Peptic Ulcers Support Group

Most ulcers are now known to be associated with Helicobacter pylori, a spiral-shaped bacterium that lives in the acidic environment of the stomach. Ulcers can also be caused or worsened by drugs such as Aspirin and other NSAIDs. About 4 % of gastric ulcers are caused by a malignant tumour, which is one reason to be vigilant in their detection. Duodenal ulcers are generally non-malignant.

In patients in whom peptic ulcer is suspected, the correct test is esophagogastroduodenoscopy (EGD), a form of endoscopy, sometimes known as just gastroscopy. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.

Classical causes of ulcers (tobacco smoking, blood groups, spices and a large array of strange things) are of relatively minor importance in the development of peptic ulcers.

A major causative factor (75% of gastric and 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori, a spirochaete that inhabits the antral mucosa and increases gastrin production. Gastrin, in turn, stimulates the production of gastric acid by parietal cells.

Another major cause is the use of NSAIDs. The gastric mucosa protects itself from gastric acid with a layer of mucous, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins. Newer NSAIDs (celecoxib, rofecoxib) only inhibit cox-2, which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration.

Glucocorticoids lead to atrophy of all epithelial tissues. Their role in ulcerogenesis is relatively small.

Stress in the psychological sense has not been proven to influence the development of peptic ulcers. Burns and head trauma, however, can lead to "stress ulcers", and it is reported in many patients who are on mechanical ventilation.

Smoking leads to atherosclerosis and vascular spasms, causing vascular insufficiency and promoting the development of ulcers through ischemia.

A family history is often present in duodenal ulcers, especially when blood group O is also present. Inheritance appears to be unimportant in gastric ulcers.

Gastrinomas (Zollinger Ellison syndrome), rare gastrin secreting tumors, cause multiple and difficult to heal ulcers.

Younger patients with ulcer-like symptoms are often treated with antacids or H2 antagonists before EGD is undertaken. Bismuth compounds may actually reduce or even clear organisms.

When H. pylori infection is present, the most effective treatments are combinations of 2 antibiotics (e.g. Erythromycin, Ampicillin, Amoxicillin, Tetracycline, Metronidazole) and 1 proton pump inhibitor (PPI). An effective combination would be Amoxicillin + Metronidazole + Pantoprazole (a PPI). In the absence of H. pylori, long-term higher dose PPIs are often used.

Treatment of Helicobacter usually leads to clearing of infection, relief of symptoms and eventual healing of ulcers. Recurrence of infection can occur and retreatment may be required, if necessary with other antibiotics. Since the widespread use of PPI's in the 1990s, surgical procedures (like "highly selective vagotomy") for uncomplicated peptic ulcers became obsolete.

Perforated peptic ulcer is a surgical emergency and requires surgical repair of the perforation. And most bleeding ulcers require endoscopy urgently to stop bleeding with cautery or injection.