Editorial: Safety and Effects of Direct Oral Anticoagulants for Portal Vein Thrombosis

医学 门静脉血栓形成 肝硬化 腹水 门脉高压 经颈静脉肝内门体分流术 胃肠道出血 肝移植 门静脉压 血栓形成 凝血病 血栓 外科 内科学 移植
作者
Nina Kimer,Lise Hobolth,Lise Lotte Gluud
出处
期刊:Alimentary Pharmacology & Therapeutics [Wiley]
标识
DOI:10.1111/apt.18512
摘要

Portal vein thrombosis (PVT) is a serious complication in chronic liver disease, mainly occurring in patients with portal hypertension [1]. The pathophysiology of PVT includes a combination of venous stasis, hypercoagulability and endothelial dysfunction, leading to reduced portal flow velocity and stagnation of blood in the splanchnic circulation [2, 3]. PVT is associated with a range of complications in cirrhosis, including variceal bleeding and ascites and PVT may become a contraindication for liver transplantation [4]. Many cases are asymptomatic and detected incidentally during routine imaging. Symptomatic presentations include abdominal pain, worsening ascites or gastrointestinal bleeding. Treatment aims at achieving recanalisation with anticoagulation [5]. The safety of anticoagulation in cirrhosis requires consideration, especially in those with coagulopathy or varices. Acute-on-chronic PVT involves thrombus formation superimposed on a background of long-standing partial obstruction, often presenting more subtly but with potential for worsening liver function. PVT in people without cirrhosis is mainly acute and often due to an acquired or inherited prothrombotic condition [5, 6]. Although treatment principles are similar, non-cirrhotic cases generally have fewer risks related to coagulopathy, altering the safety and efficacy profile of anticoagulation therapy. In a study of 102 patients with acute PVT without cirrhosis, recanalisation of the portal vein was achieved in 39% following anticoagulation with vitamin K antagonists (VKA) and nine experienced gastrointestinal bleeding [6]. Treating PVT with direct oral anticoagulants (DOACs) offers several advantages over VKA including a more predictable effect eliminating the need for frequent monitoring. In a meta-analysis of 10 observational studies and one randomised trial including patients with cirrhosis and PVT, DOACs were associated with recanalisation in 87% [7]. Premkumar et al. report their experience with dabigatran for benign PVT [8]. The rate of recanalisation was assessed for 72 patients with cirrhosis and 47 without cirrhosis receiving dabigatran. Comparison groups consisted of 28 patients (18 with cirrhosis) who declined treatment and six patients with CP > 10 who received VKA. Recanalisation occurred in 56 (47.1%) patients treated with dabigatran and more frequently in acute compared to acute-on-chronic PVT. The large proportion of patients with acute on chronic PVT may partly explain the relatively low number of patients who achieved recanalisation. A large number of patients were identified through screening for portal hypertension rather than based on symptoms or incidental findings, which may impact results. None of the patients treated with VKA and 6 (21.4%) without treatment experienced spontaneous recanalisation. The overall adverse event rate of dabigatran was 6.7% including one patient with variceal bleeding and three with epistaxis [8]. This aligns with the result of a meta-analysis comparing anticoagulants versus no anticoagulation where 4% in the treatment group experienced variceal bleeding and 11% experienced major bleeding episodes [7]. Although the non-randomised design and the heterogeneity of patients should be considered when making conclusions, the overall result is very promising. The evidence suggests that DOACs are considered for the treatment of PVT, especially in patients with acute PVT. Additional evidence is needed to evaluate the benefit–risk ratio in patients with decompensated cirrhosis and in patients with acute on chronic PVT. Nina Kimer: writing – review and editing. Lise Hobolth: writing – review and editing. Lise Lotte Gluud: conceptualization, writing – original draft, writing – review and editing. N.K. and L.H. declare no conflicts of interest. L.L.G.: Novo Nordisk, Pfizer, Becton Dickinson, Gilead, Sobi, Alexion, Astra Zeneca, Boehringer Ingelheim, Immunovia and Norgine. This article is linked to Premkumar et al paper. To view this article, visit https://doi.org/10.1111/apt.18474. Data sharing not applicable to this article as no datasets were generated or analysed during the current study.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
刚刚
啊噢发布了新的文献求助10
刚刚
刚刚
干干脆脆发布了新的文献求助10
1秒前
1秒前
蒋丞完成签到,获得积分10
1秒前
muyassar完成签到,获得积分10
1秒前
1秒前
霜叶完成签到,获得积分10
1秒前
Hello应助苹果孤云采纳,获得10
2秒前
FashionBoy应助怕孤单的石头采纳,获得10
2秒前
李健应助大胆的平蓝采纳,获得10
2秒前
2秒前
cds发布了新的文献求助10
3秒前
肖文泽发布了新的文献求助10
3秒前
3秒前
aho发布了新的文献求助20
3秒前
zzz完成签到,获得积分10
3秒前
Owen应助大漂亮采纳,获得10
3秒前
4秒前
ddd完成签到,获得积分10
4秒前
5秒前
NexusExplorer应助香芋派采纳,获得10
5秒前
Mavis完成签到,获得积分10
5秒前
5秒前
小小完成签到 ,获得积分10
5秒前
希望天下0贩的0应助诺曦采纳,获得10
5秒前
5秒前
丫丫发布了新的文献求助10
6秒前
沉静的友灵完成签到,获得积分10
6秒前
6秒前
大模型应助帅气的老五采纳,获得10
6秒前
长弓橙子完成签到,获得积分10
6秒前
天地一浮游完成签到,获得积分20
7秒前
LZX发布了新的文献求助10
7秒前
柯柯发布了新的文献求助10
8秒前
小丸子发布了新的文献求助10
8秒前
9秒前
9秒前
咩咩完成签到 ,获得积分10
10秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Developing Genetic Editing Tools for Lysobacter 2000
Моделирование процессов самоорганизации в кристаллообразующих системах 1000
History of U.S. Space Surveillance and Satellite Cataloging 1000
Adhesion Science: Principles & Practice 800
Signals, Systems, and Signal Processing 610
Fundamentals of Pharmaceutical and Biologics Regulations: A Global Perspective, Second Edition 600
热门求助领域 (近24小时)
化学 材料科学 医学 生物 纳米技术 工程类 有机化学 化学工程 生物化学 计算机科学 物理 内科学 复合材料 催化作用 物理化学 光电子学 电极 细胞生物学 基因 无机化学
热门帖子
关注 科研通微信公众号,转发送积分 6525791
求助须知:如何正确求助?哪些是违规求助? 8318977
关于积分的说明 17804480
捐赠科研通 5627443
什么是DOI,文献DOI怎么找? 2929379
邀请新用户注册赠送积分活动 1906078
关于科研通互助平台的介绍 1765712