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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endoscopic evaluation of upper gastrointestinal tract in 82 patients with liver cirrhosis, versus 82 controls was performed. In part of them presence of Helicobacter pylori infection was also analyzed. We found significantly higher prevalence of endoscopic changes in cirrhotic patients (87%). Diagnoses of oesophangeal candidiasis and varices, gastritis, ventricular or duodenal erosions and ulcers, duodenal deformations were more frequent in this group of patients in comparison to group of non-cirrhotic patients. Helicobacter pylori infection was found in 83% of cirrhotic patients, that was significantly higher than in non-cirrhotic control group (43%).
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PMID:[Macroscopic changes in endoscopy of upper digestive tract and Helicobacter pylori infections in patients with liver cirrhosis]. 759 83

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

Thirty-seven patients aged 36-75 years with cirrhosis of the liver secondary to chronic hepatitis were included in the study. They were divided into three groups according to the modified Child's classification for cirrhotic severity, where A = good, B = fair and C = poor. In addition, the patients were divided according to the presence or absence of each of the following: ascites, splenomegaly and oesophageal varices. Radionuclide-labelled solid meals were used to evaluate gastric emptying and the 14C-urea breath test was used to detect Helicobacter pylori infection. Gastric emptying was represented by the gastric retention ratio of the solid meal at 90 min (RR90) and calculated using the following formula: the residual radioactivity within the region of interest (ROI) covering the whole stomach at 90 min divided by the initial radioactivity within the ROI at 0 min. We found that 75.7% (28/37) of the patients had abnormal gastric emptying and 45.9% (17/37) had H. pylori infection. No significant correlation was found between abnormal gastric emptying and H. pylori infection. There were no significant differences among the three groups regarding gastric emptying or H. pylori infection according to the modified Child's classification. However, the highest rates of abnormal gastric emptying and H. pylori infection were in patients in Child's class C. The differences in RR90 among patients with and without ascites, and patients with and without splenomegaly, were not significant (P > 0.05). However, there was a significant difference between the patients with and without oesophageal varices (P < 0.05). In addition, poor correlations (R2 < 0.01) were found between RR90 and serum levels of bilirubin and albumin.
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PMID:Abnormal gastric emptying and Helicobacter pylori infection in patients with cirrhosis of the liver. 895 15

Helicobacter pylori infection is being correlated to a number of human diseases, among which also those of the liver. From a clinical point of view, 4 "areas of interest" for the suggested correlation can be identified: 1. Helicobacter pylori and portal hypertension-related congestive gastropathy in cirrhotics. There are, in the literature, at least 7 studies confirming that the microorganism has no role in causing or worsening the disease. 2. Helicobacter pylori and duodenal ulcer in cirrhotic patients. Apparently, in the cirrhotic patient, the microorganism has no role in causing duodenal ulcer. 3. Helicobacter pylori, ammonia production and hepatic encephalopathy. In this case, there are at least three studies showing that Helicobacter pylori infection increases the risk of developing encephalopathy in the cirrhotic patient, this being a somewhat expected finding. 4. Helicobacter pylori infection in chronic liver disease and its diagnosis. Evidence in the literature suggests: a) that hypertensive gastropathy might not represent a favourable environment for Helicobacter pylori thus making the diagnostic sensitivity of the biopsy lower than expected, and b) that even serological diagnosis might provide data of difficult interpretation, as shown in non alcoholic cirrhosis and, by our own group, in primary biliary cirrhosis. More intriguing are the data generated with respect to the potential capacity of Helicobacter pylori and Helicobacter pylori-like bacteria such as, in particular, Helicobacter hepaticus to damage the liver by producing toxins with a granulating effect on liver cell lines which, in vivo, through the portal tract, might reach the liver, thus causing hepatocellular damage. The point has been addressed by a number of investigators and autoimmune mechanisms have also been suggested. In summary, from the clinical point of view, some evidence suggests that Helicobacter pylori infection might be relevant in the pathogenesis of hepatic encephalopathy in cirrhosis. The data being generated with respect to a direct hepatotoxicity are, at present, stimulating but only speculative.
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PMID:Helicobacter pylori and the liver: any relationship? 961 80

Gastrointestinal bleeding sometimes causes life-threatening state. It is important to understand the underlining risk factors for prevention and treatment of this condition. In 1997, 81 patients with massive gastrointestinal bleeding were admitted to the life-saving center in Kyoto First Red Cross Hospital. In these patients, 14 subjects (17%) had been receiving hemodialysis. Eight patients (10%) were taking anti-coagulant or antiplatelet drugs. Eight patients (10%) had hypertension and were given calcium antagonists. Seven subjects (9%) had liver cirrhosis and/or hepatocellular carcinoma. Because these patients often fall into life-threating state, we must pay special attention to the prevention and cure for gastrointestinal bleeding. For example, it may be necessary to change to heparin free hemodialysis for patients having active bleeding. In anticoagulated patients, it may be required that sufficient hemostatic therapy without risking thromboembolic sequelae. In addition to careful managements, we have better to consider the eradication therapy for all of these high risk groups with Helicobacter pylori infection.
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PMID:[Risk factors for gastrointestinal bleeding]. 978 Jul 11

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

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

The importance of ammonia-producing Helicobacter pylori infection as a cause of subclinical encephalopathy in cirrhosis was investigated. In addition, a single psychometric test that can reliably detect subclinical hepatic encephalopathy was sought. Out-patients with cirrhosis and no overt encephalopathy underwent [14C]urea breath testing once and psychometric testing on two separate occasions, with an intervening course of clarithromycin/omeprazole if they had subclinical encephalopathy (two of four psychometric tests abnormal). Subclinical encephalopathy was present in 27 of 69 patients (39%), and Helicobacter pylori infection in 14 of 69 (20%). There was no association between the two conditions (P = 0.769). Subclinical encephalopathy resolved in 75% of treated Helicobacter pylori-positive patients and 37.5% of treated Helicobacter pylori-negative patients (P = 0.285). Number connection test-B had high reproducibility among untreated patients (R = 0.655) and high correlation (P < or = 0.01) with three surrogate gold standards. In stable cirrhotic patients, subclinical hepatic encephalopathy was found to: (1) have a high prevalence, (2) not be associated with Helicobacter pylori infection, and (3) be readily detected with the number connection test-B alone.
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PMID:Helicobacter pylori infection is not associated with subclinical hepatic encephalopathy in stable cirrhotic patients. 1176 68

Chronic hepatitis may progress to cirrhosis and hepatocellular carcinoma (HCC). HCC represents one of the most common human cancers. Incidence rates for this tumor vary widely on a worldwide, suggesting that environmental factors such as infectious microorganisms, carcinogens, or nutrition play a role in its pathogenesis. Several Helicobacter spp. colonize the liver of animals and induce hepatitis. The aim of this study was to determine whether Helicobacter infection was associated with HCV-related liver diseases in humans. Liver tissue samples, including biopsy and surgically excised tissues, were collected from patients positive for hepatitis C viruses (HCV) RNA in the serum. Genomic DNA was extracted from sections of formalin-fixed paraffin-embedded tissues by using the QIAamp Tissue Kit and subjected to polymerase chain reaction (PCR) analysis using two sets of Helicobacter-specific 16S ribosomal RNA primers. To identify positive samples for H. pylori, a set of primers specific for a conserved region in the H. pylori vacA gene were also used. The patients' H. pylori status was determined by ELISA. Forty-one patients (mean age 54.9, range 19-78 years; 24 men) were studied. Thirty patients had chronic viral hepatitis (CH) without (N = 18) or with (N = 12) cirrhosis (CIR), and 11 patients had HCC. Anti-H. pylori IgG was detected in 54%. The expected 422- and 210-bp fragments of Helicobacter 16S rRNA were amplified from 27% of liver samples, including 17% of CH-CIR and 55% of HCC (P = 0.004). The vacA sequence was amplified in 10 of 41(24%) samples (27% of those with HCC). These data confirm the presence of H. pylori DNA sequences in human liver and suggest an association of Helicobacter spp. with HCV-related chronic liver diseases. Further studies are needed to ascertain whether Helicobacter spp. infection plays a role in the development of HCC.
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PMID:Helicobacter infection in patients with HCV-related chronic hepatitis, cirrhosis, and hepatocellular carcinoma. 1214 29

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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