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3%; 95% confidence interval: 6.7�C19.9; P?Afatinib mouse response to inhaled stimuli.[2] CAL-101 ic50 Attention has focussed on genetic[3] and environmental factors[4] that might explain this. Less attention has been paid to the possibility that other endogenous chronic inflammatory conditions may contribute to the amplification process in susceptible subjects. There is growing evidence that chronic inflammation of structures that are embryologically related to the lungs such as the intestines, liver and thyroid gland is associated with airway inflammation,[5] respiratory symptoms,[5, 6] airway dysfunction[5] and accelerated decline in lung function.[7] One of the commonest causes of chronic foregut inflammation worldwide is gastritis secondary to Helicobacter Pylori infection.[8] This infection is often acquired early in life and causes an intense cytokine-mediated infiltration of the gastric epithelium by neutrophils and Sitaxentan mononuclear cells[9] which most commonly presents clinically in the form of peptic ulceration.[8] Previous studies have shown that COPD and peptic ulcer disease coexist more commonly than expected.[10, 11] However, many of these studies are limited by the absence of objective confirmation of the diagnosis of peptic ulcer disease and COPD, limited information on the chronology of the development of these conditions and a failure to account for shared risk factors such as smoking and social class. These deficiencies make it difficult to form firm conclusions about the mechanism of the association. Here, we present an audit of the prevalence of peptic ulcer disease and COPD defined using objective criteria in a well-defined population of miners. We also present a case�Ccontrol study investigating the prevalence of H.?Pylori seropositivity in patients with varying degrees of COPD compared with an age-, smoking history- and social class-matched population with normal spirometric values.