Effect of Helicobacter pylori eradication on gastric mucosal phospholipid content and its fatty acid composition.

BACKGROUND AND AIMS: Whether Helicobacter pylori eradication alters gastric mucosal phospholipid contents and their fatty acid composition remains unclear. The aim of the present study was to clarify the effect of H. pylori eradication on gastric mucosal phosphatidylcholine (PC) content and its fatty acid composition. METHODS: Endoscopic biopsy specimens were taken from the antrum and body of each of 19 asymtomatic male volunteers for detection of H. pylori, histopathological assessment of gastritis, phospholipid determination and fatty acid analysis. All the subjects with H. pylori infection were treated with eradication therapy. Endoscopy and tissue sampling were repeated again 1 and 6 months after all treatment. RESULTS: In eight subjects, H. pylori infection was evident and was successfully eradicated. Pretreatment degrees of lymphocytes and plasma cells (inflammation) and polymorphonuclear neutrophils (activity) were greater in H. pylori-positive subjects compared with H. pylori-negative subjects (P<0.001), whereas the degree of inflammation decreased (P<0.001), and neutrophils had completely disappeared at 6 months after eradication. Moreover, the gastric mucosal PC contents at the antrum and body were unchanged within 1 month after cessation of treatment, but increased at 6 months after eradication (P<0.05). At 6 months after cessation of treatment, H. pylori-eradicated subjects had an increase (+30% at antrum, +18% at body) in linoleic acid composition and a decrease (-37%, -43%) in arachidonic acid composition of PC at the antrum and body, respectively. CONCLUSIONS: These findings suggest that H. pylori eradication reduces the production of various eicosanoids, resulting in the normalization of gastric mucosal PC content and its fatty acid composition, which may consequently cause the gastric mucosal hydrophobicity to be normalized.

Etiology and prognosis of cryptogenic liver cirrhosis: possible contribution of hepatitis B virus.

Three female patients without type B or type C viral hepatitis, alcoholic, metabolic or autoimmune liver disease, were selected from 250 cases with histologically proven liver cirrhosis (M:F = 183:67). All three cases showed at least one positive aspect among three parameters of serum anti-HBc (RPHA, x1), HBV-DNA (gene S, nested PCR) and liver HBs and/or pre-S2 antigen (immunoperoxidase methods). Two cases may suggest a spontaneous disappearance of HBV from sera. Another case may suggest a contribution of mutant HBV which can not be detected by the routine tests. These HBV-related cirrhotic patients have done well clinically and have not been associated with hepatocellular carcinoma during the period from 6 to 12 years of follow-up when compared with 59.6% and 65.4% prevalence of hepatocarcinogenesis in type B and type C hepatitis-associated cirrhosis during the observation period of six and seven years on average, respectively.