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

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
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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高低密度脂蛋白胆固醇血症的患病率同时增加,但体重不会增加

DOI:
10.1111/hepr.13899
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发表时间:
2023
影响因子:
4.2
通讯作者:
Sho Takuya et al.,
Sho Takuya et al.,
中科院分区:
医学2区
文献类型:
--
作者:
Tokuchi Yoshimasa;Sho Takuya et al.,

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目的丙型肝炎病毒(HCV)感染可引起肝脏脂肪变性。因此,用直接作用的抗病毒药物(DAA)根除丙型肝炎病毒有望减少肝脏脂肪变性。我们的目的是阐明在使用DAA成功根除丙型肝炎病毒的患者中脂肪肝和超低密度脂蛋白(LDL)胆固醇血症的长期变化及其相关性。方法回顾研究包括在DAA治疗后获得持续病毒学应答的丙型肝炎患者,分析在DAA治疗后控制衰减参数(CAP)、高低密度脂蛋白胆固醇血症诊断的脂肪肝患病率的变化及其相互关系。结果在100名参与者中,受试者分别在基线(n=100)、24周(SVR24,n=100)、96周(SVR96,n=100)和144周(SVR144,n=990)进行研究。在SVR96的体重没有变化的情况下,脂肪肝(19%对32%,p=0.0349)和高低密度脂蛋白血症(6%对15%,p=0.0379)的患病率显著增加。SVR24、SVR96和SVR144的中位数总胆固醇、低密度脂蛋白胆固醇(LDL-C)和小密度脂蛋白胆固醇(SdLDL)水平和CAP值显著高于基线。在每个观察点,基线CAP值与CAP值的变化呈显著负相关:在SVR24,r=−0.5305,p<;在SVR96,r=−0.3617,p=0.0005;在胆固醇水平上也观察到了类似的关系。与基线不同,DAAS后各观察点的CAP值与LDL-C和sdLDL-C水平呈显著正相关。结论直接作用的抗病毒药物可能导致脂肪肝合并高低密度脂蛋白血症的患病率增加,而不增加体重。由于SVR后的肝脏脂肪变性可能导致肝细胞癌,可能需要仔细的随访。
AimHepatitis 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.MethodsThis 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.ResultsIn 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; andr= −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.ConclusionsDirect‐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.
DOI: 10.1016/j.virol.2010.07.041
发表时间: 2010-11
期刊: Virology
影响因子: 3.7
作者:
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影响因子: 21.3
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