Abstract
A key factor in many lung diseases and in lung allograft deterioration is an inflammatory response leading to fibroproliferation. What is the evidence for gastroduodenal reflux and aspiration being a driver of these processes? The potential damaging agents in aspirated refluxate are food particles, and microbes (particularly when patients are treated with proton pump inhibitors (PPI) and microbial overgrowth of the stomach occurs). In addition gastric juice contains enzymes e.g. pepsin and lipase and gastric acid which all have the potential to damage airway mucosa [1]. If duodenal reflux into the stomach has occurred then the gastric juice will contain conjugated bile acids, bilirubin, phospholipids and digestive enzymes in particular trypsin, chymotrypsin and lipases. These pancreatic enzymes could survive in the stomach retaining activity if the pH has been elevated by the alkaline refluxate coming from the duodenum, or in patients on PPI treatment. For example trypsin retains functionality when exposed to pepsin at pH 4.0 for 6 h but was denatured by incubation with pepsin at pH 2.2 for 4 h [2].
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Pearson, J.P., Aldhahrani, A., Chater, P.I., Wilcox, M.D. (2018). Pathological Processes. In: Morice, A., Dettmar, P. (eds) Reflux Aspiration and Lung Disease. Springer, Cham. https://doi.org/10.1007/978-3-319-90525-9_4
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DOI: https://doi.org/10.1007/978-3-319-90525-9_4
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