Abstract

BACKGROUND: Several studies have suggested that idiopathic pulmonary fibrosis (IPF) may be related to repeated aspiration of gastric contents over long periods of time. We aimed to investigate differences between pH measured directly in the lung, and biomarkers of acute inflammation in patients with newly diagnosed IPF and in patients with newly diagnosed GERD.

MATERIAL AND METHODS: All subjects (N=61) underwent collection of medical history, physical examination, pulmonary function testing, bronchoscopy, endoscopy, arterial blood gas analyses, and biochemical testing.

RESULTS: Previously diagnosed GERD was found in 56.7%, typical symptoms of reflux in 80%, and Helicobacter pylori in gastric biopsy specimens in 76.6% of the cases. pH in peripheral branches of bronchi in the cases was 5.32±0.44 and was 6.27±0.31 (p<0.001) in the control group. The average values of LDH, ALP, and CRP in bronchoalveolar aspirate and in serum, as well as TNF-alpha in bronchoalveolar aspirate, were significantly higher in IPF patients.

CONCLUSIONS: The more acidic environment in the bronchoalveolar aspirate of the IPF subjects could contribute to the development or progression of IPF, possibly via changes in local metabolism or by damaging local cells and tissue. However, further studies with larger numbers of patients are required to clarify the role of gastric fluid aspiration in IPF pathogenesis. Our preliminary work has identified inflammatory biomarkers LDH, ALP, and TNF-alpha as potentially important in the pathologic processes in IPF. Further research is needed to determine their importance in clinical intervention and patient care.

Keywords: idiopathic pulmonary fibrosis, Inflammatory markers, Gastroesophageal Reflux, Alkaline Phosphatase - metabolism, Biological Markers - metabolism, Blood Gas Analysis, Bronchoalveolar Lavage Fluid - chemistry, Bronchoscopy, C-Reactive Protein - metabolism, Case-Control Studies, Gastroesophageal Reflux - metabolism, Hydrogen-Ion Concentration, Idiopathic Pulmonary Fibrosis - metabolism, L-Lactate Dehydrogenase - metabolism, Tumor Necrosis Factor-alpha - metabolism