Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

From history-taking and from analysis of plasma salicylate levels it is shown that a link exists between aspirin and gastrointestinal bleeding in 68% of cases. Salicylate levels alone indicate that aspirin has been taken in 22% of cases. Plasma salicylate measurement and endoscopy allow a better understanding of haemorrhagic lesions due to aspirin. Aspirin is responsible especially for haemorrhage from ulcers and acute gastritis or duodenitis. Aspirin is seen to be dangerous in a moderate number of susceptible individuals: those with peptic ulcer constitution or cirrhosis.
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PMID:Aspirin and gastrointestional bleeding. Interest of plasma salicylate determination. 31 93

Duodenitis was investigated by endoscopy in 93 cases from among 1242 subjects. Endoscopic duodenitis was classified into three types endoscopically--reddening type, erosive type and nodular type. There was a relatively high correlation between the endoscopic and the histological diagnosis of duodenitis. Severely inflamed cases were found histologically more frequently in erosive- or nodular-type duodenitis than in reddening-type duodenitis. During the follow-up period, changes in endoscopic findings were observed more frequently, from the erosive type to the reddening type, and from the reddening type to normal. There were no cases which subsequently developed duodenal ulcers. We found a significantly high incidence of "endoscopic duodenitis" in uremic patients who had been given regular dialysis, and not in hepatic cirrhosis patients.
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PMID:Clinical and histologic study of endoscopic duodenitis. 136 60

Endoscopic studies were performed to determine whether changes occurred in the duodenum related to portal hypertension in patients with liver cirrhosis. The total of 271 patients studied were subdivided into three groups: 83 patients with liver cirrhosis and portal hypertension, 53 with liver cirrhosis but no portal hypertension, and 135 controls. In the duodenum of cirrhotic patients with portal hypertension several changes were observed on endoscopy that were also present in the other two groups. Atrophy and vascular malformations, however, were present only in the duodenum of cirrhotic patients with portal hypertension, although in only a few patients and with statistical significance only for vascular malformations (p less than 0.01, phi = 0.21). Eleven percent of the patients had more than one endoscopic finding, but the associations of findings were without statistical significance. No statistically significant correlation was observed between the clinical severity of cirrhosis or the severity of esophageal varices and the endoscopic findings. Finally, there was no statistically significant difference between the histological findings of duodenitis in the three groups of patients.
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PMID:The duodenum in liver cirrhosis: endoscopic, morphological and clinical findings. 191 36

Clinical studies show that patients with liver cirrhosis associated with portal hypertension have a high incidence of duodenal ulcer and duodenitis. However, little information is available concerning pathophysiological process of such duodenal diseases in liver cirrhosis. Hemodynamics of the duodenal mucosa was studied in cirrhotics with esophageal varices (68 cases) and in noncirrhotics with non-ulcer dyspepsia (37 cases) as well. In each group, hemoglobin concentration in the peripheral venous blood was measured, and mucosal hemodynamics was examined in 4 regions of the duodenum by endoscopic reflectance spectrophotometer. No significant intergroup difference was noted in the mean age or sex ratio. Hemoglobin concentration in the peripheral venous blood was significantly lower (p less than 0.01) in the cirrhotics. There were no significant intergroup differences in duodenal mucosal blood volume. However, the cirrhotics showed significantly lower oxygen saturation of hemoglobin in all regions of the duodenum (p less than 0.01). These results show that the cirrhotics with esophageal varices had relative increase in blood volume and decrease in oxygen saturation of hemoglobin in the duodenal mucosa. Such microcirculatory disturbances seem to predispose liver cirrhosis patients to duodenal injury.
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PMID:Duodenal mucosal hemodynamics in patients with liver cirrhosis. 226 Apr 99

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

Controversial data have been reported on gastric acid secretion in patients with chronic pancreatitis. Moreover, studies on gastroduodenal morphological changes in patients with this disease and with other alcohol-related conditions have given different results. Basal and penta-gastrin-stimulated gastric secretion, histological changes of gastric and duodenal mucosa, and basal and meal-stimulated gastrin were measured in 21 patients with chronic alcoholic pancreatitis and in the following pair-matched groups: 21 chronic alcoholics and 21 control subjects (nonulcer dyspepsia), and in 19 patients with proven liver cirrhosis of alcoholic origin. No patient suffered from peptic ulcers. Moreover, gastric secretion was also measured in 51 patients with proven duodenal ulcers and in 34 healthy subjects. Basal acid output in patients with chronic pancreatitis was significantly higher (p less than 0.05) than in the other groups, except for the patients with duodenal ulcers. Peak acid output values in patient with chronic pancreatitis were similar to those measured in patients with duodenal ulcer, and they were higher than in the healthy subject group and in patients with liver cirrhosis, but statistical significance was not attained for patients with nonulcer dyspepsia. An increased frequency of duodenitis was found in patients with chronic pancreatitis, whereas an increased frequency of gastric metaplasia in the duodenal bulb was observed in all the patients with alcohol-related conditions considered. No relevant differences among the considered groups were found relating to gastric histological changes. Basal and meal-stimulated gastrin were similar in all the studied groups. This study suggests that in patients with chronic pancreatitis there is increased gastric secretion and probably an increased capacity for secretion of acid. Moreover, in patients with chronic pancreatitis, duodenitis seems to be frequent, but it probably is not directly related to chronic alcohol consumption.
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PMID:Gastric secretion, gastroduodenal histological changes, and serum gastrin in chronic alcoholic pancreatitis. 707 77

Electron microscopy of epithelial cells of the mucous membrane of the duodenum and jejunum was performed in 20 patients with chronic hepatitis and liver cirrhosis to reveal changes in the structure of intracellular formations of epithelial cells of the cryptae and villi, of goblet and enterochromaffin cells. The most essential differences were found in mitochondria, granular cytoplasmic network, ribosomes, microvilli and glycocalix. There were no differences in the pattern of cellular changes in chronic hepatitis and liver cirrhosis. However, the degree of lesions increased in patients with liver cirrhosis. Morphologic changes seen in the mucous membrane of the small intestine (duodenitis and jejunitis) in chronic liver diseases present the morphologic substrate of digestion impaired by these diseases.
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PMID:[Ultrastructural changes in the epithelial cells of the small intestine mucosa in chronic liver diseases]. 736 72

Long-term treatment with triethylene tetramine dihydrochloride, (trientine, TETA) was evaluated in 19 patients with Wilson's disease (WD). Two were given the drug as first choice and 17 after treatment with penicillamine. The change was made because of side-effects, lack of improvement or worsening of neurological symptoms. All penicillamine-induced side-effects reverted. Thirteen patients still receive trientine, and the mean total observation time on this treatment is 8.5 years/patient. Seven of the 13 are free from symptoms related to WD, five have mild to moderate neurological symptoms, mainly dysarthria. One patient with neurological symptoms who received trientine from the start of treatment deteriorated rapidly and is now severely dystonic. The symptoms initially worsened and later improved in one patient. All other patients improved during trientine treatment. Three patients died: two from a multifocal cancer including the liver and one non-complier from a ruptured spleen. Two patients underwent liver transplantation for progressive liver failure: one non-complier and one with liver cirrhosis whose liver function deteriorated despite treatment; both are now free from symptoms. Unexpectedly, two patients developed a serious colitis, one with duodenitis as well, that improved after withdrawal of the drug. No other unfavourable effects of trientine were recorded.
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PMID:Long-term treatment of Wilson's disease with triethylene tetramine dihydrochloride (trientine). 758 74

Morphologic investigation of 72 gastroduodenal biopsy samples from 29 children with chronic persistent and chronic active hepatitis, hepatic cirrhosis, revealed signs of chronic gastroduodenitis. The degree of the gastroduodenal zone lesion was directly related to severity of the primary condition. Comparative data on histopathological changes in the stomach and duodenum in concurrent pathologies suggest that chronic duodenitis may be the primary condition.
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PMID:[Morphological changes in the stomach and duodenum in chronic liver diseases of HB viral etiology]. 783 15

We studied the association between esophageal varices as the course of upper gastrointestinal bleeding and hepatic cirrhosis. 154 patients were admitted 43 patients in which esophageal varices bleeding was diagnosed were considered "CASES". 111 patients in which the source of bleeding was different (peptic ulcer, duodenitis, gastritis or tumor) were considered "CONTROL". The diagnosis of hepatic cirrhosis was confirmed in 69 patients in this group the main cause of bleeding was varices (62%). The "CASES" and "CONTROL" were crossed in 2 x 2 tables with the cirrhosis variable. Hepatic cirrhosis showed statistic and epidemiological association with variceal bleeding by means of CHi Square (p less .005) and Odds ratio about 138.92 with 95% confidence interval about 18.92 to 2844.8. In the control group this associations was not proved.
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PMID:[Esophageal varices as a cause of upper digestive hemorrhage in cirrhotic patients: clinical and epidemiologic investigation]. 792 13


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