Clinical epidemiology and natural history of gastroesophageal reflux disease

Citation
A. Sonnenberg et Hb. El-serag, Clinical epidemiology and natural history of gastroesophageal reflux disease, YALE J BIOL, 72(2-3), 1999, pp. 81-92
Citations number
46
Categorie Soggetti
Medical Research General Topics
Journal title
YALE JOURNAL OF BIOLOGY AND MEDICINE
ISSN journal
00440086 → ACNP
Volume
72
Issue
2-3
Year of publication
1999
Pages
81 - 92
Database
ISI
SICI code
0044-0086(199903/06)72:2-3<81:CEANHO>2.0.ZU;2-Z
Abstract
In the MUSE classification of gastroesophageal reflux disease (GERD), esoph agitis is assessed by the presence of metaplasia, ulcer stricture, or erosi on, each being graded as absent, mild or severe. Daily reflux symptoms affe ct about 4 to 7 percent of the population; erosive esophagitis occurs in ab out 2 percent; the prevalence rate of Barrett's metaplasia is 0.4 percent; and esophageal adenocarcinoma lends to two deaths per million living popula tion. In persons with GERD symptoms, about 20 percent are found to have ero sive esophagitis, while ulcers or strictures are found in less than 5 perce nt of all patients with erosive esophagitis. No clear-cut temporal progress ion exists between successive grades of disease severity, as the most sever e grade of GERD is reached at the onset of the disease. Mild forms of GERD tend to be more common in women than men, while severe GERD characterized b y erosive esophagitis, esophageal ulcer; stricture or Barrett's metaplasia are far more common irt men than women. All forms of GERD affect Caucasians more often than African Americans or Native Americans. The prevalence of G ERD is high among developed countries irt North America and Europe and rela tively low in developing countries in Africa and Asia. During the past thre e decades, hospital discharges and mortality rates of gastric cancer gastri c ulcer and duodenal ulcer have declined, while those of esophageal adenoca rcinoma and GERD have markedly risen. These opposing time trends suggest th at corpus gastritis secondary to Helicobacter pylori infection protects aga inst GERD. This hypothesis is consistent with the geographic and ethnic dis tributions of GERD. Case-control studies also indicate that cases with eros ive esophagitis are less likely to harbor active or chronic corpus gastriti s than controls without esophagitis.