Helicobacter pylori infection and duodenal ulcer disease.

H. pylori is undoubtedly the dominant factor in the multifactorial peptic ulcer diathesis. We should not ignore the other contributing factors but rather try to identify how they interact with the organism and initiate the ulcerative process. The interplay of acid attack and mucosal defence is modulated by genetics, gender, blood group, smoking, age, and various physiologic considerations, which include acid output. These and other considerations probably explain the discrepancy between the high frequency of H. pylori infection in the population and the comparatively small proportion of individuals who develop a DU. Most agents used in DU are aimed at reducing acid secretion and achieve healing by minimizing acid attack. Such treatments, however, have no effect on H. pylori status and do not remedy the underlying gastroduodenitis. The mucosa therefore remains ill and vulnerable. After cessation of acid suppressive therapy, ulcer relapse is likely. Goodwin has likened the inflamed mucosa to a leaking roof, in which temporary dryness (healing) is assured if the rain (acid) is removed but permanent protection can be achieved only by mending the roof through healing of the mucosa. Therefore, therapy that fails to address the role of H. pylori in the causation of the mucosal inflammation, which predisposes to ulceration, is likely to confer only short-term benefit. Eradication of the infection has been shown beyond doubt to markedly alter the natural history of the disease, a number of series showing no recurrence at the end of 1 year, compared with a natural recurrence of > 70%. The economic savings after not only eradication but even suppression of H. pylori in DU disease have been estimated to be enormous. Despite these striking findings indicating H. pylori inflammation as the dominant factor in the DU diathesis and the possibilities of cure after H. pylori eradication, a large proportion of the medical community is still not willing to accept the consequences. There are presumably several reasons for this skeptical attitude. First, it takes time before physicians are willing to accept such drastic changes in their conventional way of thinking about DU disease, because it has been stressed during decades that DU disease is dominated by excessive acid as the main culprit. Second, current acid-suppressive therapy is highly efficacious in healing DU and in keeping those ulcers healed with maintenance therapy. These drugs are well tolerated and have a low side effect profile.(ABSTRACT TRUNCATED AT 400 WORDS)