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ORIGINAL ARTICLE
Year : 2014  |  Volume : 139  |  Issue : 2  |  Page : 260-266

A single hospital study on portal vein thrombosis in cirrhotic patients - clinical characteristics & risk factors


Division of Gastroenterology & Hepatology, Digestive Disease Institute, Tongji Hospital, Tongji University School of Medicine, Shanghai, China

Correspondence Address:
Changqing Yang
Professor of Medicine, Tongji Hospital, Tongji University School of Medicine Shanghai 200065
China
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Source of Support: None, Conflict of Interest: None


PMID: 24718401

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Background & objectives: Discrepancies exist in the reported prevalence of portal vein thrombosis (PVT), and its clinical characteristics and sites of occurrence need to be elucidated. The risk factors for PVT are also poorly understood. This single centre study was undertaken to determine the clinical characteristics, sites of occurrence, and risk factors associated with PVT in patients with liver cirrhosis. Methods: Hospitalized cirrhotic patients (N = 162) were segregated into the PVT and non-PVT groups. Indices possibly associated with PVT were measured and PVT was detected by both Doppler ultrasonography and computed tomography portal angiography. The portal vein diameter and flow velocity and splenic thickness were measured by ultrasonography. Results: PVT was found in 40 patients (24.7%); in 34 PVT patients (85%), the liver cirrhosis resulted from hepatitis B virus infections. Most (90%) patients were Child-Pugh classes B and C, with similar distribution between the groups. PVT was seen in 20 patients in the portal and superior mesenteric veins; ascites, abdominal pain, gastrointestinal bleeding, and jaundice were common findings in PVT patients. Haemoglobin levels and blood platelet counts (BPCs) were significantly lower and splenic thickness was greater in PVT than in non-PVT patients (P<0.01). There was a significant positive correlation between BPCs and platelet aggregation rates (R = 0.533, P<0.01). Interpretation & conclusions: The occurrence of PVT was 24.7 per cent, primarily in post-hepatitis B liver cirrhosis patients. PVT occurred mainly in the portal vein trunk and superior mesenteric vein. Different PVT sites may account for the differing clinical presentations. The lower levels of haemoglobin and BPCs as well as splenic thickening were associated with PVT. Splenic thickening may be a risk factor for PVT.


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