INTRODUCTION: Peptic ulcer disease, with or without complications, is more common in patients with liver cirrhosis than in the general population. Factors associated with portal hypertension are involved in its pathogenesis. The prevalence of Helicobacter pylori infection in patients with liver cirrhosis and the general population is similar. The aim of the present study was to determine the influence of nonsteroidal antiinflammatory drugs (NSAIDs) in the etiology of bleeding peptic ulcer disease in patients with liver cirrhosis. PATIENTS AND METHODS: We studied 35 patients with liver cirrhosis and gastrointestinal bleeding due to gastroduodenal ulcers or erosions (group A), 125 noncirrhotic patients with gastrointestinal bleeding due to gastroduodenal ulcers or erosions (group B), and 70 patients with liver cirrhosis who were admitted to hospital without gastrointestinal bleeding (group C). All patients were questioned about NSAID consumption, including aspirin, during the week prior to hospital admission. RESULTS: NSAID consumption was reported by 15 patients (42.8%) in group A, 102 patients (58.2%) in group B, and 6 patients (8.5%) in group C. Statistically significant differences were obtained when the results for group A were compared with those for group C. CONCLUSIONS: NSAID consumption in patients with liver cirrhosis without gastrointestinal bleeding was low (8.5%) and was much lower than that observed in patients with cirrhosis admitted to hospital for bleeding due to gastroduodenal ulcers or erosions (42.8%). As occurs in the general population, NSAIDs play a significant role in the pathogenesis of bleeding due to peptic ulcer disease in patients with liver cirrhosis and portal hypertension.
INTRODUCTION:Peptic ulcer disease, with or without complications, is more common in patients with liver cirrhosis than in the general population. Factors associated with portal hypertension are involved in its pathogenesis. The prevalence of Helicobacter pyloriinfection in patients with liver cirrhosis and the general population is similar. The aim of the present study was to determine the influence of nonsteroidal antiinflammatory drugs (NSAIDs) in the etiology of bleeding peptic ulcer disease in patients with liver cirrhosis. PATIENTS AND METHODS: We studied 35 patients with liver cirrhosis and gastrointestinal bleeding due to gastroduodenal ulcers or erosions (group A), 125 noncirrhotic patients with gastrointestinal bleeding due to gastroduodenal ulcers or erosions (group B), and 70 patients with liver cirrhosis who were admitted to hospital without gastrointestinal bleeding (group C). All patients were questioned about NSAID consumption, including aspirin, during the week prior to hospital admission. RESULTS: NSAID consumption was reported by 15 patients (42.8%) in group A, 102 patients (58.2%) in group B, and 6 patients (8.5%) in group C. Statistically significant differences were obtained when the results for group A were compared with those for group C. CONCLUSIONS: NSAID consumption in patients with liver cirrhosis without gastrointestinal bleeding was low (8.5%) and was much lower than that observed in patients with cirrhosis admitted to hospital for bleeding due to gastroduodenal ulcers or erosions (42.8%). As occurs in the general population, NSAIDs play a significant role in the pathogenesis of bleeding due to peptic ulcer disease in patients with liver cirrhosis and portal hypertension.