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在接受直接抗病毒治疗并获得持续病毒学应答的慢性丙型肝炎感染患者中,使用受控衰减参数评估肝脏脂肪变性的变化。

Changes in Liver Steatosis Using Controlled Attenuation Parameter among Patients with Chronic Hepatitis C Infection Treated with Direct-Acting Antivirals Therapy Who Achieved Sustained Virological Response.

作者信息

Trifan Anca, Stratina Ermina, Rotaru Adrian, Stafie Remus, Zenovia Sebastian, Nastasa Robert, Huiban Laura, Sfarti Catalin, Cojocariu Camelia, Cuciureanu Tudor, Muzica Cristina, Chiriac Stefan, Girleanu Irina, Singeap Ana-Maria, Stanciu Carol

机构信息

Department of Gastroenterology, Grigore T. Popa University of Medicine and Pharmacy, 700111 Iasi, Romania.

Department of Gastroenterology and Hepatology, "St. Spiridon" University Hospital, 700115 Iasi, Romania.

出版信息

Diagnostics (Basel). 2022 Mar 13;12(3):702. doi: 10.3390/diagnostics12030702.

DOI:10.3390/diagnostics12030702
PMID:35328255
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8947513/
Abstract

Chronic hepatitis C virus (HCV) infection induces hepatic steatosis due to viral and host factors. However, information regarding the effects of direct-acting antivirals (DAAs) therapy on liver steatosis and fibrosis is limited. Vibration-controlled transient elastography (VCTE) with a controlled attenuation parameter (CAP) represents a non-invasive method, which has been used in the last few years for the detection of hepatic steatosis and fibrosis before and at a sustained virological response at 12 weeks (SVR12). The aim of this study was to assess the modifications of liver steatosis and fibrosis in HCV-infected patients who achieved SVR12. Consecutive patients with chronic HCV infection that were treated with DAAs in a tertiary gastroenterology center from Romania were included. Demographics, laboratory data, and VCTE evaluation were recorded in all patients. Patients with previous hepatic decompensation and those who did not achieve SVR were excluded. Two hundred and eighty patients (67.1% females) who achieved SVR12 were included. Regarding the changes in biological parameters, including liver enzymes such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), reduced to normal levels at SVR12 compared to the baseline (28.72 ± 24.71 U/L vs. 40.72 ± 27.34 U/L for ALT, p < 0.013 and 27.21 ± 11.15 U/L vs. 33.35 ± 23.37 U/L for AST, p = 0.029). On the contrary, the levels of triglycerides increased significantly from the baseline to SVR12 (124.03 ± 113.49 mg/dL to 153.78 ± 94.53, p = 0.004). Regarding hepatic steatosis by CAP evaluation, at SVR12, 186 (66.4%) of the individuals had a CAP score of ≥248 dB/m, an increase of 4.6% from the baseline. After viral eradication with DAAs, we observed an increase in hepatic steatosis. Hence, a long-term follow-up is mandatory to identify HCV-infected patients with hepatic steatosis post-SVR and the risk factors for more severe outcomes.

摘要

慢性丙型肝炎病毒(HCV)感染由于病毒和宿主因素会导致肝脂肪变性。然而,关于直接抗病毒药物(DAA)治疗对肝脏脂肪变性和纤维化影响的信息有限。带有受控衰减参数(CAP)的振动控制瞬时弹性成像(VCTE)是一种非侵入性方法,在过去几年中已用于在12周持续病毒学应答(SVR12)之前及之时检测肝脂肪变性和纤维化。本研究的目的是评估实现SVR12的HCV感染患者肝脏脂肪变性和纤维化的变化。纳入了罗马尼亚一家三级胃肠病学中心接受DAA治疗的连续慢性HCV感染患者。记录了所有患者的人口统计学、实验室数据和VCTE评估结果。排除既往有肝失代偿的患者以及未实现SVR的患者。纳入了280例实现SVR12的患者(女性占67.1%)。关于生物学参数的变化,包括丙氨酸氨基转移酶(ALT)和天冬氨酸氨基转移酶(AST)等肝酶,与基线相比,在SVR12时降至正常水平(ALT:28.72±24.71 U/L vs. 40.72±27.34 U/L,p<0.013;AST:27.21±11.15 U/L vs. 33.35±23.37 U/L,p = 0.029)。相反,甘油三酯水平从基线到SVR12显著升高(124.03±113.49 mg/dL至153.78±94.53,p = 0.004)。通过CAP评估肝脂肪变性,在SVR12时,186例(66.4%)个体的CAP评分≥248 dB/m,较基线增加了4.6%。在用DAA根除病毒后,我们观察到肝脂肪变性增加。因此,必须进行长期随访,以识别SVR后有肝脂肪变性的HCV感染患者以及更严重后果的危险因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1204/8947513/227df06b4fa8/diagnostics-12-00702-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1204/8947513/ca4dbceabd9f/diagnostics-12-00702-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1204/8947513/360491a586ae/diagnostics-12-00702-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1204/8947513/2d5fa2645c14/diagnostics-12-00702-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1204/8947513/227df06b4fa8/diagnostics-12-00702-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1204/8947513/ca4dbceabd9f/diagnostics-12-00702-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1204/8947513/360491a586ae/diagnostics-12-00702-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1204/8947513/2d5fa2645c14/diagnostics-12-00702-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1204/8947513/227df06b4fa8/diagnostics-12-00702-g004.jpg

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