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Lookup NU author(s): Professor Jeffrey Pearson,
Dr Shruti Parikh
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Gastric juice contains many damaging agents against which the stomach has effective defences including a mucus bilayer which generates an unstirred layer which supports surface neutralisation of acid and forms a diffusion barrier to pepsin. However, once gastric contents leave the stomach and enter the oesophagus and the upper airways the protective mechanisms are much reduced. The major aggressors in gastric refluxate are acid, pepsin and bacteria. In addition, gastric refluxate will contain, but not always, duodenal factors such as bile acids and pancreatic enzymes. Acid in the majority of reflux events will remain at a damaging level, i.e. below pH 4.0 for a significant amount of time in the oesophagus. Bile acids have been demonstrated to be damaging in many experimental models; however, great care needs to be taken when interpreting these results because the concentrations and the form of the bile acids used do not always reflect the in vivo situation. Pepsin is an acidic protease but has the potential to damage extra-gastric tissues at pHs up to 6.0 and will not be irreversibly inhibited until pH 7.5 or above. Trypsin, if it passes through the stomach at pH 4.0 or above or rapidly though low pH of 2 or less, will retain activity and can go on to cause damage. With the increase in the use of proton pump inhibitors to treat gastro-oesophageal reflux the elevation of gastric pH has allowed bacterial over-growth of the stomach. Consequently, a reflux event can lead to the establishing of bacterial colonies outside of the stomach, notably into the airways and lungs.
Author(s): Pearson JP, Parikh S
Publication type: Conference Proceedings (inc. Abstract)
Publication status: Published
Conference Name: Alimentary Pharmacology and Therapeutics: 9th International Symposium on Human Pepsin (ISHP)
Year of Conference: 2011
Publisher: Wiley-Blackwell Publishing Ltd.
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