Helicobacter pylori and dyspepsia: a population-based study of the organism and host.

Abstract

The role of Helicobacter pylori (HP) infection in dyspepsia in the absence of peptic ulcer remains controversial. Specific attributes of the organism or the host response may be important. We aimed to determine whether HP infection overall, CagA status, serum gastrin, or serum pepsinogen levels are associated with dyspepsia in the community. A self-report bowel disease questionnaire was mailed to a random sample of Olmsted County, Minnesota residents, aged 20-50 yr. All respondents who reported symptoms of dyspepsia or irritable bowel syndrome (cases) and all respondents without significant GI symptoms (controls) were invited to participate (n = 260). They were each assessed by a physician and their medical records reviewed. Serum was obtained to measure HP and CagA antibodies, pepsinogen I and II levels, and basal serum gastrin using validated assays. Of the 148 (57%) subjects who agreed to participate, 36 had dyspepsia (17 had ulcer-like dyspepsia), 35 had irritable bowel syndrome (IBS) without dyspepsia, and 77 were asymptomatic. The proportion who were seropositive for HP were 17% in dyspepsia (24% in ulcer-like dyspepsia), 20% in IBS, and 12% in asymptomatic controls. HP was not associated with dyspepsia, ulcer-like dyspepsia, or IBS after adjusting for age. Pepsinogen levels and serum gastrin were not associated with any of the conditions studied. However, CagA antibody positivity was associated with IBS (p < 0.05), and a borderline statistically significant association with dyspepsia was detected (p = 0.08). In this community, HP infection overall does not seem to explain dyspepsia, although the role of CagA-positive HP strains deserve further study.