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)

A 2-year feeding study of methylmercury chloride (MMC: 0, 0.4, 2, or 10 ppm) was conducted in B6C3F1 mice (60 mice of each sex/group) to compare chronic toxicity and carcinogenicity results with those for ICR mice from our previous study in which males of the 10-ppm group showed an increased incidence of renal tumors without any abnormal in-life parameters. In B6C3F1 mice of the 10-ppm group, neurotoxic signs characterized by posterior paralysis were observed in 33 males after 59 weeks and in 3 females after 80 weeks. In males, a marked increase in mortality and a remarkable decrease in body weight gain were observed after 60 weeks. Toxic encephalopathy consisting of neuronal necrosis of the brain and toxic peripheral sensory neuropathy were induced in both sexes in this group. Chronic nephropathy, testicular atrophy, and glandular stomach ulcer increased in incidence in the males; chronic nephropathy also increased in incidence in females. In proliferative lesions, there were significant increases in the incidence of renal adenoma and/or carcinoma (16/60) and tubular cell hyperplasia (14/60) in males of the 10-ppm group, as compared to the control group. The incidence of chronic nephropathy also increased in males of the 2-ppm group. The results of this study indicate that the susceptibility of B6C3F1 mice to renal toxicity and renal carcinogenicity is comparable to that of ICR mice, and B6C3F1 mice are more sensitive to the chronic neurotoxic effects of MMC than are ICR mice.
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PMID:Chronic toxicity and carcinogenicity of methylmercury chloride in B6C3F1 mice. 230 16

Upper gastrointestinal hemorrhage is one of the more important complications of cirrhosis and a major cause of death in such patients. The main sites of bleeding are esophageal varices, gastritis, and peptic ulcers. In order to determine the prevalence of either potential bleeding lesions or of other endoscopic findings in hemodynamically stable individuals with various etiologies of cirrhosis, 510 consecutive cirrhotic patients, evaluated for possible orthotopic liver transplantation (OLTx) underwent an upper gastrointestinal endoscopy for combined diagnostic and therapeutic purposes. The patients were divided into two main groups: 319 patients with parenchymal liver disease and 191 patients with cholestatic liver disease. Gastritis was found significantly more often in patients with parenchymal liver disease than in those with cholestatic liver disease (49.8% vs 30.9%; P less than 0.001). In contrast, the prevalence of esophagitis, esophageal and gastric varices, gastric ulcer, duodenal ulcer, and duodenitis was similar in both groups. Normal endoscopic findings were present in 5.0% of the parenchymal group and 11.5% of the cholestatic group (P less than 0.02). Ascites and encephalopathy were found significantly more often in subjects with parenchymal liver disease as compared to those with cholestatic liver disease. Portal hypertension and its degree, as assessed by the presence and size of esophageal varices, was similar in both groups, and in both groups there was a statistically significant qualitative trend of increasing prevalence of esophageal varices with increasing severity of disease as estimated using Pugh-Child's criteria.
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PMID:Prevalence of endoscopic findings in 510 consecutive individuals with cirrhosis evaluated prospectively. 234 4

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

Seven patients with decompensated posthepatitis B cirrhosis were treated with low doses of interferon alpha. The initial plasma level of HBV-DNA ranged from 3.0 to 189.3 pg/ml, and that of ALT from 37 to 156 IU/l. Liver biopsies demonstrated ongoing piecemeal necrosis. In sera of all but one patient, HBV-DNA became undetectable by hybridisation techniques within 10 to 28 weeks. Plasma HBeAg became negative in four and HBe-antibodies positive in three patients. Serum transaminase levels showed a marked initial rise 3 to 13 weeks after onset of therapy; they dropped to normal values later in all except one patient. Therapy was initiated at 1 MU (million units) three times a week for 2 weeks and was increased to 2.5 MU for 16 weeks. Later, this dosage was raised to 5 MU three times a week in some patients. Complications included variceal haemorrhage, aggravation of ascites or of encephalopathy, development of pneumonia, recurrence of spontaneous bacterial peritonitis or of gastric ulcer bleeding. One year after stopping the therapy, three patients are well and without any feature of liver decompensation. Three patients died before they could undergo a liver transplantation. In one patient treatment was interrupted because of marked exacerbation of liver cell necrosis. It thus seems possible to suppress HBeAg and HBV-DNA in patients with decompensated cirrhosis. This is important to prepare them for possible liver transplantation. Interferon should be initiated at low doses and the patients be very carefully monitored. Prophylactic therapy for bacterial peritonitis and for variceal haemorrhage is warranted.
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PMID:Treatment of decompensated viral hepatitis B-induced cirrhosis with low doses of interferon alpha. 845 21

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

A 66-year-old woman had had recurrent episodes of disturbed consciousness whenever she had been constipated or dehydrated. She had been inactive and afflicted with obstinate constipation since she had menopause at age of 32. She underwent gastrectomy for gastric ulcer at age of 37. Laboratory examination showed marked hyperammonemia, reduction in Fisher ratio, and poor excretion of ICG. Furthermore, hypopituitarism and secondary hypothyroidism were found. She was diagnosed as Sheehan's syndrome. A T1-weighted MRI demonstrated symmetrical high intensity in the bilateral globus pallidus and empty sella. The histological examination of the liver revealed a mild lymphocytic infiltration without liver cirrhosis. Abdominal angiography showed a large shunt vessel between the splenic vein and the left renal vein. After embolization of the shunt vessel, hyperammonemia and neurological impairment improved. Additionally multiple hormones replacement has been useful to reduce the drugs of standard therapy for hepatic coma. In this case, we speculated that Sheehan's syndrome accelerated the constipation and worsened the shunt encephalopathy.
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PMID:[A case of portal-systemic encephalopathy associated with Sheehan's syndrome]. 1083 32

A 74-year-old man noted dysarthria and right hemiparesis. His history included a gastric ulcer 2 years previously, and he had gradually lost 10 kg over a 2-year period due to appetite loss. He daily consumed 120 mg of alcohol. Upon arrival, he had clear consciousness and stable vital signs. He was malnourished. Neurologic findings included a positive finding of Barre sign in the right hand and dysarthria. A venous blood gas analysis demonstrated the following: pH 7.059; PCO2, 21.5 mm Hg; PO2, 59.1 mm Hg; HCO(3-), 5.8 mmol/L; base excess, -22.7 mmol/L; lactate,17 mmol/L; and glucose, 4 mg/dL. After the administration of an infusion of thiamine and glucose, his abnormal neurologic findings subsided completely. Head magnetic resonance image (MRI; diffusion weighted image) disclosed 3 spotty, high-intensity signals in the brain. The main results of biochemical analyses of the blood collected on arrival were as follows: hemoglobin, 5.5 g/dL; glucose, 5 mg/dL; aspartate aminotransferase, 89 IU/L. He was admitted for further examination and was diagnosed as having alcoholic ketoacidosis with hypoglycemic encephalopathy and anemia due to colon cancer.
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PMID:A patient with clear consciousness even with a glucose level of 5 mg/dL (0.2 mmol/L). 2652 Nov 93

Specific risk factors for gastroduodenal surgery in cirrhotic patients have been identified, which dictates for a more personalized management. The retrospective study was conducted between 2012-2019 on twelve patients (7 cases of duodenal ulcer, 2 cases of gastric ulcer and 3 patients with gastric cancer). We took into account a number of possible factors involved in the unfavorable evolution of patients, based on data published in the literature so far. In order to follow the involvement of each factor we compared two groups of patients, one with unfavorable evolutions, exitus and another with favorable evolutions. Emergency surgery, the presence of ascites at the time of intervention, a higher than 30 MELD score, alcoholic cirrhosis, liver encephalopathy and liver failure are common factors that are found in a high percentage (between 75% and 100%) in patients who have had an unfavorable evolution, exitus. The same risk factors are found in much lower percentages in patients who have evolved favorably postoperatively, most between 12.5% and 25%. We analyzed preoperative aspects, surgical approach, complications and risk factors for these patients, compared them with the results of our study and identified future therapeutic possibilities. For CHILD B or C patients, the indication for surgery should be discussed in advance with a multidisciplinary team. Endoscopic submucosal dissection or discontinuation of D2 dissection should be considered in these patients.
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PMID:Gastroduodenal Surgery in Cirrhotic Patients - Case Series and Literature Review. 3236 26