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作 者:高婷[1] 章鹏[1] 宫钰[1] 沈黎蔚[1] 夏强[2] 李海[1]
机构地区:[1]上海交通大学医学院附属仁济医院消化科、上海市消化疾病研究所,200001 [2]上海交通大学医学院附属仁济医院肝移植中心
出 处:《胃肠病学》2012年第8期453-456,共4页Chinese Journal of Gastroenterology
摘 要:背景:乙型肝炎后肝硬化失代偿行肝移植术患者的肝脏组织病理学特点鲜有报道。目的:评估乙型肝炎后肝硬化失代偿行肝移植术患者的肝脏组织炎症活动度情况,并分析其与血清HBV DNA、临床生化指标的相关性。方法:收集乙型肝炎后肝硬化失代偿行肝移植术的连续病例72例,取肝组织行HE、网状纤维和Masson染色,观察肝脏组织炎症活动度。以Spearman秩相关分析血清HBV DNA和临床生化指标与肝脏组织炎症活动度的相关性。结果:81.9%(59/72)的乙型肝炎后肝硬化失代偿患者肝脏组织有严重的活动性炎症(G3、G4级);43.1%(31/72)患者经抗病毒治疗后血清HBV DNA阴性,其中77.4%(24/31)的患者肝脏组织炎症活动度≥G3级。MELD评分、总胆红素和凝血酶原时间与肝脏组织炎症活动度呈正相关,而ALT、HBeAg和HBV DNA水平不能反映乙型肝炎后肝硬化失代偿患者肝脏组织炎症活动度。结论:持续存在的活动性炎症是乙型肝炎后肝硬化失代偿患者的主要病理学特征以及接受肝移植的主要原因,HBV DNA载量并不能反映患者的肝脏组织炎症活动度。Background: Histopathologic analysis of patients with hepatitis B-related decompensated cirrhosis has been seldomly reported. Aims: To assess the hepatic inflammatory activity in patients undergoing liver transplantation for hepatitis B- related decompensated cirrhosis, and its correlation with HBV DNA, as well as biochemical parameters was analyzed. Methods: Seventy-two consecutive patients undergoing liver transplantation for hepatitis B-related decompensated cirrhosis were enrolled. Hepatic inflammatory activity was evaluated by HE staining, reticular fiber staining and Masson staining. Correlation of serum HBV DNA level and biochemical parameters with hepatic inflammatory activity was analyzed by Spearman rank correlation. Results: High-grade inflammation (grade 3 or 4) was found in 81.9% (59/72) of cases. After antiviral therapy, 43.1% (31/72) of patients had HBV DNA 〈 1000 eopies/mL, of whom 77.4% (24/31) had high-grade inflammation ( grade 3 or 4). MELD score, serum total bilirubin and prothrombin time were correlated with hepatic inflammatory activity. No correlation was found between inflammatory activity and ALT level, HBeAg seropositivity and HBV DNA level. Conclusions : Persistence of hepatic active inflammation is the main histological feature and cause for liver transplantation in patients with hepatitis B-related decompensated cirrhosis. HBV DNA load does not reflect hepatic inflammatory activity in patients with hepatitis B-related decompensated cirrhosis.
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