METHODS

Using linear regression, we modeled cross-sectional associations between loge IL-6 or loge CRP levels and HCV, HIV, injection drug use, and comorbidity among 1191 injection drug users.

RESULTS

Mean age was 47 years, 46.0% reported currently injecting drugs, 59.0% were HCV monoinfected, and 27% were HCV/HIV coinfected. In multivariable models, higher loge IL-6 was associated with HCV monoinfection [β = 0.191, 95% confidence interval (CI): 0.043 to 0.339] and HCV/HIV coinfection (β = 0.394, 95% CI: 0.214 to 0.574). In contrast, HCV monoinfection (β = -0.523, 95% CI: -0.275 to -0.789) and HCV/HIV coinfection (β = -0.554 95% CI: -0.260 to -0.847) were associated with lower CRP. Lower CRP with HCV infection was independent of liver fibrosis severity, synthetic function, or liver injury markers; CRP decreased with higher HCV RNA. Increased injection intensity was associated with higher IL-6 (P = 0.003) and CRP (P < 0.001); increasing comorbidity (P < 0.001) and older age (P = 0.028) were associated with higher IL-6; older age was associated with higher CRP among HCV-uninfected participants (P = 0.021).

CONCLUSION

HIV and HCV infections contribute to chronic inflammation; however, reduced CRP possibly occurs through HCV-mediated mechanisms. Findings highlight potentially modifiable contributors to inflammation.

摘要

背景

艾滋病毒和丙型肝炎病毒(HCV)感染可能会增加白细胞介素-6(IL-6)和 C 反应蛋白(CRP)。然而,炎症生物标志物、慢性病毒感染、临床因素和行为因素之间的关系仍知之甚少。

方法

我们使用线性回归模型,对 1191 名注射吸毒者中 loge IL-6 或 loge CRP 水平与 HCV、HIV、注射吸毒和合并症之间的横断面关联进行建模。

结果

平均年龄为 47 岁,46.0%的人目前正在注射吸毒,59.0%的人是 HCV 单感染,27%的人是 HCV/HIV 合并感染。在多变量模型中,较高的 loge IL-6 与 HCV 单感染相关(β=0.191,95%置信区间[CI]:0.043 至 0.339)和 HCV/HIV 合并感染(β=0.394,95%CI:0.214 至 0.574)。相反,HCV 单感染(β=-0.523,95%CI:-0.275 至-0.789)和 HCV/HIV 合并感染(β=-0.554 95%CI:-0.260 至-0.847)与 CRP 降低相关。HCV 感染时 CRP 降低与肝纤维化严重程度、合成功能或肝损伤标志物无关;CRP 随 HCV RNA 增加而降低。注射强度增加与 IL-6(P=0.003)和 CRP(P<0.001)升高相关;合并症增加(P<0.001)和年龄增加(P=0.028)与 IL-6 升高相关;HCV 未感染者年龄与 CRP 升高相关(P=0.021)。

结论

艾滋病毒和丙型肝炎病毒感染会导致慢性炎症;然而,CRP 的降低可能是通过 HCV 介导的机制发生的。研究结果突出了炎症的潜在可调节因素。

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