Abstract

The few published studies on the relationship between Helicobacter pylori infection and metabolic homeostasis were relatively small and yielded inconsistent results. We examined the prevalence of metabolic syndrome in relation to H. pylori infection and its symptoms in a large and unselected population. Coded data from the computerised database of a large health maintenance organisation in Israel were accessed for 147,936 individuals 25–95 years of age who performed the urea breath test during 2002–2012. The classification of metabolic syndrome followed a modified definition of the international diabetes federation. Prevalences of H. pylori infection and metabolic syndrome were 52.0% and 11.4% respectively. H. pylori infected patients had increased likelihood of metabolic syndrome: adjusted odds ratio (aOR) 1.15 (95% confidence intervals (CI) 1.10–1.19), as did patients with gastric ulcer: aOR 1.15 (95% CI 1.03–1.28) vs patients without these conditions. Duodenal ulcer was associated with metabolic syndrome only in persons aged 25–34 years: aOR 1.59 (95% CI 1.19-2.13), but not in older persons (P = 0.001 for heterogeneity). In conclusion, the likelihood of metabolic syndrome appeared significantly increased in relation to H. pylori infection and gastric and duodenal ulcers. These findings suggest that H. pylori long-term gastric inflammation might play a role in metabolic homeostasis.

Highlights

  • Metabolic syndrome is a cluster of metabolic factors that increase the risk for atherosclerotic cardiovascular disease and type 2 diabetes mellitus[1]

  • If H. pylori infection and gastric inflammation are important in the development of metabolic syndrome, a stronger association is expected in symptomatic H. pylori patients

  • H. pylori tested positive by urea breath test (UBT) in 76,965 (52.0%; [95% CI 51.8–52.3]) persons

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Summary

Introduction

Metabolic syndrome is a cluster of metabolic factors that increase the risk for atherosclerotic cardiovascular disease and type 2 diabetes mellitus[1]. It has been postulated that some infectious agents might play a role in the pathogenesis of metabolic syndrome, as they can induce persistent inflammation. The pathogenesis of peptic disease and gastric cancer usually involves strong and persistent inflammatory response that does not clear the infection (reviewed in[5]). Conflicting findings exist regarding such association[12,13], its magnitude[14] and specificity[15] It is unclear whether the observed association is specific to H. pylori infection or is the result of exposure to infectious agents in general, such as Chlamydia pneumoniae, herpes simplex virus 1 and cytomegalovirus[15]. The aims of the current study were to examine the prevalence of metabolic syndrome in relation to H. pylori infection, and to peptic ulcer disease, as a proxy for gastric inflammation. If H. pylori infection and gastric inflammation are important in the development of metabolic syndrome, a stronger association is expected in symptomatic H. pylori patients

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