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State-of-the-Art Pathogenesis of GERD

State-of-the-Art Pathogenesis of GERD

20 Aug 2021 14:00 14:12
(12 mins)
Kenneth McColl Speaker
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Title – Pathogenesis of Gastroesophageal Disease

There are three main factors involved in the pathogenesis and pathophysiology of gastroesophageal (GE) disease. 1) Abnormalities in the structure and function of GE junction. The normal GE junction comprises the intrinsic sphincter, the extrinsic sphincter formed by right crus of diaphragm, and the flap valve. In addition, the phreno-esophageal ligament holds the GE junction within the diaphragmatic foramen. Degenerative changes cause weakening and stretching of the extrinsic sphincter and phreno-esophageal ligament causing proximal migration of proximal stomach forming hiatus hernia and loss of flap valve. This allows reflux and impaired clearance. 2) The second factor is central obesity and associated increase in intra-abdominal pressure and abdomino-thoracix pressure gradient. Intra-abdominal pressure ranges from 7mmHg in thin subjects to 25mmHg in those with central obesity ( Derakhshan et al Gut 2012;61:337-43 ). Increasing intra-abdominal pressure experimentally by even 5mmHg causes an eight-fold increase in reflux after meals in patients with reflux disease ( Mitchell et al. Gatroenterology 2017;152:1881-88 ). Causing similar rise in intra-abdominal pressure in patients without reflux does not increase reflux (Lee YY et al.Gut, 2014; 63: 1053-1060). . Central obesity therefore promotes reflux in subjects with dysfunction of the GE sphincter. 3) The third factor is the acidity and peptic activity of the gastric juice and this is mainly related to H.pylori gastritis. We recently studied the intragastric pH at multiple location in the stomach along with measuring the density of parietal and chief cells in healthy middle aged volunteers with and without H.pylori infection ( Mitchell et al. Gut 2017;66:1555-62 ). Those with H.pylori had substantially reduced acidity and this was most marked within the 5cm segment distal to the GE junction which is also known as the acid pocket and source of GE refluxate. The density of parietal cells was also reduced by more than 50% in the H.pylori positive volunteers. This explains the protective effect of H.pylori in aetiology of reflux. In conclusion, Abnormality the of GE junction is an essential factor in pathogenesis of reflux but the promoting effect of central obesity and protective effect of H.pylori gastritis are important co-factors

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