Download Sucralfate: From Basic Science to the Bedside by F. Halter (auth.), Daniel Hollander M.D., Guido N. J. Tytgat PDF

By F. Halter (auth.), Daniel Hollander M.D., Guido N. J. Tytgat M.D. (eds.)

International researchers summarize the present figuring out of peptic illness and hint the advance of a singular new drug for peptic ailment therapy-sucralfate. participants current laboratory examine along with info from scientific trials in addition to from the perform of drugs. Articles speak about the background of sucralfate's improvement, mechanisms of motion, scientific efficacy, and destiny instructions for study. This quantity should be of curiosity to scientists and clinicians operating in gastroenterology and gastrointestinal physiology.

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3) Continuous mucosal cell renewal from the progenitor cells in the mucosal proliferative zone. (4) "Alkaline tide"—parietal cells secrete HCI into the gastric gland lumen and concurrently secrete bicarbonate into the lumen of adjacent microvessel. (5) Mucosal microvessels. (6) Continuous generation of prostaglandin Ej and prostacyclin by the mucosa is crucial for the maintenance of mucosal integrity. Most mucosal defensive mechanisms are stimulated or facilitated by endogenous or exogenous prostaglandins.

Pylori eradication. At the time being the unifying hypothesis that H. pylori directly causes peptic ulcers through combined enhancement of acid secretion and breakdown of mucosal protection still contains speculative elements. Indeed the most crucial argument against the dominant role of H. pylori in the pathogenesis of this disease stems from the observation that no more than 10-20% of H. py/ori-infected subjects develop peptic ulcers. Whether or not H. pytori-infected patients develop peptic ulcers appears to depend on several factors such as adherence to the gastric surface epithelium, virulence of the H.

Pathophysiological Abnormalities in Gastric Ulcer Patients" Decreased acid secretion and increased H^ backdiffusion Chronic superficial and atrophic gastritis Increased concentration of bile acids and pancreatic juice in stomach (duodenogastric reflux) Delayed gastric emptying Inappropriately decreased pyloric sphincter pressure under basal conditions and in response to stimuli "Reproduced from: Mahachai V. Bedard B: Update in peptic ulcer therapy. Med North Am 19 March:3628-3642. 1988, with permission.

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