JGH open : an open access journal of gastroenterology and hepatology · 2021
Gastric antral vascular ectasia in hepatitis C virus related liver cirrhosis: Fetching for predictors.
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Fouad Magdy, Khalaf Fath-Elbab Hanaa, Mostafa Alaa Mohamed, Moness Hend M, Adel Nashwa Mohamed, Ahmed Elham
Аннотация
BACKGROUND AND AIM: Gastric antral vascular ectasia (GAVE) is observed in patients with liver cirrhosis and portal hypertension. The exact pathophysiologic mechanism that underlies this condition is unknown. In our study, we estimate the prevalence of GAVE in hepatitis C virus (HCV) cirrhosis and attempted to determine if any of the hepatocellular manifestations, liver functions, serum gastrin, abdominal ultrasound and endoscopic picture have a relation to, or could predict, the occurrence of GAVE in cirrhotic patients.
METHODS: This study includes 500 HCV-related liver cirrhosis patients. According to endoscopic assessment, we detected 30 patients with GAVE (Group 2). From the 470 patients without GAVE, we randomly selected 120 patients (Group 1), to avoid statistical bias, for comparison with Group 2. Comparison included clinical manifestations, laboratory findings, serum gastrin, ultrasound findings, and endoscopic findings (esophageal and/or gastric varices and gastropathy).
RESULTS: The percentage of GAVE in HCV-related liver cirrhosis is 0.06%. We can predict GAVE by platelets, palmer erythema, diabetes mellitus (DM), marked ascites > with area under the curve of 0.67, 75.5, 0.62, and 0.40%, and accuracy of 82.5, 72, 70.7, and 79.3%, respectively. There was no correlation found between occurrence of GAVE and endoscopic findings. Also, there was no correlation found between occurrence of GAVE and serum gastrin levels, which reflect another pathophysiology, and we found no statistically significant correlation with GAVE.
CONCLUSIONS: Palmer erythema, low platelets, DM, and ascites might help in the prediction of GAVE. GAVE is not linked to the presence, type or grade of varices, and gastropathy.
METHODS: This study includes 500 HCV-related liver cirrhosis patients. According to endoscopic assessment, we detected 30 patients with GAVE (Group 2). From the 470 patients without GAVE, we randomly selected 120 patients (Group 1), to avoid statistical bias, for comparison with Group 2. Comparison included clinical manifestations, laboratory findings, serum gastrin, ultrasound findings, and endoscopic findings (esophageal and/or gastric varices and gastropathy).
RESULTS: The percentage of GAVE in HCV-related liver cirrhosis is 0.06%. We can predict GAVE by platelets, palmer erythema, diabetes mellitus (DM), marked ascites > with area under the curve of 0.67, 75.5, 0.62, and 0.40%, and accuracy of 82.5, 72, 70.7, and 79.3%, respectively. There was no correlation found between occurrence of GAVE and endoscopic findings. Also, there was no correlation found between occurrence of GAVE and serum gastrin levels, which reflect another pathophysiology, and we found no statistically significant correlation with GAVE.
CONCLUSIONS: Palmer erythema, low platelets, DM, and ascites might help in the prediction of GAVE. GAVE is not linked to the presence, type or grade of varices, and gastropathy.