Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Upper gastrointestinal hemorrhage is one of the more important complications of cirrhosis. Most of the available data regarding the prevalence of upper and lower gastrointestinal sites of bleeding in cirrhotic patients have been obtained in individuals with alcoholic cirrhosis evaluated in the course of an acute gastrointestinal bleeding episode. Few data exist, however, as to the prevalence of either potential bleeding sites or of normal endoscopic findings in hemodynamically stable individuals with cirrhosis of any etiology. Five hundred ten cirrhotic subjects, who were evaluated for possible liver transplantation (OLTx) between January 1985 and June 1987, were included in this study. Seventy-five had alcoholic cirrhosis and 435 had nonalcoholic cirrhosis of various etiologies. Of these 510 patients, 412 underwent combined upper and lower gastrointestinal endoscopy and 98 underwent upper gastrointestinal endoscopy alone. Gastritis, gastric and duodenal ulcer disease were found significantly (each at least p less than 0.025) more often in patients with alcoholic liver disease than in those with nonalcoholic liver disease. The prevalence of the various lower gastrointestinal lesions in both groups was similar. Of particular interest is the fact that in alcoholic cirrhotics, the prevalence of gastritis, gastric ulcer and duodenal ulcer disease was unrelated to the degree of portal hypertension, whereas in the nonalcoholic cirrhotics the prevalence of gastritis and duodenal ulcer disease but not gastric ulcer disease was associated significantly with the degree of portal hypertension as assessed by the presence or absence of large esophageal varices, ascites, and hepatic encephalopathy.
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PMID:Combined upper and lower gastrointestinal endoscopy: a prospective study in alcoholic and nonalcoholic cirrhosis. 269 Jun 64

Acute hepatic failure is characterized by a sudden catastrophic compromise of hepatic failure that causes clinical signs such as anorexia, depression, vomiting, diarrhea, icterus, and encephalopathy. Injurious hepatotoxins, drugs, infectious agents, or metabolic disturbances can cause acute hepatic failure; however, in many cases, the inciting cause is not determined. Treatment is aimed at controlling complications such as fluid-electrolyte imbalances, hepatic encephalopathy, hypoglycemia, bleeding diathesis, gastric ulcer, sepsis, and endotoxemia, in order to provide time for liver regeneration and recovery.
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PMID:Acute hepatic failure. 387 99

A 57-year-old man was admitted to our hospital for hepatic encephalopathy. He previously had undergone a partial gastrectomy for gastric ulcer, and also had been on maintenance hemodialysis because of diabetic nephropathy. Despite treatment with branched-chain amino acids and lactulose, encephalopathy occurred repeatedly. The findings of his laboratory examinations, computed tomography, and liver biopsy were not suggestive of chronic liver damage. Angiography revealed a portal-systemic shunt from the superior mesenteric vein via the left gastric vein to the left renal vein. A ligation of the gastrorenal shunt was performed. After the shunt ligation, hepatic encephalopathy no longer recurred, and no medication was required to prevent it. The insulin requirements also decreased, the plasma ammonia concentration then decreased, and serum concentration of several amino acids related to the ammonia metabolism also decreased. The molar ratio of branched-chain amino acids to aromatic amino acids increased. The ligation of the portal-systemic shunt was thus considered to be the key to the successful treatment of hepatic encephalopathy in this unusual case.
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PMID:Recurring encephalopathy abolished by gastrorenal shunt ligation in a diabetic hemodialysis patient. 946 59

It has been clearly established that Helicobacter pylori (H. pylori) infection plays a pivotal role in the pathogenesis of chronic gastritis, peptic ulcer, gastric adenocarcinoma, and gastric lymphoma MALT (mucosa-associated lymphoid tissue) in the general population, but data regarding the prevalence and the role of H. pylori infection in liver cirrhosis are conflicting. Most serological studies estimated a high prevalence of H. pylori infection in patients with liver cirrhosis; however, when other methods (urea breath test, histology, culture, rapid urease test) were used, the overall H. pylori prevalence was similar to that in controls. Although the prevalence of both gastric ulcer (GU) and duodenal ulcer (DU) is higher in cirrhotic patients than in general population, the relationship between H. pylori infection and peptic ulcer in cirrhosis remains controversial. Our data regarding peptic ulcer prevalence in cirrhotic patients are in agreement with previous studies that suggest an increased prevalence of both GU and DU. The incidence of bleeding peptic ulcer is high in cirrhotic patients and carries an increased risk of complications or death in these patients and therefore eradication of H. pylori infection might be as effective in preventing ulcer relapse and bleeding as it is in noncirrhotic ulcer patients. Hepatic encephalopathy is a frecquent complication of liver cirrhosis, and it is widely accepted that ammonia plays a major role in its pathogenesis. The ammonia production by H. pylori urease does not increase blood ammonia levels during cirrhosis, and eradication of H. pylori infection does not affect hepatic encephalopathy status.
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PMID:[Prevalence and role of Helicobacter pylori infection in some gastroduodenal and hepatic complications in cirrhotic patients]. 2020 58