Hung Chao-Hung, Kuo Fang-Ying, Wang Jing-Houng, Lu Sheng-Nan, Hu Tsung-Hui, Chen Chien-Hung, Lee Chuan-mo, Eng Hock-Liew
Division of Hepatogastroenterology, Department of Internal Medicine, Chang Gung Memorial Hospital, Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Antivir Ther. 2006;11(4):483-9.
BACKGROUND/AIMS: Steatosis is recognized as a cofactor influencing the presence and progression of fibrosis in chronic hepatitis C. It has been reported that antiviral therapy may reduce the progression of fibrosis and leads to regression in chronic hepatitis C patients achieving a sustained virological response (SVR). Whether steatosis might affect the long-term histological outcome of antiviral therapy remains unclear.
One-hundred and sixty-one consecutive patients (genotype 1, n=76; genotype 2, n=73) receiving interferon-alpha2b and ribavirin were analysed. Ninety patients had paired biopsies with a mean interval of 29.1 +/- 7.1 months.
Variables associated with baseline steatosis were higher body mass index (> or = 25, P=0.002) and higher fibrosis stage (> or = 2, P=0.019). Neither the presence nor the severity of steatosis was associated with SVR. Evaluation of paired biopsies showed no different distribution of steatosis evolution between patients with and without SVR (P=0.374). Among patients achieving a SVR, there was a significant difference in fibrosis changes between those with grade 0 or 1 steatosis and with grade 2 or 3 steatosis at post-treatment biopsy (-0.6 +/- 1.2 vs 0.3 +/- 1.3, P=0.041), whereas changes in histological activity index did not differ (-3.7 +/- 2.6 vs -4.0 +/- 2.9, P=0.740). Stepwise logistic regression analysis showed that SVR (odds ratio [OR]: 16.33, P=0.004) and grade 0 or 1 post-treatment steatosis (OR: 12.82, P=0.018) were independently associated with fibrosis regression.
In patients with chronic hepatitis C, steatosis not only correlates with advanced fibrosis at baseline but also affects fibrosis regression after antiviral therapy.
背景/目的:脂肪变性被认为是影响慢性丙型肝炎纤维化存在和进展的一个辅助因素。据报道,抗病毒治疗可能会减缓纤维化进展,并使获得持续病毒学应答(SVR)的慢性丙型肝炎患者的纤维化出现消退。脂肪变性是否会影响抗病毒治疗的长期组织学结果仍不清楚。
对161例连续接受α-干扰素2b和利巴韦林治疗的患者(基因1型,n = 76;基因2型,n = 73)进行分析。90例患者接受了配对活检,平均间隔时间为29.1±7.1个月。
与基线脂肪变性相关的变量包括较高的体重指数(≥25,P = 0.002)和较高的纤维化分期(≥2,P = 0.019)。脂肪变性的存在与否及严重程度均与SVR无关。配对活检评估显示,有和没有SVR的患者之间脂肪变性进展的分布没有差异(P = 0.374)。在获得SVR的患者中,治疗后活检时脂肪变性为0级或1级与2级或3级的患者在纤维化变化方面存在显著差异(-0.6±1.2对0.3±1.3,P = 0.041),而组织学活动指数的变化无差异(-3.7±2.6对-4.0±2.9,P = 0.740)。逐步逻辑回归分析显示,SVR(优势比[OR]:16.33,P = 0.004)和治疗后脂肪变性0级或1级(OR:12.82,P = 0.018)与纤维化消退独立相关。
在慢性丙型肝炎患者中,脂肪变性不仅与基线时的严重纤维化相关,而且还会影响抗病毒治疗后的纤维化消退。