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Background and study aims White opaque substance (WOS) in gastric epithelial neoplasia is helpful for qualitative diagnosis of neoplasia. We hypothesized that WOS of neoplasia is strongly influenced by acid recovery after Helicobacter pylori eradication, similar to that of gastric intestinal metaplasia. The aim of this study was to investigate whether antacids increase the appearance of the WOS in H. pylori -eradicated neoplasia. Patients and methods A total of 38 gastric epithelial neoplasias (12 adenomas and 26 adenocarcinomas) detected after H. pylori eradication were retrospectively evaluated. Presence or absence of WOS was evaluated by magnifying endoscopy with narrow band imaging before and after antacid administration. The pH of collected gastric juice was also measured. Study endpoints were (1) prevalence of WOS in the neoplasia before and after antacid administration, and the histological difference (adenoma and adenocarcinoma); and (2) relationship between the prevalence of WOS and gastric juice pH. Results WOS prevalence increased from 0â% (0/38) to 44.8% (17/38) after antacid administration. WOS prevalence in adenomas was more significantly increased compared to that in adenocarcinomas (83.3â% vs 26.9â%, P â=â0.0077). Prevalence of WOS in gastric neoplasias was only observed at neutral levels of gastric juice pH, and WOS was not observed at strong acidic levels. Conclusions Antacid administration may increase the appearance of WOS in gastric epithelial neoplasia (especially adenomas) detected after H. pylori eradication with acid recovery.
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BACKGROUND AND STUDY AIMS: The presence of white opaque substance (WOS) is an endoscopic marker of intestinal metaplasia. Considering that the nature of WOS is absorbed lipid droplets, lipase plays an important role in the lipid absorption process and is inactivated at strong acidity. WOS may only be present in a hypochlorhydria state following Helicobacter pylori infection, and, thus, may not be highly sensitive marker, especially in H. pylori- eradicated patients. We investigated the relationship between WOS and gastric acid conditions. PATIENTS AND METHODS: A total of 501 patients were retrospectively evaluated for the presence of WOS at 2 regions of interest using magnifying narrow-band imaging. The pH level of collected gastric juice was also measured. Study end points were (1) prevalence of WOS and its relationship with gastric juice pH in 3 groups: H. pylori- uninfected , H. pylori- infected, and H. pylori -eradicated; (2) the relationship between prevalence of WOS and gastric juice pH before and after proton pump inhibitor (PPI) administration in 29 H. pylori -eradicated cases. RESULTS: Prevalence of WOS was 0â% (0â/206), 28.4â% (31/109), and 3.2â% (6/186) in the H. pylori -uninfected, H. pylori -infected, and H. pylori -eradicated groups, respectively. Mean gastric juice pH was significantly higher in WOS-positive cases than in WOS-negative cases in the H. pylori -infected and H. pylori -eradicated groups ( P â<â0.0001). Mean gastric juice pH increased from 1.1 to 6.9 after PPI administration and WOS prevalence increased from 0â% (0/29) to 45â% (13/29) of cases. CONCLUSION: The prevalence of WOS is closely associated with the neutralization of intragastric pH.
RESUMEN
Gastric fundic gland polyps (FGPs) are common non-adenomatous gastric polyps arising from normal fundic mucosa without Helicobacter pylori (H. pylori) infection. Although systemic FGPs associated with familial adenomatous polyposis (FAP) often have dysplasia, there are few reports of dysplasia occurring in sporadic FGPs, especially when detected by magnifying endoscopy with narrow band imaging (ME-NBI). We experienced two cases of adenocarcinoma occurring in sporadic FGPs, and their ME-NBI findings were very useful for differentiating FGP with cancer from non-dysplastic FGP. A 68-year-old man and a 63-year-old woman were referred to our institution for medical checkup. H. pylori was negative in both patients. Endoscopic examination revealed a small reddish polypoid lesion on the anterior wall of the upper gastric body and several FGPs. ME-NBI showed an irregular microvascular architecture composed of closed loop- or open loop-type vascular components, plus an irregular microsurface structure composed of oval-type surface components which was different from that of FGPs. FAP was denied because of the absence of colon polyps and no familial history of FAP. Pathological diagnosis was adenocarcinoma occurring in sporadic FGP.