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)

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

The coagulation parameters of fourteen patients with advanced liver cirrhosis (3 in Child class B and 11 in class C) were prospectively determined quarterly for one year in order to evaluate the possible relationship between high D-dimer levels and incidence of disseminated intravascular coagulation (DIC) and of gastrointestinal bleeding. The values of D-dimer, fibrin(ogen) degradation products, platelets, fibrinogen, prothrombin activity and antithrombin III were fairly stable in almost all patients and no patient developed an overt DIC; one patient had a significant increase in D-dimer three months after the first control. During the one year follow-up, four patients died, one by the occurrence of hepatocellular carcinoma and three by digestive bleeding. Overall, four patients had upper digestive tract bleeding, three from esophageal varices and one from hemorrhagic gastritis. Hemorrhage was more frequent in patients with high D-dimer levels (3/7, 43%) than in patients with normal D-dimer levels (1/7, 14%). In conclusion, the detection of high D-dimer levels in patients with advanced cirrhosis is not predictive for the occurrence of a overt DIC but seems to be related with an increased risk of gastrointestinal bleeding.
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PMID:High D-dimer levels: a possible index of risk of overt disseminated intravascular coagulation and/or digestive bleeding in advanced liver cirrhosis? 801 48

Review of the literature presented deals with the state of connective tissue and some aspects of its metabolism in ulcer disease, chronic gastritis, chronic hepatitis, hepatic cirrhosis, acute and chronic pancreatitis. Disorders of synthesis and degradation of collagen, changes in metabolism of glycosaminoglycans, glycoproteins and aminoglycans are described, their pathogenetical role in development end exacerbation of diseases of digestive organs is demonstrated.
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PMID:[Connective tissue function in diseases of the digestive organs (a review of the literature)]. 820 30

A higher incidence of gastric and duodenum ulcer was well recognized in patients with liver cirrhosis, but the mechanism has not been fully identified. In this study, serum gastrin, free portal pressure (FPP) were measured in 24 consecutively admitted cirrhotic portal hypertensive patients, and preoperative basic acid output (BAO) was measured in 13 randomized patients. Among the 24 patients, concomitant duodenal ulcers were found in 3 by both gastroduodenoscopy and barium series, and gastritis was found in all patients. It was found that most patients (71%) with liver cirrhosis have a elevated level in serum gastrin, whereas BAO is lower than normal in all patients, and the higher the FPP, the lower the BAO is. We believe that the congestive gastroduodenal mucosal lesion was underlying the ulceration most often seen in patients with portal hypertension.
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PMID:[The level of serum gastrin and ulceration in cirrhotic patients with portal hypertension]. 858 18

The fluorescence spectroscopy of porphyrin molecule in blood was determined with photoluminescence fluorescence spectroscope in 139 patients with gastric carcinoma, 76 with hepatic carcinoma, 110 with gastric ulcer and chronic gastritis, 168 with liver cirrhosis and 33 normals as controls. The results showed that the peaks of Zinc porphyrin and protoporphyrin in patients with cancer were significantly higher than those in patients with benign disease, the peak of protoporphyrin being two to three times higher in the former groups of patients than that in the latter (P < 0.01). Protoporphyrin could be used as a marker to screen and diagnose gastric and hepatic carcinoma.
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PMID:[Changes in hematoporphyrin in patients with gastric and hepatic carcinoma and their clinical significance]. 873 9

In this research we evaluated the prevalence of Hp in the gastric mucosa in patients suffering for chronic liver disease, either chronic hepatitis or liver cirrhosis. Sixty-three patients 27 with chronic hepatitis and 36 with liver cirrhosis, were examined by EGDS; of them we evaluated: endoscopic findings of stomach and duodenum, histology of gastric mucosa (antrum and corpus-fundus), presence of Hp in the histologic samples. We compared the positivity for Hp with the following parameters: presence of esophageal varices, macroscopic aspect of the gastric and duodenal mucosa, presence of hystological findings of gastritis, gastritis's activity, grading of the hepatic damage. In the our research we didn't point out greater prevalence of the Hp in the gastric mucosa with respect to hepatic damage, esophageal varices or macroscopic signs of gastric pathology. The Hp is significantly associated with histologic evidence of gastritis and also with the grade of gastritis's activity. The data of the present work don't suggest any correlation within the pathologic changes of the gastric mucosa caused from the liver cirrhosis and the presence or the growth of Hp.
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PMID:[Endoscopic and histologic findings of gastric mucosa and Helicobacter pylori prevalence in patients suffering from chronic liver disease]. 876 78

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

The abnormal composition of the fatty acids in gastric mucosal phospholipids was examined in 11 patients with non-alcoholic liver cirrhosis accompanied by gastritis and in 10 healthy subjects without liver disease and gastritis. The cases positive for serum anti-Helicobacter pylori immunoglobulin G antibody were excluded. The arachidonic acid (AA, C20:4n-6) contents of the two main components of phospholipid, the phosphatidylcholine (PC) and phosphatidylethanolamine (PE) fractions, in gastric biopsy specimens were significantly lower in the cirrhosis group, although PC and PE contents in gastric biopsy specimens were not altered. In the cirrhosis group, AA contents of the PC fractions in gastric biopsy specimens were significantly correlated with AA contents of plasma PC fractions and serum albumin levels. Soft oil capsules containing polyunsaturated fatty acid (PUFA) such as AA, eicosapentanoic acid (EPA, C20:5n-3) and docosahexanoic acid (DHA, C20:6n-3) were administered after each meal daily for 4 weeks to six cirrhotic patients and four control subjects, who were randomly selected from the patients and control subjects. After administration of PUFA-enriched oil capsules, gastric mucosal AA contents of PC and PE fractions were significantly improved almost to the control levels. In three cirrhotic patients with severe or mild gastritis whose gastric mucosal lesions were endoscopically shown to have responded to PUFA-enriched oil capsules, AA contents of plasma PC and PE fractions before administration were much lower than in the remaining three cirrhotics that did not respond to the PUFA-enriched oil capsules, but significantly improved to the control levels after administration of oil capsules. The results demonstrate that administration of PUFA-enriched soft oil capsules increased AA contents of the phospholipids in gastric mucosa and thus improved gastric mucosal lesions endoscopically in cirrhotic patients with gastritis.
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PMID:Abnormality in fatty acid composition of gastric mucosal phospholipids in patients with liver cirrhosis and its correction with a polyunsaturated fatty acid-enriched soft oil capsule. 940 27

The article presents summarized results of treatment and examinations of 216 patients with gastro-intestinal bleedings due to acute errosive hemorrhagic gastritis and gastroduodenitis, cancer and polyposis of the stomach, liver cirrhosis and portal hypertension, hemorrhage against the background of atherosclerosis and arterial hypertension by administration of hemostatic medicine into the lymphatic system for activation and reinforcement of the reserve monocyte-macrophage mechanism of hemocoagulation. The results obtained confirm the expedience of this method of influencing the monocyte-macrophage hemostasis, having no complications and giving better medical effects.
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PMID:[Hemostatic therapy of gastroduodenal hemorrhage of non-ulcer genesis by the use of reserve mechanisms of hemostasis]. 961 18

The gastrointestinal bleeding commonly observed in patients with liver cirrhosis is usually from esophageal and gastric varices, gastroduodenal ulcer, and congestive gastropathy. Portal hypertension is the major causative factor of pathogenesis of GI lesions. In the present review, we focus in gastric mucosal defense and Helicobacter pylori infection in liver cirrhosis. Gastric mucosal defense is reduced in liver cirrhosis, especially prostaglandins which play a role in the gastric mucosal defense decreased in the gastric mucosal of patients with liver cirrhosis and rat portal hypertension model. Although H. pylori is strongly associated with peptic ulcer disease and chronic gastritis, several studies showed no relationship between H. pylori infection and gastroduodenal ulcer or the infection and congestive gastropathy in liver cirrhosis. Reduced gastric mucosal defense may account for the pathogenesis of GI lesions in liver cirrhosis.
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PMID:[Gastrointestinal lesions in liver cirrhosis]. 978 Jul 25


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