ABSTRACT
PURPOSE: We aimed to evaluate the difference in fluorodeoxyglucose (FDG) uptake in sedated healthy subjects after they underwent esophagogastroduodenoscopy (EGD) and colonoscopy procedures. METHODS: The endoscopy group (n = 29) included healthy subjects who underwent screening via F-18 FDG positron emission tomography/computed tomography (PET/CT) after an EGD and/or colonoscopy under sedation on the same day. The control group (n = 35) included healthy subjects who underwent screening via PET/CT only. FDG uptake in the tongue, uvula, epiglottis, vocal cords, esophagus, stomach, duodenum, liver, cecum, colon, anus, and muscle were compared between the two groups. RESULTS: Maximum standardized uptake value (SUVmax) in the tongue, pharynx, larynx, and esophagus did not significantly differ between the endoscopy and control groups. In contrast, mean SUVmax in the whole stomach was 18 % higher in the endoscopy group than in the control group (SUVmax: 2.96 vs. 2.51, P = 0.010). In the lower gastrointestinal track, SUVmax from the cecum to the rectum was not significantly different between the two groups, whereas SUVmax in the anus was 20 % higher in the endoscopy group than in the control group (SUVmax: 4.21 vs. 3.50, P = 0.002). SUVmax in the liver and muscle was not significantly different between the two groups. Mean volume of the stomach and mean cross section of the colon was significantly higher in the endoscopy group than in the control group (stomach: 313.28 cm3 vs. 209.93 cm3, P < 0.001, colon: 8.82 cm2 vs. 5.98 cm2, P = 0.001). CONCLUSIONS: EGD and colonoscopy under sedation does not lead to significant differences in SUVmax in most parts of the body. Only gastric FDG uptake in the EGD subjects and anal FDG uptake in the colonoscopy subjects was higher than uptake in those regions in the control subjects.
ABSTRACT
AIM: To investigate the effect of Helicobacter pylori (H. pylori) status test and H. pylori eradication on the occurrence of metachronous gastric cancer (MGC) after endoscopic submucosal dissection (ESD) of early gastric cancer (EGC) and risk factors of MGC. METHODS: The authors retrospectively reviewed the medical records of 433 patients (441 lesions) who underwent ESD for EGC from January 2005 to January 2015 in Yeungnam University Hospital. Patients were categorized into two groups; the H. pylori tested group (n = 257) and the H. pylori non-tested group (n = 176) based on performance of H. pylori status test after ESD of EGC. The H. pylori tested group was further categorized into three subgroups based on H. pylori status; the H. pylori-eradicated subgroup (n = 120), the H. pylori-persistent subgroup (n = 42), and the H. pylori-negative subgroup (n = 95). Incidences of MGC and risk factors of MGC were identified. RESULTS: Median follow-up duration after ESD was 30.00 mo (range, 6-107 mo). Total 15 patients developed MGC during follow-up. MGC developed in 11 patients of the H. pylori tested group (7 in the H. pylori-negative subgroup, 3 in the H. pylori-eradicated subgroup, and 1 in the H. pylori-persistent subgroup) and 4 patients of the H. pylori non-tested group (P > 0.05). The risk factors of MGC were endoscopic mucosal atrophy in the H. pylori tested group and intestinal metaplasia in all patients. CONCLUSION: H. pylori eradication and H. pylori status test seems to have no preventive effect on the development of MGC after ESD for EGC. The risk factors of MGC development were endoscopic mucosal atrophy in the H. pylori tested group alone and intestinal metaplasia in all patients.
