Liver disease and Helicobacter.

The human upper gastrointestinal tract is often infected with Helicobacter pylori (H. pylori). This urea splitting bacterium is now considered to be a causal agent in some diseases, including antral gastritis and frank duodenal ulceration, in addition to an association with gastric carcinoma and mucosa associated lymphoid tissue (MALT) lymphoma[1]. Since the discovery of H. pylori, a number of additional Helicobacter species have been isolated from the stomachs and intestinal tracts of a variety of mammalian species. At least eighteen separate Helicobacter species have been recognized (Table ​(Table11)[2,3]. The discovery of these Helicobacter species, has raised the possibility of a relationship between Helicobacter infection and liver diseases[3]. Table 1 Helicobacter species and their hosts HELICOBACTER PYLORI AND PEPTIC ULCER IN CIRRHOSIS Historically, it is well recognized that duodenal ulcer disease is more common in patients with cirrhosis as compared with non-cirrhotic patients[4]. However, a number of early studies suggested that in cirrhotic patients there was no clear relationship between duodenal ulcers and H. pylori infection, suggesting the possibility of other causes[5]. Other studies suggested that H. pylori infection, as measured by IgG, H. pylori serum antibodies, was more common in cirrhotic patients than in non-cirrhotics[6]. A study showed that cirrhotic patients were more likely to have a positive H. pylori ELISA with a negative histologic examination for H. pylori as compared with noncirrhotic patients[7]. Whether H. pylori is a risk factor for peptic ulcer in cirrhosis remains controversial. In a cross-sectional study by Wang et al[3,8], 49 cirrhotic patients underwent upper gastrointestinal endoscopy and 75 controls (healthy examinees) without liver disease were also examined by endoscopy. Thirty (61%) of the 49 cirrhotic patients had peptic ulcers as compared with 24 (32%) of the 75 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 wit h gastric (75%) and duodenal ulcers (95%) than nonulcerous control patients (59%), the difference between patients with and without peptic ulcer (40% vs 37%) was not significant in cirrhotic patients. H. pylori was identified in 40% of the cirrhotic patients with duodenal ulcers as against 95% of controls with duodenal ulcer (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 nonulcerous patients between the cirrhotic and control groups (37% vs 59%). No evidence was found to substantiate an etiologic role of H. pylori in the development of duodenal ulcer in cirrhotic patients[8]. In 153 consecutive patients with cirrhosis, Siringo et al[9] assessed the prevalence of IgG to Helicobacter pylori and compared it with that in 1010 blood donor-residents in the same area and the relationship of IgG to H. pylori with clinical and endoscopic features and with the risk of peptic ulcer. The prevalence of IgG to H. pylori of cirrhosis was significantly higher than in blood donors (76.5% vs 41.8%; P < 0.0005) and was not associated with sex, cirrhosis etiology, Child class, gammaglobulins and hypertensive gastropathy. In both groups, the prevalence of IgG to H. pylori was significantly higher in subjects aged over 40. Multivariate analysis identified high age and males as risk factors for a positive H. pylori serology and no independent risk factors for peptic ulcer. The high prevalence of H. pylori positive serology found in this series was related to age and sex and might also be explained by previous hospital admissions and/or upper gastrointestinal endoscopy. Their results did not confirm the role of H. pylori as a risk factor for peptic ulcer in patients with liver cirrhosis. H. pylori infection is the major pathogenic factor for peptic ulcer disease. Its epidemiology is not fully known; few data are available in patients with chronic liver disease. To investigate the seroprevalence and factors associated with H. pylori infection, a series of studies or liver cirrhosis patients is necessary. Two hundred and twenty consecutive patients were prospectively included in a study aimed to evaluate the effect of dietary intervention on cirrhosis complications and survival. An epidemiological and clinical questionnaire was completed. Sera were obtained and stored at -70 °C until analyzed. They were tested for H. pylori antibodies using a commercial ELISA kit. Eleven of 220 patients had borderline anti-H. pylori-IgG titers. Of the remaining 209 patients, 105 (50.2%) showed positive titers of H. pylori-IgG. Univariate analysis showed that H. pylori infection was more frequent in older patients, those born outside Catalonia, and in patients with a low educational level. Past ethanol consumption and current smoking were correlated negatively with H. pylori infection. Selected age (OR = 3.1, 95%CI: 1.46-6.45), educational level (OR = 2.2, 95%CI: 1.18-4.2) and alcohol consumption (OR = 0.7, 95%CI: 0.45-0.99) as the variables were independently related to H. pylori infection in multivariate analysis. Their conclusions of H. pylori infection in cirrhosis has the same epidemiological pattern as in the general population. Suggestions that the etiology or the severity of the liver disease could be related to H. pylori infection were not confirmed by their study[10].