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AbstractBackground and objectiveWe have suggested that chronic inflammation of other foregut derivatives might be associated with airway inflammation and amplification of the response to inhaled stimuli such as cigarette smoke leading to chronic obstructive pulmonary disease (COPD). One of the commonest causes of chronic foregut inflammation is gastritis secondary to Helicobacter Pylori infection. We tested the hypothesis that peptic ulceration and H. Pylori seropositivity are associated with COPD independently of other shared risk factors.MethodsWe reviewed primary care medical records and performed full lung function tests on 329 miners seen over 2 years as part of a compensation scheme. We also performed H. Pylori serology in patients with varying degrees of severity of COPD compared with a matched control population.ResultsThe prevalence of peptic ulcer disease in the groups classed as normal, chronic bronchitis, mild, moderate and severe COPD was 3.2%, 16.2%, 21.4%, 42.4% and 56.2%, respectively. There was a strong and independent relationship between the presence of peptic ulcer disease and percent of predicted forced expiratory volume in 1 s (−13.3%; 95% confidence interval: 6.7–19.9; P < 0.001) and forced expiratory volume in 1 s/forced vital capacity ratio (−5.06%; 95% confidence interval: 1.8–8.2; P < 0.001). Positive H. pylori serology was present in 54.7% of 58 patients with COPD and 23.5% of 17 controls (P = 0.026).ConclusionsOur findings suggest a relationship between peptic ulcer disease and COPD that is more that just a shared susceptibility to different environmental stimuli.

More information Original publication

DOI

10.1111/resp.12075

Type

Journal article

Publisher

Wiley

Publication Date

2013-05-01T00:00:00+00:00

Volume

18

Pages

728 - 731

Total pages

3