Acid secretion and duodenal ulcer
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Ulcerative lesions of the gastroduodenal area are classified as peptic ulcer diseases. Peptic ulcer disease is associated with a high rate of recurrence. The saying, “no acid, no ulcer”, has withstood test of the time and still accepted by most physicians and researcher are generally true. One possible cause of gastric and duodenal ulcers is reduced mucosal defense mechanisms. Human and animal data, however, have demonstrated that duodenal ulcers do not occur with reduced mucosal defense mechanism alone but also require the presence of sufficient amounts of acid. In one study, patients suffering from duodenal ulcer had a significantly increased mean number of gastric parietal cells and appeared to have increased sensitivity to gastrin when compared with healthy subjects. Although the reason is unknown, the stomach emptying rate may be greatly increased in duodenal ulcer patients. Another abnormality in duodenal ulcer patients is decreased inhibition of gastrin release by acid and a reduced rate of duodenal bicarbonate secretion. It should be emphasized, however, that a significant number of patients with duodenal ulcer do not have excessive secretion of acid.
An exciting development in the field of peptic ulcer disease is the finding of a possible correlation between Helicobacter pylori (H.pylori) infection and the incidence of gastric and duodenal ulcers. The role of H.pylori infection in the genesis of peptic ulcer is unclear, but in a significant number of patients, eradication of the bacteria reduces the rate of ulcer recurrence. H.pylori produces large quantities of the enzyme urease, which hydrolyzes urea to produced ammonia. The ammonia neutralizes acid in the stomach, protecting the bacteria for the injurious effects of hydrochloric acid.
Although the mechanism has not been elucidated, the presence of H.pylori in the stomach enhances the secretion of gastrin by the gastric mucosa. Whether increased gastrin release by the presence of H.pylori is responsible for the increased recurrence of gastric and duodenal ulcers in patients has yet to be proven. It has been demonstrated That H2 receptor blockers (cimentidine and ranitidine) have no effect on H.pylori infection. In contrast, omeprazole (an inhibitor of the H+/K+-ATPase) appears to be bacteriostatic. A combination therapy using omeprazole 20 mg twice a day plus metronidazole 500mg two times a day or Amoxicillin 1 gm two times a day and clarithromycin 500mg twice a day appears to be effective in the eradication of H.pylori in 50 to 80% of patients with peptic ulcer disease, resulting in a significant reduction of duodenal ulcer recurrence.
References:
- Medical physiology, Lippincott Williams & Wilkins 3rd edi.
- Harrison’s Principles of Internal Medicine, 17th edition.
- Davidson’s Principles and Practice of Medicine, 20th Edition
- www.aafp.org
Filed Under: Gastroenterology
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