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肝胆相照论坛 论坛 学术讨论& HBV English 从富马酸替诺福韦酯切换到艾拉酚胺替诺福韦酯对乙型肝炎 ...
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从富马酸替诺福韦酯切换到艾拉酚胺替诺福韦酯对乙型肝炎 [复制链接]

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发表于 2022-1-21 14:14 |只看该作者 |倒序浏览 |打印
从富马酸替诺福韦酯切换到艾拉酚胺替诺福韦酯对乙型肝炎患者血脂谱的影响
铃木和晴 1 2 , 须田刚树 1 , 山本佳也 2 , 阿彦子聪 2 , 木下健二 2 , 宫本秀一 2 , 杉浦亮 2 , 木村惠 1 , 前原修 1 , 山田连 1 , 北方谷隆 1 , 重泽拓 1 , 征继大原 1 , 川岸直树 1 , 中井雅人 1 , 庄拓哉 1 , 夏坂光辉 1 , 森川健一 1 , 小川浩司 1 , 坂本直也 1
隶属关系

    PMID:35051189 DOI:10.1371/journal.pone.0261760

抽象的

对于乙型肝炎病毒 (HBV) 感染的长期治疗,从富马酸替诺福韦二吡呋酯 (TDF) 转换为替诺福韦艾拉酚胺 (TAF) 可能会预防肾功能障碍和骨质流失。然而,这种转换对血脂谱的确切影响仍有待阐明。这是一个重要的问题,因为已知 TDF 对低密度和高密度脂质都有影响。因此,我们的回顾性多中心研究旨在评估从 TDF 转换为 TAF 对 HBV 感染患者血脂谱的影响。在从 TDF 转换为 TAF 之前和 TAF 开始后 6-12 个月时获得样品。在某些情况下,TDF 给药前后获得的额外样本可用于分析。根据 NCEP-ATP III 脂质风险分类,分析了血清胆固醇水平,包括氧化低密度脂蛋白 (LDL) 和非高密度脂蛋白胆固醇 (HDL-c),以及血脂异常发生率。分析了 69 名患者的数据,其中 33 名患者的 TDF 启动前后血清样本。转换为 TAF 后,总胆固醇 (T-chol)、HDL-c、LDL-c、非 HDL-c 和氧化 LDL 水平显着增加。关于 TAF 前后的连续变化,TDF 与显着降低血清 T-chol、HDL-c 和氧化 LDL-c 水平相关,与 T-chol、HDL-c、LDL-c 和氧化 LDL -c 切换后水平显着增加。根据 T-chol 和 LDL-c,从 TDF 到 TAF 的转换也与血脂异常的发生率增加有关,从 33% 增加到 39%,严重血脂异常的发生率分别增加了 1.4% 和 5.8%水平。值得注意的是,在 TAF 治疗前未检测到严重血脂异常病例。由于氧化的 LDL-c 和非 HDL-c 与动脉粥样硬化的发展密切相关,因此在该临床人群中从 TDF 转换为 TAF 后需要仔细监测脂质。
利益冲突声明

Naoya Sakamoto 教授获得 Bristol Myers Squibb 和 Pharmaceutical KK 的讲座费用,MSD KK 和 Chugai Pharmaceutical Co., Ltd. 的资助和捐赠,以及 Gilead Sciences, Inc. 的研究资助。Goki Suda 博士获得 Bristol Myers Squibb 的研究资助、Pharmaceutical KK、MSD KK、Chugai Pharmaceutical Co., Ltd 和 Gilead Sciences, Inc.。其他作者没有任何可披露的信息,包括与雇佣、咨询、专利、开发中的产品、已上市产品等有关的任何其他相关声明。这不会改变我们对共享数据和材料的 PLOS ONE 政策的遵守。

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发表于 2022-1-21 14:14 |只看该作者
Effect of switching from tenofovir disoproxil fumarate to tenofovir alafenamide on lipid profiles in patients with hepatitis B
Kazuharu Suzuki  1   2 , Goki Suda  1 , Yoshiya Yamamoto  2 , Satoshi Abiko  2 , Kenji Kinoshita  2 , Shuichi Miyamoto  2 , Ryo Sugiura  2 , Megumi Kimura  1 , Osamu Maehara  1 , Ren Yamada  1 , Takashi Kitagataya  1 , Taku Shigesawa  1 , Masatsugu Ohara  1 , Naoki Kawagishi  1 , Masato Nakai  1 , Takuya Sho  1 , Mitsuteru Natsuizaka  1 , Kenichi Morikawa  1 , Koji Ogawa  1 , Naoya Sakamoto  1
Affiliations

    PMID: 35051189 DOI: 10.1371/journal.pone.0261760

Abstract

For long-term treatment of hepatitis B virus (HBV) infection, switching from tenofovir-disoproxil-fumarate (TDF) to tenofovir-alafenamide (TAF) may prevent renal dysfunction and bone loss. However, the precise effects of this switch on the blood lipid profile remain to be clarified. This is an important issue as TDF is known to have effects on both low- and high-density lipids. Therefore, our retrospective multi-center study aimed to evaluate the effects of switching from TDF to TAF on the lipid profile of patients with HBV infection. Samples were obtained prior to the switch from TDF to TAF and at 6-12 months after TAF initiation. In some cases, additional samples obtained pre- and post-TDF administration were available for analysis. Serum cholesterol levels, including oxidized-low-density lipoprotein (LDL) and non-high-density lipoprotein-cholesterol (HDL-c), and the rate of dyslipidemia, according to the NCEP-ATP III lipid risk classification, were analyzed. The data from 69 patients were analyzed, including 33 patients with pre- and post-TDF-initiation serum samples. Total cholesterol (T-chol), HDL-c, LDL-c, non-HDL-c, and oxidized LDL levels increased significantly after switching to TAF. With regard to sequential changes pre- to post-TAF, TDF was associated with significantly lower serum T-chol, HDL-c, and oxidized LDL-c levels, with T-chol, HDL-c, LDL-c, and oxidized LDL-c levels increasing significantly after the switch. The switch from TDF to TAF was also associated with an increase in the rate of dyslipidemia, from 33% to 39%, with an increase in the rate of severe dyslipidemia of 1.4% and 5.8%, based on T-chol and LDL-c levels. Of note, no cases of severe dyslipidemia were detected pre-TAF treatment. As oxidized LDL-c and non-HDL-c are strongly associated with atherosclerosis development, careful monitoring of lipid is needed after switching from TDF to TAF in this clinical population.
Conflict of interest statement

Professor Naoya Sakamoto received lecture fees from Bristol Myers Squibb and Pharmaceutical K.K, grants and endowments from MSD K.K and Chugai Pharmaceutical Co., Ltd., and a research grant from Gilead Sciences, Inc. Dr. Goki Suda received research grants from Bristol Myers Squibb, Pharmaceutical K.K, MSD K.K, Chugai Pharmaceutical Co., Ltd, and Gilead Sciences, Inc. The other authors have nothing to disclose, including any other relevant declarations relating to employment, consultancy, patents, products in development, marketed products, etc. This does not alter our adherence to PLOS ONE policies on sharing data and materials.

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