Background/AimsObesity is reported to be associated with erosive esophagitis (EE). However, the temporal association of obesity and abdominal obesity with EE is unclear. We conducted this study to investigate the temporal association of obesity, especially abdominal obesity with EE.MethodsAmong 1,182 subjects who underwent health screening examinations including upper endoscopy in both 2003 and 2006, a total 1,029 subjects with a normal esophagogastric junction on upper endoscopy in 2003 were enrolled. All subjects completed questionnaires and anthropometric measurements were obtained twice by trained personnels. The patients with newly developed EE were compared to the subjects without newly developed EE.ResultsAmong 1,029 subjects, 42 (4.1%) were newly diagnosed with EE and 82 (8.0%) with hiatal hernia. The mean body mass index (BMI) in both examinations was significantly different between the two groups based on the development of erosive esophagitis (p<0.05 in both examinations). The mean waist circumference (WC) in both examinations was also significantly different between the two groups (p<0.01 in both examinations). The multivariate analysis demonstrated that EE was not associated with the BMI in 2003 and the increase of BMI; however, it was associated with the WC in 2003 (Odds ratio, 7.21; 95% CI, 1.78 to 29.19; >90 cm vs <80 cm).ConclusionsOur study showed that abdominal circumference is an independent risk factor for EE, demonstrating a temporal relationship between abdominal obesity and EE.
To investigate the pancreatic exocrine function in noninsulin-dependent diabetes mellitus (type 2 DM), we evaluated the pure pancreatic juice obtained by endoscopic cannulation of the main pancreatic duct in 13 healthy control subjects and 22 patients with type 2 DM who had no evidence of pancreatic disease. Samples of pancreatic juices were collected in six fractions for 30 minutes at 5-minute intervals after an intravenous bolus injection of secretin (0.25 CU/kg) and cholecystokinin-8 (CCK) (40 ng/kg). The responses of plasma glucose, insulin, and C-peptide to intravenous administration of glucose (50%, 40 mL) were measured. The levels of plasma insulin and C-peptide levels in type 2 DM were the same as in healthy controls in the basal state but did not further increase in response to an intravenous glucose. This suggested that patients with type 2 DM had insulin secretion defect rather than insulin deficiency. Pancreatic secretions including volume, bicarbonate, and protein output in response to stimulation with secretin, and CCK were significantly reduced when compared to the healthy controls. We conclude that patients with type 2 DM exhibit impairment of pancreatic exocrine secretion and that this impairment might not be related to insulin deficiency. Therefore, we recommended that careful evaluation for exocrine pancreatic function in type 2 diabetics who have any clinically suspicious symptoms of pancreatic insufficiency.
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