The American Journal of Digestive Diseases

, Volume 14, Issue 9, pp 655–677 | Cite as

Current concepts of peptic ulceration

  • S. P. Bralow
Progress Report


These observations support the theory that peptic ulceration results from failure of adequate local repair to mucosal injury. The resultant ulcer may be acute or chronic depending upon the duration of the stress or the mucosal contact of the irritative substance and on the ability of the local tissue to achieve cellular homeostasis. The role of acid and pepsin secretion would be secondary, the substances exerting their destructive influence only on susceptible tissue. In 15–20% of the duodenal ulcer patients, chronic damage in the first portion of the duodenum may lead to partial pyloric obstruction resulting in enlargement of the stomach and hyperplasia of the parietal and peptic cell masses. Whether mild impairment of gastric emptying may stimulate continuous gastrin release from the antrum is not known as yet. Such stimulation may initiate further hyperplasia of the PCM and increase gastric secretion. In gastric lesions the apparent normal volume and low acidity of gastric secretion probably results from reabsorption of hydrogen ions through the damaged mucosa.

It is extremely difficult to review the controversial literature pertaining to peptic ulcer genesis without concluding as did an editorial writer forLancet: “He, who investigates the etiology and behavior of peptic ulcer must be prepared for a poverty of rewards such as plagues few other areas of medical research.”123 To compensate for this frustration, we have postulated our own theory based on the inability of the mucosa to maintain cellular homeostasis following mucosal injury.


Peptic Ulcer Duodenal Ulcer Gastric Secretion Mucosal Injury Cellular Homeostasis 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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Copyright information

© Hoeber Medical Division • Harper & Row 1969

Authors and Affiliations

  • S. P. Bralow
    • 1
  1. 1.From the Department of Medicine, Gastrointestinal SectionTemple University School of MedicinePhiladelphia

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