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)

At present in vivo NMR spectroscopic studies of brain glutamate and glutamine concentrations relative to encephalopathy have mainly been performed in hepatic encephalopathy (HE). In vivo proton NMR studies were performed in rats with hyperammonemia and acute HE due to acute liver ischemia as well as in rats with hyperammonemia due to either repeated urease i.p. injection or i.p. administration of methionine sulfoximine, a well known inhibitor of glutamine synthetase. In man, in vivo proton NMR is described in patients with chronic liver disease: cirrhosis of different etiology and associated with different degrees of HE. In the experimental models proton NMR spectroscopy of the cerebral cortex revealed an increase in glutamine concentration, a decrease in glutamate concentration and a decrease in phosphocholine compounds. In humans no clear distinction between cerebral cortex glutamate and glutamine concentration could be made by in vivo 1H NMR spectroscopy. However, the combined glutamate/glutamine peak increased in a way compatible with an increased cerebral cortex glutamine concentration during chronic HE. In the cirrhotic patients too a decrease in cerebral cortex phosphocholine compounds was observed, the explanation of which is unclear. Both the experimental work and the clinical observations support the hypothesis that impairment of the glutamate/glutamine cycle between astrocytes and neurons plays a role in the pathogenesis of hepatic encephalopathy.
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PMID:What the clinician can learn from MR glutamine/glutamate assays. 167 85

An unusual campylobacter strain, a urease positive thermophilic variant of Campylobacter lari, was isolated from the urine of a patient with urinary tract infection who was hospitalized because of cirrhosis and haemorrhage. The strain was isolated from urine specimens on three separate occasions. A significant serological response to the organism was also detected. This is the first documented case of extra-intestinal infection due to this group of organisms.
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PMID:Isolation of a urease positive thermophilic variant of Campylobacter lari from a patient with urinary tract infection. 207 1

Urease is an enzyme found in plants and bacteria, but not mammals. It catalyzes the conversion of urea to carbon dioxide and ammonia. Ammonia shortens the life span of cells; and higher concentrations cause tissue necrosis and cytolysis. Twenty percent of total body urea is converted to ammonia by bacterial urease in the colon. Small injections of urease immunize animals by producing antiurease, a gamma globulin, which inactivates urease. Immunization eliminates the colonic conversion of urea to ammonia. Injection of urease produces ammonia intoxication making immunization hazardous. Although previously impossible, a non enzymatic urease antigen was synthesized by covalently bonding jack bean urease with glutaraldehyde. This antigen stimulated the production of antiurease that inactivates native urease. Helicobacter pylori, a potent urease producer, has been implicated in peptic ulcer, gastritis and other inflammatory bowel lesions. The pathogenicity of H pylori is dependent on its urease production. Immunization to urease can render H pylori non pathogenic. Cirrhotics develop encephalopathy and hyperammonemia because their livers fail to convert all the ammonia in portal venous blood to urea and collaterals develop by passing the liver. Colonic ammonia increases the turnover rate of colonic mucosa. Ammonia absorbed into the portal venous system is transported to the liver where it is reconverted to urea. Absorbed ammonia adversely influences liver function. Infections with urease producing organisms destroy the renal parenchyma and produce struvite stones. Urease immunization aids colonic healing and prevents uremic colitis. Absorbed ammonia is a noxious influence on the liver. Animals immunized to urease regenerate the liver faster and are less susceptible to hepatotoxins. Immunization to urease ameliorates cirrhosis. Proteus and other urease producers become non toxic and do not damage the renal parenchyma. Urease is responsible for the pathogenicity of infections with urease producing organisms. Immunization to urease renders urease producing organisms non pathogenic.
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PMID:Awakenings to the pathogenicity of urease and the requirement for continuous long term therapy. 799 80

In cirrhosis, Helicobacter pylori infection may be implicated, together with portal hypertension, bile reflux and alcohol abuse, in damage to gastric mucosa. Aim of this study was to define the influence of non-alcoholic liver disease on the incidence of Helicobacter pylori infection and on the diagnostic accuracy of specific serology. Enrolled in the study were 232 individuals, 105 also had cirrhosis. Infection by Helicobacter pylori, diagnosed by a positive concordance of quick urease test and histology, was detected in 97 (48 with cirrhosis) out of 184 patients. Severe gastritis was more frequent in patients with Helicobacter pylori infection than in patients without. Cirrhosis did not significantly affect the prevalence of Helicobacter pylori infection or the histological features of gastritis. Specific anti-Helicobacter pylori IgG and IgA assay (Bio-Rad GAP test) was used for serological diagnosis. Anti-Helicobacter pylori IgG showed a high sensitivity (85% in cirrhotics, 89% in non-cirrhotics) and low specificity being more evident in cirrhotics (38% vs 56% non-cirrhotics). Serum specific IgA showed low sensitivity (approximately 25% in both groups) and specificity of 79% in cirrhotics vs 84% in non-cirrhotics. In conclusion, non-alcoholic cirrhosis does not affect the incidence of Helicobacter pylori infection and the histological features of chronic gastritis but does decrease diagnostic efficiency of serological tests for Helicobacter pylori.
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PMID:Cirrhosis negatively affects the efficiency of serologic diagnosis of Helicobacter pylori infection. 889 48

There is a higher prevalence of peptic ulcer disease in cirrhotic patients than in the general population. Whether Helicobacter pylori is a risk factor for peptic ulcer in cirrhosis remains controversial. The aim of this study was to determine whether there is a significant correlation between H.pylori infection and peptic ulcer in liver cirrhosis. In a cross-sectional study, 49 cirrhotic patients underwent upper gastrointestinal endoscopy and 75 controls (health examinees) without liver disease were also examined by endoscopy. The presence of H. pylori was assessed by culture, histologic findings and rapid urease test of gastric antrum biopsy specimens. Thirty of the 49 (61%) cirrhotic patients had peptic ulcers as compared to 24 of the 75 (32%) controls. The frequency of H. pylori in the antrum in the cirrhotic group was significantly lower than in the control group (39% vs 69%). The presence of H. pylori was more frequent in control patients with gastric (75%) and duodenal ulcers (95%) than nonulcer control patients (59%) whereas the difference between patients with peptic ulcer and nonulcer (40% vs 37%) was not significant in cirrhotic patients. H. pylori was identified in 40% of the cirrhotic patients with duodenal ulcers compared with 95% of controls with duodenal ulcers (p < 0.05). Nevertheless, this difference was not significant among patients with a gastric ulcer between the two groups (40% vs 75%). There was no significant difference in the frequency of H. pylori infection among nonulcer patients between the cirrhotic and control groups (37% vs 59%). In conclusion, we found no evidence to substantiate an etiologic role of H. pylori in the development of a duodenal ulcer in cirrhotic patients.
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PMID:Helicobacter pylori infection and risk of peptic ulcer among cirrhotic patients. 903 84

The prevalence of Helicobacter pylori in Egyptian patients with different stages of liver diseases was compared to those with normal liver status. Eighty patients subjected to upper gastrointestinal endoscopy were enrolled. They were divided according to their liver status into two groups; the first patients with liver cirrhosis and the second who had no liver affection. Gall bladder diseases were excluded by abdominal ultrasound examinations. Endoscopic antral mucosal biopsies were used for H. pylori screening by both culture and urease test, and for histopathological examinations. Both groups were matched as regards age, sex, and socioeconomic conditions. Culture was positive in 42.2% and 40.7% of patients in both groups respectively (P > 0.05). Urease test showed positive results in 58% and 76.6% in both groups respectively (P > 0.05). Helicobacter pylori prevalence showed no significant differences between both studied groups as regards age, sex, or type of gastric lesions. Furthermore, liver status in patients with chronic liver diseases does not play a role in distribution of infection. The study shows the high prevalence of H. pylori among Egyptians and the absence of a relation between H. pylori and chronic liver diseases.
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PMID:Helicobacter pylori among Egyptian patients with chronic liver diseases. A comparative study. 925 95

An increased frequency of peptic ulcer disease is noted in patients with cirrhosis, but the role of H. pylori in this disorder remains to be determined. The diagnosis of cirrhosis was confirmed by a combination of clinical, biochemical, radiological, and histological methods. The severity of cirrhosis was assessed by Pugh's modification of Child's criteria. Upper gastrointestinal endoscopy was performed consecutively to evaluate the presence of varices and gastroduodenal mucosa. H. pylori status was assessed by histology, urease test, and serology. In all, 130 patients with cirrhosis were recruited into the study; there were 86 males and 44 females with a mean (SD) age of 54.4 (12.7) years. The H. pylori prevalence was 76.2%. There was no difference in age between the H. pylori-positive and -negative cirrhotics (P = 0.29). The H. pylori prevalence revealed no difference among cirrhotics with Child A (77.8%), Child B (72.9%), and Child C (78.6%) (P = 0.8), and neither was there a difference in H. pylori prevalence in cirrhotics with and without congestive gastropathy (77% vs 73.7%, P = 0.84). The prevalence of H. pylori in cirrhotics with and without varices did not show a statistical difference (75% vs 81.8%, P = 0.68). There also was no difference in the H. pylori prevalence between cirrhotic patients with and without peptic ulcers (84.4% vs 69.7%, P = 0.09). In conclusion, the prevalence of H. pylori or peptic ulcer is independent of the severity of cirrhotic liver disease. The association between H. pylori infection and peptic ulcer disease is weak in cirrhosis.
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PMID:Helicobacter pylori infection and peptic ulcer disease in cirrhosis. 963 11

An increased risk for gastric cancer in patients with liver cirrhosis has recently been reported. This study was performed in order to determine gastric epithelial cell proliferation in cirrhotic patients and to evaluate the role of congestive gastropathy (CG) and Helicobacter pylori infection in this process. Thirty-six cirrhotic patients and 18 controls were enrolled in the study. All patients underwent endoscopy and three biopsies were performed in the antrum and three in the gastric body. The presence of H. pylori infection was assessed by a rapid urease test and histology. The antral biopsies were used for gastric cell proliferation assessment by an immunohistochemical analysis (Ki-67). There was no significant difference in epithelial cell proliferation between cirrhotics and controls. Gastric proliferation values were higher in patients with H. pylori infection compared with uninfected patients, both in cirrhotic (P = 0.003) and in control groups (P = 0.06). Among the cirrhotic group, we found a progressive increase in gastric cell proliferation values related to the degree of CG, the highest values being observed in cirrhotic patients with severe CG. Moreover, cirrhotics with both severe CG and H. pylori infection had the highest proliferation values when compared with all other subgroups. In conclusion, this study found that: (1) CG significantly affects epithelial cell proliferation in gastric mucosa in cirrhotic patients, (2) H. pylori infection plays a similar role in gastric cell proliferation in both cirrhotic and non-cirrhotic patients, and (3) CG and H. pylori could act synergistically in this process.
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PMID:Gastric epithelial cell proliferation in patients with liver cirrhosis. 1131 31

Helicobacter pylori urease activity is a potential source of ammonia in the stomach of patients with cirrhosis. However, the possible role of H. pylori in the pathogenesis of hepatic encephalopathy deserves further investigations. The current study evaluates the relationship among H. pylori infection, gastric juice ammonia concentrations, and arterial ammonia levels in patients with cirrhosis. Overall, 14 patients with cirrhosis with overt hepatic encephalopathy, 19 with subclinical hepatic encephalopathy, and 13 without encephalopathy were enrolled. All patients underwent upper endoscopy, and gastric biopsy specimens were taken for H. pylori assessment (rapid urease test, histology, and culture). A gastric juice sample and an arterial blood sample were obtained for ammonia level assessment. Patients with overt encephalopathy had both higher arterial ammonia levels and a more severe hepatic impairment than the remaining patients, whereas gastric juice ammonia concentrations did not differ among the three groups. H. pylori prevalence was similar among groups. Patients with H. pylori infection had significantly higher gastric juice ammonia concentrations than those without infection (2.3 +/- 1.3 vs. 0.9 +/- 0.6 mmol/L, respectively; p = 0.003); however, no difference in arterial ammonia levels emerged between the two groups (37.7 +/- 18.6 vs. 37.6 +/- 18.8 micromol/L, respectively). No significant correlation was found between gastric juice ammonia concentrations and arterial ammonia levels. The data suggest that liver impairment remains crucial in ammonia disposal in patients with cirrhosis, whereas H. pylori infection does not seem to play a major role in the pathogenesis of hyperammonemia in these patients.
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PMID:Helicobacter pylori, gastric juice, and arterial ammonia levels in patients with cirrhosis. 1196 74

Helicobacter pylori infection could play a role in different clinical alterations observed in cirrhosis, from gastroduodenal lesions to hepatic encephalopathy. Although its prevalence in cirrhotics is similar to that in controls, H. pylori infection is responsible for the increased prevalence of peptic ulcer observed in these patients. The ammonia production by H. pylori urease does not seem to increase blood ammonia levels during cirrhosis, indicating that its role in hepatic encephalopathy could be marginalized in clinical practice. Dual and triple therapies have been shown to be equally effective for H. pylori eradication in these patients.
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PMID:Helicobacter pylori infection in patients with liver cirrhosis: facts and fictions. 1277 75


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