慢性乙型肝炎的核苷（酸）类似物治疗在基线和 1 年后发生

StephenW

慢性乙型肝炎的核苷（酸）类似物治疗在基线和 1 年后发生肝细胞癌的危险因素
金子俊 1 2 , 黑崎雅之 1 , 马柴俊之 3 , 丸泽博之 4 , 近藤雅彦 5 , 小岛雄二 6 , 内田靖 7 , 藤井英树 8 , 赤羽武博 9 , 八木泽仁 10 , 草部敦典 11 , 小桥春彦 12 , Abe 13、Hideo Yoshida 14、Chikara Ogawa 15、Koichiro Furuta 16、Nobuharu Tamaki 1、Keiji Tsuji 17、Tomomichi Matsushita 18、Namiki Izumi 1、日本红十字肝脏研究小组
隶属关系
隶属关系

    1
    日本东京武藏野红十字医院消化内科和肝内科。
    2
    日本东京医科齿科大学胃肠病学和肝病学系。
    3
    日本爱媛县松山红十字医院肝胆胰疾病中心。
    4
    日本大阪日本红十字会大阪医院消化内科。
    5
    日本滋贺县日本红十字大津医院消化内科。
    6
    日本三重县日本红十字伊势医院消化内科。
    7
    日本岛根市日本红十字松江医院消化内科。
    8
    日本红十字会京都第一医院消化内科。
    9
    日本宫城县日本红十字石卷医院消化内科。
    10
    日本秋田市日本红十字秋田医院消化内科。
    11
    日本红十字会名古屋第二医院消化内科。
    12
    日本冈山市日本红十字冈山医院肝病科。
    13
    日本群马县日本红十字前桥医院消化内科。
    14
    日本东京日本红十字医疗中心消化内科。
    15
    日本香川县日本红十字高松医院消化内科。
    16
    日本岛根市日本红十字增田医院消化内科。
    17
    日本广岛市广岛红十字医院和原子弹爆油炸幸存者医院消化内科。
    18
    日本岐阜县日本红十字岐阜医院消化内科。

    PMID: 36222204 DOI: 10.1002/jmv.28210

抽象的

背景/目的：核苷（酸）类似物（NA）不能完全抑制慢性乙型肝炎（CHB）患者发生肝细胞癌（HCC）的风险。本研究旨在确定接受当前 NA 治疗的初始 CHB 患者发生 HCC 的危险因素。

方法：从日本红十字肝脏研究组的 17 家医院回顾性招募接受 NA 的患者（n = 905）。所有未接受过治疗的患者均已连续接受当前的 NA 超过一年，直至随访结束。我们使用受试者工作特征曲线下面积分析了预测风险评分的准确性。

结果：NA 治疗显着改善了白蛋白-胆红素 (ALBI) 评分（-0.171 ± 0.396；第 48 周时 p < 0.001）。中位随访时间为 6.2 (1.03-15.7) 年，共有 72 名 (8.0%) 患者发展为 HCC。根据多变量分析，HCC 发展的独立预测因素是年龄较大、肝硬化、基线血小板计数和 ALBI 评分较低，以及 NA 治疗后 1 年的甲胎蛋白 (AFP)。使用包含这些因素的 PAGE-B、mPAGE-B、aMAP、APA-B 和 REAL-B 分数评估准确性。对于这些模型，歧视通常是可以接受的。 aMAP 和 REAL-B 在 NA 治疗一年后的 3 年和 5 年预测中分别表现出 0.866/0.862 和 0.833/0.859 的高区分度。

结论：基线年龄和血小板计数，以及 NA 一年后的 ALBI 和 AFP，有助于对致癌风险进行分层。 aMAP 和 REAL-B 评分在日本 CHB 患者中得到了高精度验证。本文受版权保护。版权所有。

关键词：乙型肝炎病毒；白蛋白-胆红素评分；肝细胞癌;核苷（酸）类似物。

本文受版权保护。版权所有。

StephenW

Risk factors for hepatocellular carcinoma at baseline and 1 year after initiation of nucleos(t)ide analog therapy for chronic hepatitis B
Shun Kaneko  1   2 , Masayuki Kurosaki  1 , Toshie Mashiba  3 , Hiroyuki Marusawa  4 , Masahiko Kondo  5 , Yuji Kojima  6 , Yasushi Uchida  7 , Hideki Fujii  8 , Takehiro Akahane  9 , Hitoshi Yagisawa  10 , Atsunori Kusakabe  11 , Haruhiko Kobashi  12 , Takehiko Abe  13 , Hideo Yoshida  14 , Chikara Ogawa  15 , Koichiro Furuta  16 , Nobuharu Tamaki  1 , Keiji Tsuji  17 , Tomomichi Matsushita  18 , Namiki Izumi  1 , Japanese Red Cross Liver Study Group
Affiliations
Affiliations

    1
    Department of Gastroenterology and Hepatology, Musashino Red Cross Hospital, Tokyo, Japan.
    2
    Department of Gastroenterology and Hepatology, Tokyo Medical and Dental University, Tokyo, Japan.
    3
    Center for Liver-Biliary-Pancreatic Diseases, Matsuyama Red Cross Hospital, Ehime, Japan.
    4
    Department of Gastroenterology, Japanese Red Cross Osaka Hospital, Osaka, Japan.
    5
    Department of Gastroenterology, Japanese Red Cross Otsu Hospital, Shiga, Japan.
    6
    Department of Gastroenterology, Japanese Red Cross Ise Hospital, Mie, Japan.
    7
    Department of Gastroenterology, Japanese Red Cross Matsue Hospital, Shimane, Japan.
    8
    Department of Gastroenterology, Japanese Red Cross Kyoto Daiichi Hospital, Kyoto, Japan.
    9
    Department of Gastroenterology, Japanese Red Cross Ishinomaki Hospital, Miyagi, Japan.
    10
    Department of Gastroenterology, Japanese Red Cross Akita Hospital, Akita, Japan.
    11
    Department of Gastroenterology, Japanese Red Cross Nagoya Daini Hospital, Nagoya, Japan.
    12
    Department of Hepatology, Japanese Red Cross Okayama Hospital, Okayama, Japan.
    13
    Department of Gastroenterology, Japanese Red Cross Maebashi Hospital, Gunma, Japan.
    14
    Department of Gastroenterology, Japanese Red Cross Medical Center, Tokyo, Japan.
    15
    Department of Gastroenterology, Japanese Red Cross Takamatsu Hospital, Kagawa, Japan.
    16
    Department of Gastroenterology, Japanese Red Cross Masuda Hospital, Shimane, Japan.
    17
    Department of Gastroenterology, Hiroshima Red Cross Hospital & Atomic-bomb Survivors Hospital, Hiroshima, Japan.
    18
    Department of Gastroenterology, Japanese Red Cross Gifu Hospital, Gifu, Japan.

    PMID: 36222204 DOI: 10.1002/jmv.28210

Abstract

Background/aims: Nucleos(t)ide analogs (NA) cannot completely suppress the risk of hepatocellular carcinoma (HCC) in patients with chronic hepatitis B (CHB). This study aimed to identify the risk factors for HCC development in naïve CHB patients treated with current NA.

Methods: Patients receiving NA (n = 905) were recruited retrospectively from the 17 hospitals of the Japanese Red Cross Liver Study Group. All treatment-naïve patients had been receiving current NA continuously for more than one year until the end of the follow-up. We analyzed the accuracy of predictive risk score using area under receiver operating characteristic curve.

Results: The albumin-bilirubin (ALBI) score was significantly improved by NA therapy (-0.171 ± 0.396; p < 0.001 at week 48). A total of 72 (8.0%) patients developed HCC over a median follow-up of 6.2 (1.03-15.7) years. An independent predictive factor of HCC development was older age, cirrhosis, lower platelet counts at baseline and ALBI score, and alpha-fetoprotein (AFP) at 1 year after NA therapy according to multivariate analysis. The accuracy was assessed using the PAGE-B, mPAGE-B, aMAP, APA-B, and REAL-B scores that included these factors. Discrimination was generally acceptable for these models. aMAP and REAL-B demonstrated high discrimination with 0.866/0.862 and 0.833/0.859 for 3- and 5- years prediction from the status of one year after NA therapy, respectively.

Conclusion: Baseline age and platelet count, as well as ALBI and AFP one year after NA, were useful for stratifying carcinogenesis risk. The aMAP and REAL-B scores were validated with high accuracy in Japanese CHB patients. This article is protected by copyright. All rights reserved.

Keywords: Hepatitis B virus; albumin-bilirubin score; hepatocellular carcinoma; nucleos(t)ide analogs.

This article is protected by copyright. All rights reserved.