[Ulcer epidemiology: old knowledge in a new light].

Low standards of hygiene lead to frequent gastric infection by Helicobacter pylori (Hp) during early childhood and, subsequently, the development of diffuse atrophic gastric. Atrophic gastric in conjunction with environmental factors, such as high dietary salt and low consumption of fruits or vegetables, promote intestinal metaplasia of the gastric mucosa and, possibly, gastric cancer. Under improved standards of hygiene, Hp is contracted only during adulthood, and gastric atrophy becomes less marked. The remaining capacity to secrete acid suffices to induce ulcers in the gastric mucosa weakened by the Hp infection. In adults with high acid output, the strongly acidic environment of the gastric corpus is too hostile for Hp, and it colonizes mainly the antrum. Duodenal mucosa exposed to high volumes of acid changes into epithelium covered by gastric metaplasia, more suitable for colonization by Hp than the original mucosa. The ensuing duodenitis in conjunction with the increased acid load favours duodenal ulceration. Acute exogenous influences, such as smoking, stress or physical workload, shift the delicate balance of defensive and aggressive factors at the mucosal level towards ulceration. The improvement in sanitation and the development of clean water supplies deferred the infection from childhood into adulthood and later prevented its occurrence altogether. The epidemiology of Hp could explain the historic trends of peptic ulcer and gastric cancer and their similar geographic distributions.