ETIOLOGY OF BARRETT METAPLASIA AND ESOPHAGEAL ADENOCARCINOMA

The incidence of esophageal adenocarcinoma in the United States is ris ing at an epidemic rate, Although the cause for this rapid rise is unc lear, it is well established that nearly all cases of esophageal adeno carcinoma arise from a premalignant lesion of the esophagus, known as Barrett's esophagus, Although Barrett's esophagus is recognized as a p recursor lesion, the etiology, prevalence, and malignant risk of this lesion remain unclear, The relatively short, two-decade time frame for the rise in esophageal adenocarcinoma incidence and the increase acro ss populations is a strong argument for environmental factors as etiol ogical agents, perhaps interacting with genetically determined charact eristics that define personal susceptibility, Because of the strong li nk between Barrett's esophagus and esophageal adenocarcinoma and the l ink between Barrett's esophagus and gastroesophageal reflux disease, r isk factors for gastroesophageal reflux disease have been the prime su spects offered as possible explanations for the rise in esophageal ade nocarcinoma. A plethora of hypotheses have been advanced, implicating tobacco and alcohol consumption, changes in obesity and diet, and the changing pattern in use of medications that affect the upper gastroint estinal tract, The following text will review what is currently known about the epidemiology of Barrett's metaplasia, its risk for malignant transformation, and the proposed theories of etiogenesis.