Gastric cancer and Helicobacter pylori: a combined analysis of 12 case control studies nested within prospective cohorts

BACKGROUND: The magnitude of the association between Helicobacter pylori and incidence of gastric cancer is unclear. H pylori infection and the circulating antibody response can be lost with development of cancer; thus retrospective studies are subject to bias resulting from classifi- cation of cases as H pylori negative when they were infected in the past. AIMS: To combine data from all case control studies nested within prospective cohorts to assess more reliably the relative risk of gastric cancer associated with H pylori infection.To investigate variation in relative risk by age, sex, cancer type and subsite, and interval between blood sampling and cancer diagnosis. METHODS: Studies were eligible if blood samples for H pylori serology were collected before diagnosis of gastric cancer in cases. Identified published studies and two unpublished studies were included. Individual subject data were obtained for each. Matched odds ratios (ORs) and 95% confidence intervals (95% CI) were calculated for the association between H pylori and gastric cancer. RESULTS: Twelve studies with 1228 gastric cancer cases were considered. The association with H pylori was restricted to noncardia cancers (OR 3.0; 95% CI 2.3–3.8) and was stronger when blood samples for H pylori serology were collected 10+ years before cancer diagnosis (5.9; 3.4–10.3). H pylori infection was not associated with an altered overall risk of cardia cancer (1.0; 0.7–1.4). CONCLUSIONS: These results suggest that 5.9 is the best estimate of the relative risk of non-cardia cancer associated with H pylori infection and that H pylori does not increase the risk of cardia cancer. They also support the idea that when H pylori status is assessed close to cancer diagnosis, the magnitude of the non-cardia association may be underestimated

IgA antibodies in persisting Helicobacter pylori infection in Finnish adults

ABSTRACTMost individuals infected with Helicobacter pylori have elevated levels of specific IgG antibodies, but only in about two-thirds of cases does the IgA titre exceed the cut-off level. The aim of this study was to determine whether H. pylori-infected subjects with elevated IgG levels would subsequently produce IgA antibodies, and whether elevated IgA levels increased during infection. Paired sera were available from 336 adults who took part in a large population-based health survey in 1977–1980 and a follow-up study on asthma and atopic diseases in 1997–1998 (series A). Data on paired sera from 224 adults who participated in a population-based health survey in Vammala, Finland in 1973 and who gave a follow-up blood sample in 1994 (series B) were also re-analysed. H. pylori IgG and IgA levels were determined with commercially available (series A) and in-house (series B) enzyme immunoassays. Twenty-one (35%) of the 60 subjects who initially had elevated levels of IgG antibodies only were found to be IgA-positive at follow-up. In those subjects whose baseline and follow-up samples were IgG- and IgA-positive, the median IgA levels increased by 48% and 22% in series A and B (p < 0.0001 and p 0.0241), respectively, whereas the median IgG levels did not change significantly in either series. During H. pylori infection, an increase in specific IgA was reflected by the increase in the number of responders and by the rise in titres

Bactericidal effect of bovine normal and immune serum, colostrum and milk against Helicobacter pylori

vokET

Helicobacter felis infection in mouse alters the amount of peripheral blood phagocytic leukocytes

vEK

Specific immune colostrum in the treatment of Helicobacter felis induced gastritis in mouse

vokET

Immune colostrum in the prevention of Helicobacter felis infection in mouse

vokET