Pathogenesis and pathophysiology of duodenal ulcer

Abstract

Much epidemiological, clinical, and pathophysiological evidence has accumulated to indicate that the aetiology of duodenal ulcer is heterogeneous (Table 8). Recent advances in the medical therapy of duodenal ulcer support the long held concept that hyperacidity is an important physiological abnormality in the majority of patients with duodenal ulcer. It can also be shown that the origin of hyperacidity is heterogeneous. Certain specific physiological abnormalities that lead to hyperacidity may have a genetic basis. The various physiological abnormalities, alone or in combination, may lead to two final common pathways: abnormally large meal-stimulated acid secretion, and nocturnal acid hypersecretion. Indeed, success of medical therapy aiming at the control of postprandial acid secretion or of nocturnal acid secretion strongly supports their significance. It is possible that hyperacidity occurs as a temporary phenomenon and is associated with stressful life events. However, it is also possible that it occurs as a constant abnormality, bestowed perhaps genetically on the duodenal ulcer patient. In the presence of hyperacidity, mucosal repair may be affected adversely. In either situation, an acute ulcer, such as that associated with stress, is allowed to develop into a full-blown ulcer. Healing takes place if the hyperacidity recedes or is reduced therapeutically, allowing normal mucosal repair to take place.