Maternal H. Pylori Infection May Increase Leukemia Risk in Offspring

By Will Boggs, MD

NEW YORK COT 14, 2005 (Reuters Health) - Maternal infection with Helicobacter pylori may be associated with an increased risk of childhood leukemia in the offspring, according to a report in the October 1st issue of the American Journal of Epidemiology.

"Studies on possible infectious etiology of childhood leukemia are finally moving to evaluate specific micro-organisms," Dr. Matti Lehtinen from National Public Health Institute, Oulu, Finland told Reuters Health.

Dr. Lehtinen and colleagues used a cohort of 550,000 mothers and their offspring to study the role of three bacterial infections -- Mycoplasma pneumoniae, Chlamydia and H. pylori -- in childhood leukemia.  The subjects resided in Finland or Iceland.

Taken in isolation, neither M. pneumoniae nor Chlamydia was associated with an increased risk of childhood leukemia, the report indicates.

In contrast, the authors report, in the group from Iceland, maternal IgG antibody positivity to H. pylori was associated with a 2.8-fold increased total risk of childhood leukemia in the offspring. The risk was higher (3.7-fold) when the analysis was restricted to Icelandic cases diagnosed before the age of 6 years, the results indicate.

In the group from Finland, however, H. pylori IgG antibodies were not associated with an increased childhood leukemia risk, the researchers note.

"To our knowledge," the authors conclude, "we have documented for the first time the possibility of an association between maternal H. pylori infection and risk of childhood leukemia in the offspring. Independent confirmatory studies are needed."

"We have updated the registry linkages and identified more than 1100 childhood leukemia cases and their mothers," Dr. Lehtinen said. "The original (published) observation was done from a small sample size and needs to be confirmed in this larger material."

"Our studies on Epstein Barr virus and childhood leukemia are also continuing and will hopefully elaborate the etiology further," Dr. Lehtinen added.

SOURCE:

• Am J Epidemiol 2005;162:662-667.