Truscello Esther, Wang Shouao, Young Jim, Sebastiani Giada, Walmsley Sharon L, Hull Mark, Cooper Curtis, Klein Marina B
Faculty of Health, Medicine, and Life Sciences, Maastricht University, Maastricht, The Netherlands.
Department of Medicine, Division of Infectious Diseases, Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada.
J Infect Dis. 2025 Feb 4;231(1):e101-e112. doi: 10.1093/infdis/jiae487.
Both human immunodeficiency virus (HIV) and hepatitis C virus (HCV) infections increase the risk of hepatic steatosis (HS), which in turn contribute to the severity and progression of liver disease. Direct-acting antivirals (DAAs) can cure HCV but whether they reduce HS is unclear.
HS was assessed using the controlled attenuation parameter (CAP) and the Hepatic Steatosis Index (HSI) in participants coinfected with HIV and HCV from the Canadian Coinfection Cohort. Changes in HS, before, during, and after successful DAA treatment were estimated using generalized additive mixed models, adjusted for covariates measured prior to treatment (age, sex, duration of HCV infection, body mass index, diabetes, prior exposure to dideoxynucleosides, and hazardous drinking).
In total, 431 participants with at least 1 measure of CAP or HSI before treatment were included. CAP steadily increased over time: adjusted annual slope 3.3 dB/m (95% credible interval [CrI], 1.6-4.9) before, and 3.9 dB/m (95% CrI, 1.9-5.9) after DAA treatment, irrespective of pretreatment CAP. In contrast, HSI changed little over time: annual slope 0.2 (95% CrI, -0.1 to 0.5) before and 0.2 (95% CrI, -0.1 to 0.5) after, but demonstrated a marked reduction during treatment -4.5 (95% CrI, -5.9 to -3.1).
When assessed by CAP, HS was unaffected by DAA treatment and steadily increased over time. In contrast, HSI did not appear to reflect changes in HS, with the decrease during treatment likely related to resolution of hepatic inflammation. Ongoing HS may pose a risk for liver disease in coinfected people cured of HCV.
人类免疫缺陷病毒（HIV）感染和丙型肝炎病毒（HCV）感染均会增加肝脂肪变性（HS）的风险，而肝脂肪变性又会加重肝脏疾病的严重程度并促使其进展。直接抗病毒药物（DAA）可治愈HCV，但尚不清楚其是否能减轻肝脂肪变性。
在加拿大合并感染队列中，使用受控衰减参数（CAP）和肝脂肪变性指数（HSI）对HIV和HCV合并感染的参与者进行肝脂肪变性评估。使用广义相加混合模型估计在成功进行DAA治疗之前、期间和之后肝脂肪变性的变化，并对治疗前测量的协变量（年龄、性别、HCV感染持续时间、体重指数、糖尿病、先前接触双脱氧核苷情况以及有害饮酒）进行校正。
总共纳入了431名在治疗前至少有1次CAP或HSI测量值的参与者。CAP随时间稳步增加：无论治疗前的CAP如何，DAA治疗前调整后的年斜率为3.3 dB/m（95%可信区间[CrI]，1.6 - 4.9），治疗后为3.9 dB/m（95% CrI，1.9 - 5.9）。相比之下，HSI随时间变化不大：治疗前的年斜率为0.2（95% CrI，-0.1至0.5），治疗后的年斜率为0.2（95% CrI，-0.1至0.5），但在治疗期间显著降低，为-4.5（95% CrI，-5.9至-3.1）。
通过CAP评估时，肝脂肪变性不受DAA治疗影响且随时间稳步增加。相比之下，HSI似乎并未反映肝脂肪变性的变化，治疗期间的下降可能与肝脏炎症的消退有关。持续存在的肝脂肪变性可能会给HCV已治愈的合并感染患者带来肝脏疾病风险。
