Clinics and research in hepatology and gastroenterology · 2024
Predictive value of hepatic venous pressure gradient in cirrhotic portal vein thrombosis development.
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Zhong Huan, Lu Sizhu, Xu Min, Liu Na, Ye Wei, Yang Yongfeng
Аннотация
BACKGROUND & AIMS: There are lots of risk factors reported for cirrhotic portal vein thrombosis (PVT) development, however, the relationship between hepatic venous pressure gradient (HVPG) and PVT development remains unclear.
METHODS: The clinical outcomes of cirrhotic patients who had no PVT and underwent HVPG measurement at baseline between March 2018 and March 2022 were analyzed retrospectively. Screening for non-tumoral PVT development was implemented by contrast-enhanced computed tomography and/or magnetic resonance imaging every 6-12 months.
RESULTS: Eighty-two cirrhotic patients were evaluated over a follow-up period. Of these, 12 patients (14.6%) experienced the development of PVT. The occurrence of non-tumoral PVT at one, two, and three years were 6.6%, 11.7%, and 22.2% respectively. HVPG (p=0.038;HR 1.07;95%CI 1.00-1.14) and alcohol liver disease (ALD) (p=0.019;HR 4.20;95%CI 1.27-13.89) were independently associated with a high PVT risk. The cutoff value of HVPG was 17.52 mmHg. The cumulative incidence of PVT differed significantly among groups stratified by HVPG thresholds of 16mmHg (P=0.011). The sensitivity and specificity of HVPG≥16mmHg in predicting PVT development were 100.0% and 35.7%.
CONCLUSIONS: In patients with liver cirrhosis, the value of HVPG was the independent predictive factor of PVT development. Screening for PVT was recommended during follow-up in patients with HVPG≥16 mmHg.
METHODS: The clinical outcomes of cirrhotic patients who had no PVT and underwent HVPG measurement at baseline between March 2018 and March 2022 were analyzed retrospectively. Screening for non-tumoral PVT development was implemented by contrast-enhanced computed tomography and/or magnetic resonance imaging every 6-12 months.
RESULTS: Eighty-two cirrhotic patients were evaluated over a follow-up period. Of these, 12 patients (14.6%) experienced the development of PVT. The occurrence of non-tumoral PVT at one, two, and three years were 6.6%, 11.7%, and 22.2% respectively. HVPG (p=0.038;HR 1.07;95%CI 1.00-1.14) and alcohol liver disease (ALD) (p=0.019;HR 4.20;95%CI 1.27-13.89) were independently associated with a high PVT risk. The cutoff value of HVPG was 17.52 mmHg. The cumulative incidence of PVT differed significantly among groups stratified by HVPG thresholds of 16mmHg (P=0.011). The sensitivity and specificity of HVPG≥16mmHg in predicting PVT development were 100.0% and 35.7%.
CONCLUSIONS: In patients with liver cirrhosis, the value of HVPG was the independent predictive factor of PVT development. Screening for PVT was recommended during follow-up in patients with HVPG≥16 mmHg.