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Copyright ©ERS Journals Ltd 2007
Helicobacter pylori eradication in the management of idiopathic pulmonary fibrosis
Pulmonary Division, Dept of Medicine, Hamad General Hospital, Doha, Qatar.
To the Editors:
Idiopathic pulmonary fibrosis (IPF) is a relentlessly progressive disease of unknown aetiology. Current theory regarding the pathogenesis of IPF suggests that recurrent exposure of the lungs to repeated injury and/or antigen of "unknown origin" leads to the release of pro-fibrotic growth factors and fibrosis 1. The nature of the triggering injury and/or antigen remains a mystery. A number of studies have documented high prevalence of gastro-oesophageal reflux disease (GERD) in patients with IPF in up to 90% of patients 2, 3. This has led to the assumption that recurrent micro-aspiration of acid droplets causes, or contributes to, the recurrent insults to the lungs and the development of IPF 2. However, the prevalence of GERD in the general population (10–20%) far exceeds the prevalence of IPF (13–20 cases per 100,000 population) 4, 5. So, if the acid content of the reflux is the probable triggering/injurious agent, then what makes only a small proportion of subjects with GERD develop IPF? Recent meta-analysis and epidemiological data have shown that high prevalence of GERD is associated with low Helicobacter pylori prevalence status 6. This may raise the hypothesis that IPF only develops in those patients with GERD whose gastric juice contains H. pylori 7. Put simply, IPF may result from micro-aspiration of gastric contents due to GERD, but only in the small proportion of patients with GERD who have H. pylori in their gastric juice.
Attempting to explain the development of IPF in individuals with GERD merely in terms of the chemical composition of the gastric content (acid content) or a genetic predisposition is not rewarding, because the chemical composition of gastric juice is probably similar in all individuals with GERD and no correlation between the severity of IPF and the severity of GERD was found in previous studies 2. In addition, no specific genetic markers have been identified in patients with IPF 8. Therefore, these assumptions cannot explain the low prevalence of IPF among the general population, despite a high prevalence of GERD.
Proton pump inhibitor (PPI) therapy has been shown to stabilise lung function in some patients with IPF. Previously, this effect was attributed to the acid suppression action of PPI, but it should be noted that PPI therapy does not prevent acid reflux. More importantly, PPIs have been found to exert a bacteriostatic effect on H. pylori, interfere with the bacterial energy production and cause a decrease in antral H. pylori density during therapy 9, 10. Another important reason to justify testing the role of H. pylori hypothesis is that a noninvasive, simple, highly sensitive and specific test is available to detect the presence of H. pylori, which is the "H. pylori faecal antigen test" with sensitivity and specificity of up to 98 and 94%, respectively 11. This test may be used to detect the prevalence of H. pylori infection in patients with IPF and compare it with control groups from patients with other lung diseases and healthy individuals. If the prevalence of H. pylori in IPF patients is found to be high, the next step will be the detection of H. pylori in bronchoalveolar lavage of these patients.
I think this hypothesis is a fertile area for future research and, if it proves true, prevention and treatment of a relentlessly progressive disease will be in hand.
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- Raghu G, Freudenberger TD, Yang S, et al. High prevalence of abnormal acid gastro-oesophageal reflux in idiopathic pulmonary fibrosis. Eur Respir J 2006;27:136–142.
[Abstract/Free Full Text] - Tobin RW, Pope CE, Pellegrini CA, Emond MJ, Sillery J, Raghu G. Increased prevalence of gastroesophageal reflux in patients with idiopathic pulmonary fibrosis. Am J Resp Crit Care Med 1998;158:1804–1808.
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- Raghu G, Mageto YN. Genetic predisposition of interstitial lung diseases. In: King TE Jr, Schwartz MI, eds. Interstitial Lung Diseases. 3rd Edn. Hamilton, B.C. Decker, 1998; p. 119–132
- Suerbaum S, Leying H, Memmerle B, Klemm K, Opferkuch W. Antibacterial activity of pantoprazole, omeprazole and other H+/K+–ATPase inhibitors against Helicobacter pylori. Rev ESP Enf Digest 1990;78:P256
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- Vaira D, Malfertheiner P, Megraud F, et al. Diagnosis of Helicobacter infection with a new non-invasive antigen-based assay. HpSA European study group. Lancet 1999 354:30–33.
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