Journal of digestive diseases · 2023
Prevalence and clinical characteristics of advanced portal vein thrombosis in cirrhotic patients with gastroesophageal variceal hemorrhage.
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Rao Chen Yi, Xue Chun Yan, Fang Qing Qing, Wu Ling, Huang Xiao Quan, Chen Ying, Chen Shi Yao, Li Feng
Аннотация
OBJECTIVES: Portal venous thrombosis (PVT) in cirrhotic patients is usually asymptomatic and diagnosed incidentally. In this study we aimed to investigate the prevalence and characteristics of advanced PVT in cirrhotic patients with a recent episode of gastroesophageal variceal hemorrhage (GVH).
METHODS: Cirrhotic patients with recent GVH at one month before their admission for further treatment to prevent rebleeding were retrospectively recruited. Hepatic venous pressure gradient (HVPG) measurements, contrast-enhanced computed tomography (CT) scan of the portal vein system, and endoscopy were performed. PVT was diagnosed by CT examination and classified as none, mild and advanced.
RESULTS: Of the 356 patients enrolled, 80 (22.5%) had advanced PVT. Elevated levels of white blood cells (WBC) and serum D-dimer were observed in advanced PVT patients compared with those with no or mild PVT. Moreover, HVPG was lower in patients with advanced PVT, with fewer patients having HVPG exceeding 12 mmHg, while grade III esophageal varices and varices with red signs were more prevalent. Multivariate analysis showed that WBC count (odds ratio [OR] 1.401, 95% confidence interval [CI] 1.171-1.676, P < 0.001), D-dimer level (OR 1.228, 95% CI 1.117-1.361, P < 0.001), HVPG (OR 0.942, 95% CI 0.900-0.987, P = 0.011), and grade III esophageal varices (OR 4.243, 95% CI 1.420-12.684, P = 0.010) were associated with advanced PVT.
CONCLUSIONS: Advanced PVT, which is associated with a more severe hypercoagulable and inflammatory status, causes severe prehepatic portal hypertension in cirrhotic patients with GVH.
METHODS: Cirrhotic patients with recent GVH at one month before their admission for further treatment to prevent rebleeding were retrospectively recruited. Hepatic venous pressure gradient (HVPG) measurements, contrast-enhanced computed tomography (CT) scan of the portal vein system, and endoscopy were performed. PVT was diagnosed by CT examination and classified as none, mild and advanced.
RESULTS: Of the 356 patients enrolled, 80 (22.5%) had advanced PVT. Elevated levels of white blood cells (WBC) and serum D-dimer were observed in advanced PVT patients compared with those with no or mild PVT. Moreover, HVPG was lower in patients with advanced PVT, with fewer patients having HVPG exceeding 12 mmHg, while grade III esophageal varices and varices with red signs were more prevalent. Multivariate analysis showed that WBC count (odds ratio [OR] 1.401, 95% confidence interval [CI] 1.171-1.676, P < 0.001), D-dimer level (OR 1.228, 95% CI 1.117-1.361, P < 0.001), HVPG (OR 0.942, 95% CI 0.900-0.987, P = 0.011), and grade III esophageal varices (OR 4.243, 95% CI 1.420-12.684, P = 0.010) were associated with advanced PVT.
CONCLUSIONS: Advanced PVT, which is associated with a more severe hypercoagulable and inflammatory status, causes severe prehepatic portal hypertension in cirrhotic patients with GVH.