点击显示 收起
Department of Medical Pathology and Laboratory Medicine
School of Medicine
University of California, Davis
Davis, CA 95616
School of Public Health
Department of Epidemiology
611 Church Street, Room 315
University of Michigan
Ann Arbor, MI 48104
E-mail: mnhaan{at}umich.edu
Department of Medical Pathology and Laboratory Medicine
School of Medicine
University of California, Davis
Davis, CA
US Department of Agriculture
Agricultural Research Service
Western Human Nutrition Research Center
University of California, Davis
Davis, CA
Dear Sir:
Kountouras et al raise interesting points about the potential relations between Helicobacter pylori infection, gastric function, vitamin B-12 absorption, and risk of cognitive impairment. Our research group has not specifically investigated H. pylori infection in the Sacramento Area Latino Study on Aging (SALSA), but we did report previously on the cross-sectional association between gastric function and vitamin B-12 status in a nonrandom subsample of study subjects (1). Elevated serum gastrin (100 ng/L) is a sensitive predictor of moderate-to-severe atrophy of the gastric body (2). We observed elevated serum gastrin in 30% of the SALSA subjects, with a higher percentage (48%) of elevated values in those subjects with a deficient total plasma B-12 concentration (<148 pmol/L). Moreover, we observed a highly significant inverse association between gastrin and plasma vitamin B-12 concentrations (P < 0.0001).
The association between H. pylori infection and gastric function is complex. Initial, acute H. pylori infection results in reduced secretion of gastric acid (3). If the infection persists for several months, gastric acid secretion may normalize or increase (4). If the infection and gastritis are prolonged beyond several months, there is progression to gastric atrophy, and gastric acid secretion is again reduced. This H. pylori–induced reduction in gastric acid secretion impairs the capacity to release and absorb vitamin B-12 from animal source foods and may increase the risk of intestinal bacterial overgrowth. The bacteria may compete with the host for dietary vitamin B-12 and reduce the vitamin's bioavailability. Finally, recent evidence has been presented that links previous H. pylori infection with subsequent development of autoimmune pernicious anemia (5). The pathogenesis of such an association may involve molecular mimicry by H. pylori of gastric mucosal antigen, which allows the organism to "fly below the radar screen" of host immune surveillance with subsequent risk of autoimmune consequences in a susceptible host (6). Thus, it is reasonable to predict that H. pylori infection may contribute to low vitamin B-12 status. Data from the National Health and Nutritional Examination Survey show that Mexican Americans 70 y of age and older experience a significantly higher prevalence of infection with H. pylori than do white non-Hispanics (74.0% compared with 54.8%) (7). The SALSA study involves a representative sample of the Mexican elderly population in the Sacramento area of California who are demographically similar to national samples of the same age and ethnicity (8). It is therefore likely that the SALSA population carries a high burden of H. pylori seroprevalence. It is possible that the relatively high prevalence of low plasma vitamin B-12 (6.5%) we observed in the SALSA cohort may be associated with prevalent infection by H. pylori. Whether the influence of gastric atrophy on vitamin B-12 status is of sufficient magnitude to affect cognitive function in the SALSA cohort is open to speculation. Because we did not find an effect of low plasma vitamin B-12 on dementia and CIND outcomes, the link between H. pylori and vitamin B-12 may not directly apply to these findings. We also have not yet examined the influence of related medications on vitamin B-12 or on cognitive status.
ACKNOWLEDGMENTS
None of the authors had any conflicts of interest to report.
REFERENCES