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. 1988;20(1):63-8.
doi: 10.3109/00365548809117218.

Antibody response to Campylobacter pylori in an ethnic group lacking peptic ulceration

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Antibody response to Campylobacter pylori in an ethnic group lacking peptic ulceration

B Dwyer et al. Scand J Infect Dis. 1988.

Abstract

The association between duodenal ulcer, gastritis and gastroduodenal colonization with Campylobacter pylori suggests a causal role for this newly described bacterium. In an attempt to challenge the verity of this association we studied a group of people in whom duodenal ulcer is apparently absent. Serological evidence of infection was sought with a sensitive, specific ELISA assay for C. pylori specific IgG and was compared with results from control sera from teenagers referred for respiratory viral serology, volunteer blood bank donors, patients with duodenal ulcers and patients in whom the presence or absence of C. pylori had been determined by histological and microbiological examination of gastric tissue. A relatively isolated group of Australian Aborigines in whom peptic ulceration is virtually unknown, was observed to possess age-specific mean C. pylori antibody levels comparable those found in a group of white Australian dyspeptic patients without microbiological evidence of infection with this organism. The antibody levels of Aborigines were lower than those found in an aged-matched group of 'healthy' white Australians, both of these groups having levels which were significantly lower than the levels found in culture positive white Australian dyspeptic patients. It was found that 21/144 'healthy' white Australians (14.6%) had antibody levels greater than or equal to the lower 99% confidence interval of the mean level found in culture positive patients, while only 2/274 Aborigines (0.7%) had such elevated levels. By contrast, 89/142 (62.7%) patients with endoscopically proven duodenal ulcer had similarly elevated specific antibody levels. These differences were highly significant. We consider these findings to be consistent with the hypothesis that C. pylori is important in the pathogenesis of duodenal ulcer.

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