User:Alisha, Deepa, Pamiz/Sandbox 1: Difference between revisions

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Resistance to treatment with PPIs, including Esomeprazole, has been speculated among Barrett’s Esophagus (BE) patients who did not indicate any symptomatic improvement after being placed on a standard PPI drug dose [20]. No contributory mutations causing PPI resistance have been found [20]. It is speculated that the high acid exposure in BE patients may be due to “reflux diathesis” rather than resistance to gastric acid secretion [21]. Other possible reasons for PPI failure include Helicobacter pylori infection, rapid metabolism, and bioavailability; reasons of clinical significance include delayed gastric emptying and visceral hypersensitivity [20]. More studies need to be conducted to understand the mechanisms underlying the development of resistance to PPIs [20].

Revision as of 00:16, 7 December 2013 view source Deepa Patel (talk \| contribs) 230 edits →‎Drug-Molecule Interaction ← Older edit		Latest revision as of 00:19, 7 December 2013 view source Deepa Patel (talk \| contribs) 230 edits No edit summary
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	Resistance to treatment with PPIs, including Esomeprazole, has been speculated among Barrett’s Esophagus (BE) patients who did not indicate any symptomatic improvement after being placed on a standard PPI drug dose [20]. No contributory mutations causing PPI resistance have been found [20]. It is speculated that the high acid exposure in BE patients may be due to “reflux diathesis” rather than resistance to gastric acid secretion [21]. Other possible reasons for PPI failure include Helicobacter pylori infection, rapid metabolism, and bioavailability; reasons of clinical significance include delayed gastric emptying and visceral hypersensitivity [20]. More studies need to be conducted to understand the mechanisms underlying the development of resistance to PPIs [20].		Resistance to treatment with PPIs, including Esomeprazole, has been speculated among Barrett’s Esophagus (BE) patients who did not indicate any symptomatic improvement after being placed on a standard PPI drug dose [20]. No contributory mutations causing PPI resistance have been found [20]. It is speculated that the high acid exposure in BE patients may be due to “reflux diathesis” rather than resistance to gastric acid secretion [21]. Other possible reasons for PPI failure include Helicobacter pylori infection, rapid metabolism, and bioavailability; reasons of clinical significance include delayed gastric emptying and visceral hypersensitivity [20]. More studies need to be conducted to understand the mechanisms underlying the development of resistance to PPIs [20].