1995
DOI: 10.5144/0256-4947.1995.451
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Frequency of Peptic Ulcers in Patients with Portal Hypertension

Abstract: To find the frequency of peptic ulceration in portal hypertension, 137 patients with portal hypertension were studied retrospectively. Patients with hepatocellular carcinoma, other malignancies or underlying severe systemic disease were excluded and the remaining 114 patients were included in the study. There were 81 males (mean age 49.1 ± 13.7 years) and 33 females (mean age 52.9 ± 10 years). Portal hypertension was secondary to viral liver disease in 75%. Fifty-seven patients had no evidence of peptic ulcers… Show more

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“…The damaged protective function of gastric mucosal barrier seems to have a greater role in the pathophysiology of peptic ulcers in cirrhotics, based on the occurrence of chronic atrophyc gastritis in liver cirrhosis, the reduced strength of gastric mucosa due to parietal venous congestion and protein and vitamin deficiencies [52]. Others metabolic and functional modifications should integrate the pathogenetic framework of peptic ulcer in cirrhotic patients: raised level of gastrin and histamine, increase of duodenogastric reflux, impaired gastric empting, reduced prostaglandin level in gastric mucosa and decrease of mucosal oxigen saturation [53,54]. Most recent studies confirm this proposal evaluation referring that the severity degree of liver pathological involvement plays an important role in the development of peptic ulcer disease.…”
Section: Gastric and Duodenal Ulcermentioning
confidence: 99%
“…The damaged protective function of gastric mucosal barrier seems to have a greater role in the pathophysiology of peptic ulcers in cirrhotics, based on the occurrence of chronic atrophyc gastritis in liver cirrhosis, the reduced strength of gastric mucosa due to parietal venous congestion and protein and vitamin deficiencies [52]. Others metabolic and functional modifications should integrate the pathogenetic framework of peptic ulcer in cirrhotic patients: raised level of gastrin and histamine, increase of duodenogastric reflux, impaired gastric empting, reduced prostaglandin level in gastric mucosa and decrease of mucosal oxigen saturation [53,54]. Most recent studies confirm this proposal evaluation referring that the severity degree of liver pathological involvement plays an important role in the development of peptic ulcer disease.…”
Section: Gastric and Duodenal Ulcermentioning
confidence: 99%