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Background: Epidemiological studies have confirmed that gastroesophageal symptoms are highly prevalent. However, studies linking epidemiology with clinical or chart data are scarce. We aimed to determine the frequency of endoscopy and endoscopic findings, as well as predictors of health-care utilization, among people with reflux symptoms in the community., Methods: A previous survey of 2,118 Olmsted County, MN, residents in 1993 identified 242 subjects with frequent reflux symptoms (at least weekly) who received care at a medical center in the county. Data were abstracted from Mayo Clinic records between 1988 and 1998., Results: Overall, 130 of the 242 (54%, 95% CI 47-60%) had sought care for reflux. Twenty-five patients (10%) had visited a gastroenterologist; 47 (19%) had an upper endoscopy (EGD), 64 (26%) had an upper GI X-ray, and one had an ambulatory 24-h esophageal pH study. Long segment Barrett's esophagus was detected in 4 (9%) of those having an EGD and adenocarcinoma was found in one patient with Barrett's. Three patients had surgery for gastroesophageal reflux disease. Thirteen patients (5%) died, but no deaths were due to esophageal reflux or adenocarcinoma. Age, higher education, frequent heartburn, and dysphagia were all significant, independent predictors of consulting., Conclusions: Although many people in the community have frequent reflux symptoms, few have investigations, and deaths were unrelated to reflux disease or its complications. Data from referral clinic or endoscopy series should not be extrapolated to the large numbers of people in the community with symptoms of reflux.

Specialized intestinal epithelium occurs more frequently at the gastroesophageal junction than previously anticipated. It can occur either within tongues of mucosa (short segment Barrett's) or just beneath a normal z-line (intestinal metaplasia at the gastroesophageal junction). Whether the etiopathogenesis and the natural history of these two conditions are the same is as yet unclear. The role of gastroesophageal reflux disease (GERD), Helicobacter pylori, and inflammation at the gastroesophageal junction in the pathogenesis of short segment Barrett's and intestinal metaplasia at the gastroesophageal junction needs to be carefully documented. Intestinal metaplasia at the gastroesophageal junction, short segment Barrett's, and Barrett's may represent a continuum of the same disease process. Recent evidence suggests, however, that short segment Barrett's shares similar characteristics with Barrett's but may be distinct from intestinal metaplasia at the gastroesophageal junction. It is conceivable that short segment Barrett's may remain steady or even regress if and when the noxious influence wanes but, with continuing stimulation, short segment Barrett's may lengthen further to become what we observe to be Barrett's. If correct, endogenous or exogenous factors that induce progression need to be identified. Acid and bile reflux and H. pylori are possible candidates acting either singly or synergistically. Finally, the true neoplastic potential of short segment Barrett's needs clarification.

Objective: Anecdotally, functional bowel disorders (FBD) such as the irritable bowel syndrome appears to cluster in some families, but no studies have investigated the heritability of FBD. We aimed to investigate the influence of heritable factors in FBD., Methods: Same sex twin pairs enrolled in the Australian Twin Registry completed a structured interview that included questions related to symptoms consistent with FBD: abdominal pain, diarrhea, constipation, excessive gas or bloating, and nausea. Reasons for the occurrence of each symptom, including their physicians' diagnoses, were recorded. Lisrel 7.16 software was used to fit genetic models following standard procedures., Results: Of the 686 individual twins from same-sex pairs, 33 (4.8%) had one or more symptoms diagnosed by a medical practitioner as functional bowel disorder. Complete data on this symptom scale was available for 186 monozygotic and 157 same sex dizygotic twin pairs. A model in which 56.9% (95% CI: 40.6-75.9%) of the variance was attributed to additive genetic variance, with the remaining 43.1% attributed to the individual's unique environment, closely fitted the data (chi2=0.01, df=4, p=1.0)., Conclusion: Our results suggest that a substantial proportion of the liability for FBD may be under genetic control. Whether this liability is related to the disorder itself or to other potential predisposing factors requires clarification.