Since their introduction in 1988, proton pump inhibitors (PPI) have become one of the most prescribed drugs worldwide especially for the treatment of peptic ulcer and gastroesophageal reflux disease (GERD). (1) Proton pump inhibitors (PPIs) effectively suppress gastric acid production by inhibiting the function of H+/K+-ATPase in gastric parietal cells. (2)
Also, the indications for esophagogastroduodenoscopy (EGD) have significantly increased, including GERD. These patients usually tend to be chronic PPIs users. Several studies have associated PPI use with an increased risk of hip fracture, Clostridium difficile, and community-acquired pneumonia.(3-5) In addition, the literature associated sporadic gastric fundic gland polyps (FGPs) with …show more content…
(13, 14) Both types are the same histologically, but dysplasia is common in FAP-associated FGPs (30–50%) and rare in sporadic FGPs (1%). (6, 10, 15) Histological examination of FGPs shows cystic dilatations of the oxyntic glands lined by parietal and chief cells with or without foveolar cells. (16, 17) These findings are non-specific as it can occur in the absence of PPI use and also in H2 blockers users but with milder degree. …show more content…
(10, 15, 16, 21)
Some authors link FGPs development to gastric acid suppression rather than the use of PPI per se. This is supported by observations of FGPs in patients using H2 blockers, in addition, only a subset of patients develops FGPs despite being on regular PPI use. (22-24)
Hypergastrinemia secondary to acid suppression could cause hyperplasia of enterochromaffin-like and parietal cells. (25, 26) However, evidence that gastrin can act as a growth factor in the stomach is lacking. (23, 27)
Some genetic studies showed association between beta-catenin gene mutations and sporadic FGPs and FAP-associated FGPs to mutations in the adenomatous polyposis coli (APC) tumour-suppressor gene, but these mutations may not be enough to clarify the pathogenesis of
Also, the indications for esophagogastroduodenoscopy (EGD) have significantly increased, including GERD. These patients usually tend to be chronic PPIs users. Several studies have associated PPI use with an increased risk of hip fracture, Clostridium difficile, and community-acquired pneumonia.(3-5) In addition, the literature associated sporadic gastric fundic gland polyps (FGPs) with …show more content…
(13, 14) Both types are the same histologically, but dysplasia is common in FAP-associated FGPs (30–50%) and rare in sporadic FGPs (1%). (6, 10, 15) Histological examination of FGPs shows cystic dilatations of the oxyntic glands lined by parietal and chief cells with or without foveolar cells. (16, 17) These findings are non-specific as it can occur in the absence of PPI use and also in H2 blockers users but with milder degree. …show more content…
(10, 15, 16, 21)
Some authors link FGPs development to gastric acid suppression rather than the use of PPI per se. This is supported by observations of FGPs in patients using H2 blockers, in addition, only a subset of patients develops FGPs despite being on regular PPI use. (22-24)
Hypergastrinemia secondary to acid suppression could cause hyperplasia of enterochromaffin-like and parietal cells. (25, 26) However, evidence that gastrin can act as a growth factor in the stomach is lacking. (23, 27)
Some genetic studies showed association between beta-catenin gene mutations and sporadic FGPs and FAP-associated FGPs to mutations in the adenomatous polyposis coli (APC) tumour-suppressor gene, but these mutations may not be enough to clarify the pathogenesis of