Pathophysiology of Peptic Ulcer Disease-Reference-Cited by-同舟云学术

Pathophysiology of Peptic Ulcer Disease

Published:1995 Issue: Volume: Page:1-13
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Author:

Halter F.

Publisher

Springer US

Link

http://link.springer.com/content/pdf/10.1007/978-0-585-32154-7_1.pdf

Reference42 articles.

1. Rauws EAJ, Langenberg W, Houthoff HJ, et al: Campylobacter pyloridis-associated chronic active antral gastritis: A prospective study of its prevalence and the effects of antibacterial and anticulcer treatment. Gastroenterology 94:33–40, 1988. This study showed a strong correlation between chronic active gastritis and the presence of H. pylori. It was outlined for the first time that H. pylori eradication can improve the gastric mucosa, thus supporting evidence for a true cause-effect relationship in H. pylori colonization and chronic active gastritis.

2. Graham DY: Campylobacter pylori and peptic ulcer disease. Gastroenterology 96:615–625, 1989. This study well defines the central role of H. pylori in the pathogenesis of duodenal ulcer disease.

3. Sonnenberg A: Geographic and temporal variations in the occurrence of peptic ulcer disease. Scand J Gastroenterol 20(suppl 110): 11, 1985. This overview outlines variations in peptic ulcer occurrence between different countries and different age groups. The author suggests that a cohort phenomenon is responsible for the gradual decline of prevalence of peptic ulcer disease.

4. Soll AH: Pathogenesis of peptic ulcer and implications for therapy. N Engl J Med 322:909–916, 1990. In this review the pathogenetic mechanisms of peptic ulcer disease are critically outlined. Special attention is given to the role of mucosal defense factors and the dysregulation of gastric acid secretion.

5. Cox AJ: Stomach size and its relation to chronic peptic ulcer. AMA Arch Pathol 54:407, 1952. The author presents for the first time evidence, based on autopsy studies, that patients with active or healed duodenal ulcers have in general an enlarged stomach with an increased parietal cell mass.

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