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直接抗病毒药物治疗后丙型肝炎病毒4型根除对肝脏硬度测量的影响

Impact of hepatitis C virus genotype-4 eradication following direct acting antivirals on liver stiffness measurement.

作者信息

Tag-Adeen Mohammed, Sabra Ahlam Mohamed, Akazawa Yuko, Ohnita Ken, Nakao Kazuhiko

机构信息

Department of Internal Medicine, Qena School of Medicine, South Valley University, Qena, Egypt.

Department of Gastroenterology and Hepatology, Nagasaki School of Biomedical Sciences, Nagasaki University, Nagasaki, Japan.

出版信息

Hepat Med. 2017 Oct 6;9:45-53. doi: 10.2147/HMER.S142600. eCollection 2017.

DOI:10.2147/HMER.S142600
PMID:29062242
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5638573/
Abstract

BACKGROUND

Liver fibrosis is the most important prognostic factor in chronic hepatitis C virus (HCV) patients, and Egypt shows the highest worldwide HCV prevalence with genotype-4 pre-dominance. The aim of this study was to investigate the degree of liver stiffness measurement (LSM) improvement after successful HCV eradication.

PATIENTS AND METHODS

The study included 84 chronic HCV Egyptian patients, and was conducted at Qena University Hospital from November 1, 2015 till October 31, 2016. LSM was obtained by FibroScan® before starting direct acting antiviral (DAA) treatment and after achieving sustained virologic response-24 (SVR-24). Based on baseline LSM, patients were stratified into F0-F1, F2, F3 and F4 groups (METAVIR). LSM and laboratory data after achieving SVR-24 was compared with that before starting therapy in each fibrosis group (F0-F4), -value <0.05 was statistically significant.

RESULTS

Following DAA treatment, 80 patients achieved SVR-24; of these, 50 were males (62.5%), mean age: 54.2±7.6 years, and mean body mass index: 28.6±2.2 kg/m. Mean baseline LSM dropped from 15.6±10.8 to 12.1±8.7 kPa post-SVR; the maximum change of -5.8 occurred in F4 versus -2.79, -1.28 and +0.08 in F3, F2 and F0-F1 respectively (<0.0001). At baseline, 41 patients were in the F4 group; only 16 (39%) regressed to non-cirrhotic range (<12.5 kPa), while 25 (61%) were still cirrhotic despite achieving SVR-24 (<0.0001). Patients who achieved LSM improvement (n=64) have had significantly higher baseline aspartate transferase (AST) and alanine transaminase (ALT). Also, those patients showed significant improvement in AST, AST/platelets ratio index (APRI) and fibrosis-4 index (Fib-4) after achieving SVR; 91% showed AST improvement (=0.01) and APRI improvement (=0.01) and 81% showed Fib-4 improvement (=0.04). Females, diabetics, patients with S3 steatosis and patients older than 50 years showed less LSM improvements than their counterparts. Baseline LSM ≥9 kPa, bilirubin ≥1 mg/dl, ALT ≥36 U/L and AST ≥31 U/L were significant predictors for LSM improvement.

CONCLUSION

Successful HCV genotype-4 eradication results in significant LSM improvement; the best improvement occurs in F4 patients. But as the majority of cirrhotics are still at risk for liver decompensation and hepatocellular carcinoma development despite achieving SVR-24, early detection and treatment are highly recommended.

摘要

背景

肝纤维化是慢性丙型肝炎病毒(HCV)患者最重要的预后因素,埃及是全球HCV患病率最高且以4型为主的国家。本研究的目的是调查HCV成功根除后肝脏硬度测量(LSM)的改善程度。

患者和方法

该研究纳入了84例埃及慢性HCV患者,于2015年11月1日至2016年10月31日在基纳大学医院进行。在开始直接抗病毒药物(DAA)治疗前及获得持续病毒学应答24周(SVR-24)后,通过FibroScan®获得LSM。根据基线LSM,患者被分为F0-F1、F2、F3和F4组(METAVIR)。比较每个纤维化组(F0-F4)达到SVR-24后的LSM和实验室数据与开始治疗前的数据,P值<0.05具有统计学意义。

结果

接受DAA治疗后,80例患者实现了SVR-24;其中,50例为男性(62.5%),平均年龄:54.2±7.6岁,平均体重指数:28.6±2.2kg/m²。平均基线LSM从15.6±10.8kPa降至SVR后的12.1±8.7kPa;F4组的最大变化为-5.8,而F3、F2和F0-F1组分别为-2.79、-1.28和+0.08(P<0.0001)。基线时,41例患者在F4组;尽管实现了SVR-24,但只有16例(39%)回归到非肝硬化范围(<12.5kPa),而25例(61%)仍为肝硬化(P<0.0001)。实现LSM改善的患者(n=64)基线天门冬氨酸转氨酶(AST)和丙氨酸转氨酶(ALT)显著更高。此外,这些患者在实现SVR后AST、AST/血小板比值指数(APRI)和纤维化-4指数(Fib-4)有显著改善;91%的患者AST改善(P=0.01)且APRI改善(P=0.01),81%的患者Fib-4改善(P=0.04)。女性、糖尿病患者、S3脂肪变性患者和年龄大于50岁的患者LSM改善程度低于其对应人群。基线LSM≥9kPa、胆红素≥1mg/dl、ALT≥36U/L和AST≥31U/L是LSM改善的显著预测因素。

结论

成功根除HCV 4型可导致LSM显著改善;F4患者改善最佳。但由于大多数肝硬化患者尽管实现了SVR-24仍有肝失代偿和肝细胞癌发生的风险,强烈建议早期检测和治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/050e/5638573/b735b311fc74/hmer-9-045Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/050e/5638573/c4191564bac3/hmer-9-045Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/050e/5638573/83523ef10173/hmer-9-045Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/050e/5638573/275a3876bc56/hmer-9-045Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/050e/5638573/e218292dacc3/hmer-9-045Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/050e/5638573/b735b311fc74/hmer-9-045Fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/050e/5638573/c4191564bac3/hmer-9-045Fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/050e/5638573/83523ef10173/hmer-9-045Fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/050e/5638573/275a3876bc56/hmer-9-045Fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/050e/5638573/e218292dacc3/hmer-9-045Fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/050e/5638573/b735b311fc74/hmer-9-045Fig5.jpg

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