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Pathophysiology of Peptic Ulcer Disease

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Sucralfate

Abstract

Much progress has been achieved in recent years on the understanding of the pathophysiol- ogy of peptic ulcer disease (PUD), but a single factor explaining why ulcers occur has not been found. New developments have evolved in waves concentrated on phenomena only partly responsible for the development of peptic ulcers. Every surge has brought new insight but tended to absorb a disproportionate amount of research efforts on mechanisms that can only partially explain the disease. This critique is particularly focused on studies devoted to the role of gastric acid and pepsin, if one considers that the majority of ulcer patients do not secrete excessive amounts of this “aggressive” secretory product. Similarly, the concept of “cytoprotection,” albeit of importance, has created a consider- able amount of confusion because many have confounded phenomena involved in protection against noxious agents with the considerably more complex field of develop- ment and healing of peptic ulcers. The concept of protection has nevertheless helped to better understand the important role of nonsteroidal anti-inflammatory drugs (NSAIDs) in drug-induced ulcer disease. Similarly small is the harvest from the impressive knowledge that has accumulated in recent years on gastrointestinal hormones. The advent of Helicobacter pylori is regarded as the breakthrough for the understanding of PUD because the large majority of ulcer patients harbor this infective agent in their stomachs and especially since new therapeutic options have emerged from this discovery. This should, however, not deviate from the fact that the majority of H. pylori carriers never develop PUD.

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Halter, F. (1995). Pathophysiology of Peptic Ulcer Disease. In: Hollander, D., Tytgat, G.N.J. (eds) Sucralfate. Springer, Boston, MA. https://doi.org/10.1007/978-0-585-32154-7_1

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  • DOI: https://doi.org/10.1007/978-0-585-32154-7_1

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