Abstract
It is argued that separation of chronic peptic ulcers into gastric and duodenal may be artificial and confuse the search for common factors in their etiology. Differences are often exaggerated by contrasting the extremes of a continuous distribution of ulcers from high gastric lesser curve to duodenal bulb and beyond. Genetic and epidemiological factors appearing to favor one or the other type of ulcer may act by determining the background cellular changes on which ulcers develop. The extent of the mucosal changes may influence the site of ulceration and incidentally the level of acid secretion. Thus ulcers could be driven distally or drawn proximally across the arbitrary boundary of the pylorus.