Helicobacter pylori infection and typhoid fever in Jakarta, Indonesia
We evaluated the association between typhoid fever and Helicobacter pylori infection, as the latter microorganism may influence gastric acid secretion and consequently increase susceptibility to Salmonella typhi infection. Anti-H. pylori IgG and IgA antibody titres (ELISA) and gastrin concentration...
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Published in: | Epidemiology and infection Vol. 134; no. 1; pp. 163 - 170 |
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Main Authors: | , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Cambridge, UK
Cambridge University Press
01-02-2006
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Subjects: | |
Online Access: | Get full text |
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Summary: | We evaluated the association between typhoid fever and Helicobacter pylori infection, as the latter microorganism may influence gastric acid secretion and consequently increase susceptibility to Salmonella typhi infection. Anti-H. pylori IgG and IgA antibody titres (ELISA) and gastrin concentration (RIA) were determined in the plasma of 87 blood culture-confirmed typhoid fever cases (collected after clinical recovery) and 232 random healthy controls without a history of typhoid fever, in the Jatinegara district, Jakarta. Patients with typhoid fever more often than controls were seropositive for H. pylori IgG (67% vs. 50%, P<0·008), when antibody titres were dichotomized around median titres observed in controls. H. pylori IgA seropositivity was not associated with typhoid fever. Plasma gastrin concentrations indicative of hypochlorhydria (i.e. gastrin ⩾25 or ⩾100 ng/l) were not significantly elevated in typhoid fever cases compared to controls (P=0·54 and P=0·27 respectively). In a multivariate analysis, typhoid fever was independently associated with young age (<33 years, median age of the controls) [odds ratio (OR) 7·93, 95% confidence interval (CI) 3·90–16·10], and H. pylori IgG seropositivity (OR 1·93, 95% CI 1·10–3·40). Typhoid fever was independently associated with H. pylori IgG seropositivity, but not with elevated gastrin concentration. Therefore, the association suggests a common risk of environmental exposure to both bacteria, e.g. poor hygiene, rather than a causal relationship via reduced gastric acid production. |
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Bibliography: | ArticleID:00487 PII:S0950268805004875 istex:40725897F79DFB9BCB1C05422648843DFE16C960 ark:/67375/6GQ-5TJCS27X-X ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0950-2688 1469-4409 |
DOI: | 10.1017/S0950268805004875 |