通过直接作用抗病毒药物根除丙型肝炎病毒会导致脂肪肝和极低密度脂蛋白胆固醇血症的患病率同时增加，且体重不增加。
Hepatitis C virus eradication by direct-acting antivirals causes a simultaneous increase in the prevalence of fatty liver and hyper low-density lipoprotein cholesterolemia without an increase in body weight.
作者信息
Tokuchi Yoshimasa, Suda Goki, Kawagishi Naoki, Ohara Masatsugu, Kohya Risako, Sasaki Takashi, Yoda Tomoka, Maehara Osamu, Ohnishi Shunsuke, Kubo Akinori, Yoshida Sonoe, Fu Qingjie, Yang Zijian, Hosoda Shunichi, Kitagataya Takashi, Suzuki Kazuharu, Nakai Masato, Sho Takuya, Natsuizaka Mitsuteru, Ogawa Koji, Sakamoto Naoya
机构信息
Department of Gastroenterology and Hepatology, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Laboratory of Molecular and Cellular Medicine, Faculty of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.
出版信息
Hepatol Res. 2023 Jul;53(7):595-606. doi: 10.1111/hepr.13899. Epub 2023 Apr 4.
AIM
Hepatitis C virus (HCV) infection has been reported to cause liver steatosis. Thus, eradicating HCV with direct-acting antivirals (DAAs) is expected to reduce liver steatosis. We aimed to clarify long-term changes in the prevalence of fatty liver and hyper-low-density lipoprotein (LDL) cholesterolemia and their associations in patients who achieve successful HCV eradication using DAAs.
METHODS
This retrospective study included patients with HCV who achieved sustained virologic response after interferon-free DAA and analyzed the changes in the prevalence of fatty liver diagnosed with controlled attenuation parameter (CAP), hyper-LDL cholesterolemia, and their relationships at baseline (n = 100) and 24 weeks (SVR24, n = 100), 96 weeks (SVR96, n = 100), and 144 weeks (SVR144, n = 90) after DAA.
RESULTS
In 100 participants, the prevalence of fatty liver (19% vs. 32%, p = 0.0349) and hyper-LDL cholesterolemia (6% vs. 15%, p = 0.0379) significantly increased without changes in body weight at SVR96. Median total cholesterol, low-density lipoprotein cholesterol (LDL-C), and small-dense-LDL (sdLDL) levels and CAP values were significantly greater at SVR24, SVR96, and SVR144 than at baseline. Baseline CAP values and changes in CAP values were significantly negatively correlated at every observation point: r = -0.5305, p < 0.0001 at SVR24; r = -0.3617, p = 0.0005 at SVR96; and r = -0.4735, p < 0.0001 at SVR144. A similar relationship was observed in cholesterol levels. Unlike at baseline, CAP values were significantly positively correlated with LDL-C and sdLDL-C levels at all observation points after DAAs.
CONCLUSIONS
Direct-acting antivirals may cause an increased prevalence of fatty liver accompanying hyper-LDL cholesterolemia without increased body weight. As post-SVR liver steatosis could cause HCC, careful follow-up may be required.
目的
据报道，丙型肝炎病毒（HCV）感染会导致肝脏脂肪变性。因此，使用直接抗病毒药物（DAA）根除HCV有望减少肝脏脂肪变性。我们旨在阐明使用DAA成功根除HCV的患者中脂肪肝和极低密度脂蛋白（LDL）胆固醇血症患病率的长期变化及其关联。
方法
这项回顾性研究纳入了在接受无干扰素DAA治疗后实现持续病毒学应答的HCV患者，并分析了在基线（n = 100）以及DAA治疗后24周（SVR24，n = 100）、96周（SVR96，n = 100）和144周（SVR144，n = 90）时，通过受控衰减参数（CAP）诊断的脂肪肝患病率、高LDL胆固醇血症及其关系的变化。
结果
在100名参与者中，SVR96时脂肪肝患病率（19%对32%，p = 0.0349）和高LDL胆固醇血症患病率（6%对15%，p = 0.0379）显著增加，而体重无变化。SVR24、SVR96和SVR144时的总胆固醇、低密度脂蛋白胆固醇（LDL-C）、小而密LDL（sdLDL）水平中位数以及CAP值均显著高于基线。在每个观察点，基线CAP值与CAP值变化均呈显著负相关：SVR24时r = -0.5305，p < 0.0001；SVR96时r = -0.3617，p = 0.0005；SVR144时r = -0.4735，p < 0.0001。胆固醇水平也观察到类似关系。与基线时不同，DAA治疗后的所有观察点，CAP值与LDL-C和sdLDL-C水平均呈显著正相关。
结论
直接抗病毒药物可能导致伴有高LDL胆固醇血症的脂肪肝患病率增加，且体重未增加。由于SVR后肝脏脂肪变性可能导致肝癌，可能需要进行密切随访。
Zotero 插件