Barcelona Hepatic Hemodynamic Laboratory, Liver Unit, Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain(†); Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Madrid, Spain.
Surgical Research Laboratory, Department of Surgery, University of Groningen, University Medical Center Groningen, The Netherlands.
J Hepatol. 2021 Dec;75(6):1367-1376. doi: 10.1016/j.jhep.2021.07.020. Epub 2021 Jul 30.
BACKGROUND & AIMS: Portal vein thrombosis (PVT) is a relatively frequent event in patients with cirrhosis. While different risk factors for PVT have been reported, such as decreased portal blood flow velocity (PBFV) and parameters related with severity of portal hypertension, these are based on retrospective studies assessing only a discrete number of parameters. The aim of the current study was to evaluate the incidence and risks factors for non-tumoral PVT development in a large prospective cohort of patients with cirrhosis.
We performed an exhaustive evaluation of clinical, biochemical, inflammatory and acquired/hereditary hemostatic profiles in 369 patients with cirrhosis without PVT who were prospectively followed-up. Doppler ultrasound was performed at baseline and every 6 months or whenever clinically indicated. PVT development was always confirmed by computed tomography.
Twenty-nine patients developed non-tumoral PVT, with an incidence of 1.6%, 6% and 8.4% at 1, 3 and 5 years, respectively. Low platelet count, PBFV <15 cm/sec and history of variceal bleeding were factors independently associated with a high PVT risk. No relationship between PVT development and any other clinical biochemical, inflammatory and acquired or hereditary hemostatic parameter was found.
In patients with cirrhosis, the factors predictive of PVT development were mainly those related to the severity of portal hypertension. Our results do not support the role of hemostatic alterations (inherited or acquired) and inflammatory markers in the prediction of PVT in patients with cirrhosis.
Patients with cirrhosis and more severe portal hypertension are at higher risk of non-tumoral portal vein thrombosis development. Acquired or inherited hemostatic disorders, as well as inflammatory status, do not seem to predict the development of portal vein thrombosis in patients with cirrhosis.
门静脉血栓形成（PVT）在肝硬化患者中较为常见。虽然已有研究报道了多种与 PVT 相关的风险因素，如门静脉血流速度（PBFV）降低和与门静脉高压严重程度相关的参数，但这些研究均基于回顾性研究，仅评估了少数参数。本研究旨在评估肝硬化患者中大量前瞻性队列中非肿瘤性 PVT 发展的发生率和风险因素。
我们对 369 例无 PVT 的肝硬化患者进行了详尽的临床、生化、炎症和获得性/遗传性止血特征评估，并对其进行前瞻性随访。在基线时和每 6 个月或临床需要时进行多普勒超声检查。PVT 的发展始终通过计算机断层扫描来确认。
29 例患者发生非肿瘤性 PVT，1、3、5 年的发生率分别为 1.6%、6%和 8.4%。血小板计数低、PBFV<15cm/sec 和静脉曲张出血史是与高 PVT 风险相关的独立因素。未发现 PVT 发展与任何其他临床生化、炎症和获得性或遗传性止血参数之间存在任何关系。
在肝硬化患者中，预测 PVT 发展的因素主要与门静脉高压的严重程度有关。我们的结果不支持止血异常（获得性或遗传性）和炎症标志物在预测肝硬化患者 PVT 中的作用。
肝硬化患者中，门静脉高压程度越严重，发生非肿瘤性门静脉血栓形成的风险越高。获得性或遗传性止血障碍以及炎症状态似乎不能预测肝硬化患者门静脉血栓形成的发生。
