[Physiopathological basis for the treatment of peptic ulcer].

Peptic ulcer pathophysiology has advanced in several ways during the last years; the following facts has been put forward: a) There has been recognized specific receptors controlling oxyntic cell secretion for histamine, acetylcholine, gastrin and prostaglandins. Agonists and antagonists for the above mentioned receptors has been synthesized. The physiology of the proton-pump located at the luminal side of the mucous membrane has been clarified. This pump is responsible for HCl secretion and can be blocked with omeprazole and trimeprazole. b) There is a comprehensive view of the gastric mucosal barrier, which is important for gastric self-protection, against inner or outer noxious stimuli. The mucosal barrier rupture can be the initial step of some gastroduodenal diseases, so the understanding of its functioning is very important to explain the pathophysiology of peptic ulcer. Finally, some etiopathogenic factors has been proved in the development of peptic ulcer, as Helicobacter pylori, which adheres to gastric cells mucus, damaging the cells after colonization, and producing the rupture of the mucosal barrier; which in turn favours peptic ulcer disease. The use of non-steroidal antiinflammatory drugs (NSAID) can act at several levels; the most important one seems to be the alteration of prostaglandins synthesis and consequent decrease of mucus and bicarbonate secretion. At the same time NSAID can cause antro-pyloric motor disturbances which contributes to peptic ulcer development. The understanding of all those pathophysiological factors has promoted the designs of new pharmacological approaches to the medical treatment of peptic ulcer, so new antiulcer drugs can act at different stages of peptic-acid secretion, like H2-antagonists, proton-pump blockers, cytoprotector drugs and antimicrobial agents for Helicobacter pylori eradication.