AASLD 2011:Good Response to Entecavir Reduces Risk of Hepatitis B Liver Disease

StephenW

http://www.hivandhepatitis.com/hepatitis-b/hepatitis-b-topics/hbv-treatment/3357-aasld-good-response-to-entecavir-reduces-risk-of-hepatitis-b-liver-disease-progression
AASLD: Good Response to Entecavir Reduces Risk of Hepatitis B Liver Disease Progression

    Published on Tuesday, 22 November 2011 00:00
    Written by Liz Highleyman



Chronic hepatitis B patients who achieve HBV DNA viral load suppression on entecavir (Baraclude) have a lower risk of liver failure, hepatocellular carcinoma, and death than non-responders, according to study findings presented this month at the American Association for the Study of Liver Diseases Liver Meeting (AASLD 2011) in San Francisco.

Over years or decades, chronic hepatitis B virus (HBV) infection can lead to advanced liver disease including cirrhosis and liver cancer. The nucleoside analog drug entecavir effectively inhibits HBV replication, lowers viral load, and improves liver fibrosis, but the ultimate goal of treatment is to reduce the likelihood of clinical events and premature death.

Roeland Zoutendijk from Erasmus Medical Center in Rotterdam and colleagues investigated whether entecavir-induced viral suppression is associated with improved clinical outcomes among chronic hepatitis B patients.

The researchers evaluated medical records from HBV monoinfected patients (e.g., no HIV, hepatitis C, or hepatitis delta coinfection) at 10 large European referral centers within the VIRGIL Network who were treated with entecavir monotherapy for at least 3 months.

The analysis included 372 participants; three-quarters were men, about half were white, the mean age was 43 years, and about 60% were hepatitis B "e" antigen (HBeAg) positive. About 73% had no cirrhosis, 24% had compensated cirrhosis, and 2% had decompensated cirrhosis at baseline. About one-third had previously been treated with nucleoside/nucleotide analogs, including lamivudine (Epivir-HBV) and adefovir (Hepsera), and about 20% had previously used interferon.

Virological response was defined as serum HBV DNA < 80 IU/mL. Clinical endpoints considered were liver decompensation (indicated by jaundice, ascites, bleeding varices, or hepatic encephalopathy), occurrence of hepatocellular carcinoma (HCC, a form of primary liver cancer), and death. The median follow-up period was 19 months.

Results

-Patients with compensated or decompensated cirrhosis at baseline and those without had similar likelihood of achieving virological response on entecavir.
-Patients who achieved virological response on entecavir had a significantly lower probability of disease progression compared with non-responders (hazard ratio 0.29):
        No cirrhosis: 1 event among 222 responders (0%) vs 1 event among 52 non-responders (2%);
        Compensated cirrhosis: 3 events among 73 responders (4%) vs 5 events among 16 non-responders (30%);
        Decompensated cirrhosis: 1 event among 6 responders (17%) vs 2 events among 3 non-responders (67%).
-Patient age, baseline MELD score, albumin level, prothrombin time (INR), platelet count, and pre-existing cirrhosis were also significantly associated with clinical events.
-However, occurrence of clinical events was not significantly influenced by patient sex, HBeAg status, previous nucleoside/nucleotide therapy, or baseline HBV DNA.

&quotrobability of achieving virological response to entecavir is not influenced by severity of liver disease," the investigators concluded. "Virological response to entecavir is associated with a lower probability of disease progression (HCC, hepatic decompensation, death) for cirrhotic patients."

Investigator affiliations: Department of Gastroenterology and Hepatology, Erasmus MC, Rotterdam, Netherlands; Department of Hepatology, Hospices Civils de Lyon, Lyon, France; Department of Hepatology and Gastroenterology, Imperial College , London, UK; NIHR Biomedical Research Unit and Centre for Liver Research, Queen Elizabeth Hospital, Birmingham, UK; Department of Gastroenterology, Hepatology, and Endocrinology, Medical School Hannover, Hannover, Germany; Medizinische Klinik 1, Klinikum der Johan Wolfgang Goethe-Universitat, Frankfurt am Main, Germany; Liver Unit, IFI institute, Asklepios Klinik St. Georg, Hamburg, Germany; Clinic of Infectious Diseases, University of Bari, Bari, Italy; Department of Hepatology, Hospital Vall de Hebron, Barcelona, Spain; Department of Hepatology, University Clinic Leipzig, Leipzig, Germany.

11/22/11

Reference

R Zoutendijk, JG Reijnders, F Zoulim, et al. Virological response to entecavir is associated with a lower probability of disease progression: results from 377 chronic hepatitis B patients. 62nd Annual Meeting of the American Association for the Study of Liver Diseases (AASLD 2011). San Francisco, November 4-8. 2011. Abstract 240.




(6.合.彩)足球.篮球...各类投注开户下注

第一投注现金网:招代理年薪10万以上:yyu.cc

StephenW

肝病学会：良好的反应恩替卡韦降低乙肝疾病进展的风险

分类：乙肝治疗
    周二公布，2011年11月22日00:00
    书面LIZ Highleyman



慢性乙型肝炎患者达到HBV DNA的抑制病毒载量的恩替卡韦（博路定），有一个比非应答者的肝功能衰竭，肝癌，死亡风险较低，根据美国协会为肝癌的研究，研究提出本月初的调查结果病肝会议（AASLD 2011）在旧金山。

几年或几十年，慢性乙型肝炎病毒（HBV）感染可导致晚期肝病，包括肝硬化和肝癌。核苷类似物药物恩替卡韦有效地抑制乙肝病毒复制，降低病毒载量，并改善肝纤维化，但治疗的最终目的是要减少临床事件和过早死亡的可能性。

在鹿特丹Erasmus医学中心的Roeland Zoutendijk和他的同事调查是否改善慢性乙型肝炎患者中的临床结果与恩替卡韦引起的病毒抑制。

研究人员评估了乙肝病毒monoinfected谁是恩替卡韦单药治疗至少3个月内维吉尔网络的10家大型欧洲转介中心（例如，没有感染艾滋病毒，丙型肝炎，丁型肝炎合并感染）患者的医疗记录。

分析包括372与会者;四分之三的男性中，约有一半是白人，平均年龄为43岁，约60％是B型肝炎“E”抗原（HBeAg）阳性。约73％的人没有肝硬化，24％有代偿性肝硬化，失代偿期在基线和2％肝硬化。约三分之一以前一直与核苷/核苷酸类似物，包括拉米夫定（Epivir - HBV）和阿德福韦（Hepsera），和20％左右，以前用干扰素治疗。

病毒学反应定义为血清HBV DNA <80 IU /毫升。考虑临床终点是肝功能失代偿（黄疸，腹水，静脉曲张破裂出血，或肝性脑病表示），肝癌的发生（肝癌，原发性肝癌的一种形式），和死亡。中位随访期为19个月。

结果

-补偿或失代偿性肝硬化在基线和那些没有实现对恩替卡韦的病毒学应答患者类似的可能性。
-对恩替卡韦取得病毒学应答的患者的病情恶化的可能性显着降低，与非应答者（危险比0.29）相比：
        无肝硬化：1 222应答之间的事件（0％）比1之间的52个非应答（2％）的事件;
        代偿性肝硬化：3间73急救员（4％）与16个非应答者（30％）5个事件的事件;
        失代偿期肝硬化：1间6应答者（17％）与3个非应答者（67％）之间的2个事件的事件。
-病人的年龄，基线MELD评分，白蛋白水平，凝血酶原时间（INR），血小板计数，和预先存在的肝硬化也显著相关的临床事件。
-然而，临床事件的发生并没有显著影响患者的性别，HBeAg的状态，以前的核苷/核苷酸治疗，或基线HBV DNA。

“恩替卡韦实现病毒学应答的概率并不肝脏疾病的严重程度的影响，研究人员得出结论。” “恩替卡韦是相关的病毒学应答与疾病进展的可能性降低肝硬化患者（肝癌，肝功能失代偿，死亡）。”

调查背景：胃肠病学和肝病，伊拉斯谟的MC，鹿特丹，荷兰，肝病，收容所Civils里昂，里昂，法国，英国伦敦帝国学院，肝脏和肠胃，系; NIHR的生物医学研究组和肝中心伊利沙伯医院，英国伯明翰;胃肠病，肝病，内分泌，汉诺威医学院，德国汉诺威Medizinische Klinik 1，Klinikum DER约翰沃尔夫冈歌德大学，美因河畔法兰克福，德国，肝组，研究，国际金融机构研究所Asklepios Klinik圣乔治，德国汉堡，肝病，医院瓦尔德希伯伦，巴塞罗那，西班牙;;部，德国莱比锡，莱比锡大学医院肝病，传染病，巴里，意大利巴里大学诊所。

11年11月22日

参考

ř Zoutendijk，JG Reijnders，F Zoulim，等。恩替卡韦是相关的病毒学应答与疾病进展的可能性降低：从377例慢性乙型肝炎患者的结果。美国协会第62届年会肝病（AASLD 2011）的研究。旧金山年11月4-8。 2011年。摘要240。