Abstract

Although there has been an explosion of data not only since the discovery of H. pylori in 1982, but also since the first comprehensive review of H. pylori in the Gastroenterology Clinics in 1993, much remains to be learned. In 1993, there were many skeptics doubting the importance of H. pylori in ulcer disease. Although this skepticism has dissipated, many ulcer patients infected with H. pylori still do not receive appropriate therapy. This situation possibly relates to the safety, efficacy, and simplicity of prescribing acid-suppressive therapy in contrast to the confusion regarding anti-H. pylori treatment regimens. Among the many continuing unanswered questions regarding the role of H. pylori and PUD are the still enigmatic nature of host, environmental, and H. pylori-related factors that determine outcome. Why do only some infected individuals (and why do more men than women) develop PUD, and what determines whether gastric ulcers or duodenal ulcers develop? What is the explanation for the seasonal variation in ulcer disease? Although PUD is an infectious disease, are other environmental factors critical for the manifestation of ulcers in association with infection? What factors govern the outcome of the combination of H. pylori infection and NSAID use? Has attention been too focused first on the pathophysiology of acid secretion and now on H. pylori? In curing H. pylori in association with PUD, are clinicians going to displace disease northward, substituting erosions, inflammation, and neoplasia (and associated symptoms) in the esophagus and gastroesophageal junction for an ulcer crater (and its associated symptoms) in the duodenum or stomach? The epidemiology of PUD is changing--in more recent reports of ulcer patients, H. pylori and NSAID use are less prevalent than in earlier reports. These questions and comments should not be misinterpreted as advocating a lack of aggressiveness in diagnosis and treatment of H. pylori in the setting of PUD, however. Nevertheless, the pendulum is swinging.

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