Srisopa Somkid, Pipatsatitpong Duangnate, Akekawatchai Chareeporn
Graduate Program in Medical Technology, Faculty of Allied Health Sciences, Thammasat University, Pathumthani 12121, Thailand.
Bamrasnaradura Infectious Diseases Institute, Ministry of Public Health, Nonthaburi 11000, Thailand.
Biomed Rep. 2024 Aug 13;21(4):146. doi: 10.3892/br.2024.1834. eCollection 2024 Oct.
Hepatitis C virus (HCV) coinfection in individuals living with human immunodeficiency virus (HIV) (PLWH) may affect lipid metabolism and accelerate the progression of chronic hepatitis. Therefore, the identification of risk factors for progressive liver disease is needed. The present study aimed to examine the prevalence and clinical features associated with liver fibrosis in HCV-coinfected HIV patients, including metabolic markers. A total of 105 patients coinfected with HIV and HCV were recruited and liver fibrosis was assessed using the fibrosis-4 (FIB-4) score and aspartate aminotransferase-to-platelet ratio index (APRI). Logistic regression analyses indicated that patients aged >50 years and with a CD4 cell count <350 cells/µl had an 11.4-times higher (P=0.001) and a 5.7-times higher (P=0.017) risk of liver fibrosis, as determined by FIB-4 score, compared to patients aged ≤40 years and a CD4 cell count of ≥350 cells/µl, respectively. In addition, patients naïve to HCV treatment or receiving treatment had 5.4- and 12.7-times higher risks for liver fibrosis, as determined by APRI, than those with sustained virologic response (SVR) (P=0.003 and P=0.033, respectively). Univariate analysis indicated lower risks of liver fibrosis, as determined by APRI, in the patients with abnormally high levels of cholesterol, high-density lipoprotein (HDL) and low-density lipoprotein (LDL) than those with normal levels [odds ratio (OR) 0.3, 95% confidence interval (CI) 0.1-0.9, P=0.037; OR 0.4, 95% CI 0.2-0.9, P=0.041; OR 0.2, 95% CI 0.1-0.5, P=0.001] and multivariate analysis suggested only patients with high levels of LDL had a lower risk for liver fibrosis determined by APRI (OR 0.1, 95% CI 0.3-0.8, P=0.029). Consistently, serum levels of cholesterol, HDL and LDL were significantly lower in the patient groups with more advanced fibrosis, evaluated by FIB-4 score and APRI, than those without liver fibrosis and the levels of cholesterol and LDL in the patients achieving SVR were higher than those with no response or not receiving treatment (all P<0.05). In conclusion, the present study identified serum lipid levels as associated factors of hepatic fibrosis, together with age, CD4 cell count and HCV treatment status, in HCV-coinfected PLWH on long-term suppressive anti-retroviral therapy.
人类免疫缺陷病毒(HIV)感染者(PLWH)合并丙型肝炎病毒(HCV)感染可能会影响脂质代谢并加速慢性肝炎的进展。因此,需要确定进展性肝病的危险因素。本研究旨在调查合并HCV感染的HIV患者中与肝纤维化相关的患病率和临床特征,包括代谢标志物。共招募了105例合并HIV和HCV感染的患者,并使用纤维化-4(FIB-4)评分和天冬氨酸转氨酶与血小板比值指数(APRI)评估肝纤维化。逻辑回归分析表明,年龄>50岁且CD4细胞计数<350个/μl的患者,根据FIB-4评分确定的肝纤维化风险分别比年龄≤40岁且CD4细胞计数≥350个/μl的患者高11.4倍(P=0.001)和5.7倍(P=0.017)。此外,根据APRI确定,初治或正在接受HCV治疗的患者发生肝纤维化的风险分别比获得持续病毒学应答(SVR)的患者高5.4倍和12.7倍(分别为P=0.003和P=0.033)。单因素分析表明,与血脂水平正常的患者相比,胆固醇、高密度脂蛋白(HDL)和低密度脂蛋白(LDL)水平异常升高的患者根据APRI确定的肝纤维化风险较低[比值比(OR)0.3,95%置信区间(CI)0.1-0.9,P=0.037;OR 0.4,95%CI 0.2-0.9,P=0.041;OR 0.2,95%CI 0.1-0.5,P=0.001],多因素分析表明,只有LDL水平高的患者根据APRI确定的肝纤维化风险较低(OR 0.1,95%CI 0.3-0.8,P=0.029)。同样,根据FIB-4评分和APRI评估,纤维化程度更严重的患者组血清胆固醇、HDL和LDL水平显著低于无肝纤维化的患者组,且获得SVR的患者胆固醇和LDL水平高于无应答或未接受治疗的患者(所有P<0.05)。总之,本研究确定血清脂质水平是长期接受抑制性抗逆转录病毒治疗的合并HCV感染的PLWH肝纤维化的相关因素,同时还有年龄、CD4细胞计数和HCV治疗状态。