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苏州大学附属第一医院药学部,江苏 苏州 215000
主管药师。研究方向:医院药学。E-mail:gongwei@pharm-go.com
副主任药师,硕士。研究方向:临床药学。电话:0512-67780997。E-mail:lyxfyy@aliyun.com
收稿:2025-10-11,
修回:2026-01-09,
录用:2026-01-28,
纸质出版:2026-02-28
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龚伟,李芸.肝硬化合并门静脉血栓形成患者的抗凝治疗研究进展[J].中国药房,2026,37(04):533-539.
GONG Wei,LI Yun.Research progress on anticoagulant therapy in patients with liver cirrhosis complicated with portal vein thrombosis[J].ZHONGGUO YAOFANG,2026,37(04):533-539.
龚伟,李芸.肝硬化合并门静脉血栓形成患者的抗凝治疗研究进展[J].中国药房,2026,37(04):533-539. DOI: 10.6039/j.issn.1001-0408.2026.04.21.
GONG Wei,LI Yun.Research progress on anticoagulant therapy in patients with liver cirrhosis complicated with portal vein thrombosis[J].ZHONGGUO YAOFANG,2026,37(04):533-539. DOI: 10.6039/j.issn.1001-0408.2026.04.21.
门静脉血栓(PVT)作为肝硬化常见且严重的并发症,其抗凝治疗因患者凝血功能异常与出血风险并存而颇具挑战。本文综合近年来肝硬化合并PVT抗凝治疗的研究成果及国内外指南与共识,围绕肝硬化合并PVT的高发原因、临床表现与诊断、抗凝治疗决策(包括指征确定、时机选择、疗程选择)、药物合理使用4个方面展开综述。结果表明,肝硬化患者中PVT高发是多因素共同作用的结果。目前普遍认为,门静脉血流瘀滞、机体高凝状态以及血管内皮损伤是PVT形成的三大危险因素。肝硬化合并PVT的临床表现丰富,其诊断需结合临床背景、影像学检查以及实验室检查进行综合判断,其中影像学检查是核心诊断依据。抗凝治疗能够显著提高PVT的血栓再通率,降低血栓进展风险,且不会增加门静脉高压相关的出血风险。在治疗时机上,确诊后6个月内,尤其是2周内启动抗凝治疗可显著提高血栓再通率。对于肝硬化合并PVT的抗凝治疗,临床上常用的药物主要包括肝素类药物、维生素K拮抗剂(VKA)及直接口服抗凝剂(DOACs)。其中,低分子肝素作为一线药物的证据十分充分;DOACs在代偿期肝硬化合并PVT患者中显示出良好的疗效与安全性,不过其在失代偿期肝硬化合并PVT患者中的应用仍需格外谨慎。建议疗程通常不少于6个月。对于存在肠系膜静脉受累、等待肝移植或遗传性血栓形成倾向的肝硬化合并PVT患者,应考虑进行长期抗凝治疗。
Portal vein thrombosis (PVT) is a common and severe complication of liver cirrhosis. Anticoagulant therapy for PVT in these patients is particularly challenging due to the coexistence of abnormal coagulation function and bleeding risk. This article reviews recent research findings, domestic and international guidelines, and expert consensus regarding anticoagulant therapy for liver cirrhosis complicated by PVT. The review focuses on four key aspects: the underlying causes of the high incidence of PVT, its clinical manifestations and diagnosis, anticoagulant treatment decision-making (including determining indications, timing, and course selection), and rational drug use. The evidence indicates that the high incidence of PVT in patients with liver cirrhosis results from the interplay of multiple factors. Currently, portal venous stasis, a systemic hypercoagulable state, and vascular endothelial damage are widely recognized as the three primary risk factors for PVT formation. The clinical manifestations of liver cirrhosis complicated by PVT are diverse,diagnosis requires comprehensive evaluation based on clinical context, imaging examination, and laboratory tests, with imaging examination as the cornerstone. Anticoagulant therapy can significantly improve the thrombus recanalization rate in PVT, reduce the risk of thrombus progression, and does not increase the risk of portal hypertension-related bleeding. Regarding treatment timing, initiating anticoagulation within six months of diagnosis, particularly within two weeks, can significantly enhance the recanalization rate. Commonly used anticoagulants in clinical practice for liver cirrhosis with PVT include heparins, vitamin K antagonists (VKAs), and direct oral anticoagulants (DOACs). Among these, substantial evidence supports low-molecular-weight heparin as a first-line agent. DOACs have demonstrated favorable efficacy and safety in patients with compensated liver cirrhosis and PVT; however, their use in patients with decompensated liver cirrhosis and PVT warrants extra caution. A treatment duration of at least six months is generally recommended. Long-term anticoagulation should be considered for patients with liver cirrhosis and PVT who have mesenteric vein involvement, are awaiting liver transplantation, or have an inherited thrombophilia.
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