Cirrhosis negatively affects the efficiency of serologic diagnosis of Helicobacter pylori infection.

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.

Lipids of human gastric mucosa: effect of Helicobacter pylori infection and nonalcoholic cirrhosis.

BACKGROUND/AIMS: Gastric mucosa phospholipids play an important protective role against exogenous and endogenous toxic agents. Recently, we described a significant alteration of phospholipid profile in patients with chronic atrophic gastritis without Helicobacter pylori infection. The aim of the present study was to assess the phospholipid composition of gastric biopsy specimens in 41 subjects with chronic gastritis in relation to H. pylori infection (no. 26) and nonalcoholic cirrhosis (no. 18). METHODS: Phospholipids were extracted from homogenate mucosal samples using Folch's method, purified, and separated by thin-layer chromatography, while bound fatty acids were analyzed by gas liquid chromatography. RESULTS: The amounts of five gastric phospholipid classes, their rank order, and percent distribution of the principal ones (phosphatidylcholine [PC] 58%, phosphatidylethanolamine [PE] 26%, and phosphatidylinositol 11% vs. values of 49, 19, and 14, respectively, in the earlier study) were confirmed in chronic gastritis without H. pylori infection. H. pylori infection induced a dramatic reduction (about 30%) in the absolute amount of total phospholipids (24.2 micrograms/mg protein versus 35.1 of the H. pylori-negative group; P < 0.01), PC and PE being the most affected (-36% and -26%, respectively), while bound fatty acids remained unchanged. There was no difference in cirrhotic vs. noncirrhotic subjects. CONCLUSIONS: (1) The development of gastritis is characterized by an alteration of the lipid mucosal pattern that can change with the different etiologies, the most dramatic variations being observed in the presence of H. pylori infection; and (2) cirrhosis does not affect further the alteration in the phospholipid profile of the antral mucosa caused by chronic gastritis.