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Peptic ulcer is a non-malignant ulcer of the stomach (called gastric ulcer) or duodenum (called duodenal ulcer). By far most instances are now known to be due to Helicobacter pylori, a spiral-shaped bacterium that lives in the acid environment of the stomach. These ulcers can also be caused or worsened by drugs such as Aspirin and other NSAIDs.
Signs and symptoms
Symptoms of a peptic ulcer can be:
A history of heartburn, gastroesophageal reflux disease (GERD) and use of certain forms of medication can raise the suspicion for peptic ulcer. Medicines associated with peptic ulcer are NSAID (non-steroid anti-inflammatory drugs) that inhibit cyclooxygenase 1, and most glucocorticoids (e.g. dexamethasone).
In patients over 45 with more than 2 weeks of the above symptoms the odds for peptic ulceration are high enough to warrant rapid investigation by EGD (see below).
In earlier times it was thought that the timing of the symptoms in relation to the meal could differentiate between gastric and duodenal ulcers: a gastric ulcer would give pain during the meal, as gastric acid was secreted, while duodenal ulcers would only hurt after the meal — when acidic chyme was passed down to the duodenum. This theory has not been proved in practice.
Diagnosis
In patients in whom peptic ulcer is suspected, esophagogastroduodenoscopy (EGD, a form of endoscopy) is indicated. 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.
The diagnosis of Helicobacter pylori can be by:
- Biopsy during EGD;
- Breath testing (does not require EGD);
- Direct culture from an EGD biopsy specimen;
- Direct detection of urease activity in a biopsy specimen;
- Measurement of antibody levels in blood (does not require EGD). It is still slightly controversial whether a positive antibody without EGD is enough to warrant eradication therapy.
The possibility of other causes of ulcers, notably malignancy (gastric cancer) needs to be kept in mind. This is especially true in ulcers of the large curvature of the stomach; most are also a consequence of chronic H. pylori infection.
Pathophysiology
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 (90% of gastric and 75% 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 (see above). The gastric mucosa protects itself from gastric acid with a layer of 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.
Macroscopically: Gastric ulcer is most often localized on the lesser curvature of the stomach. It is a round to oval parietal defect ("hole"), 2 to 4 cm diameter, with a smooth base and perpendicular borders. These borders are not elevated or irreguliar as in gastric cancer - ulcerative form. Surrounding mucosa may present radial folds, as a consequence of the parietal scarring.
Microscopically: Gastric peptic ulcer is a mucosal defect which penetrates the muscularis mucosae and muscularis propria, produced by acid-pepsin aggression. Ulcer margins are perpendicular and present chronic gastritis. During the active phase, the base of the ulcer shows 4 zones: inflammatory exudate, fibrinoid necrosis, granulation tissue and fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis. 1
Epidemiology
In Western countries the prevalence of Helicobacter pylori infections roughly matches age (i.e., 20% at age 20, 30% at age 30, 80% at age 80 etc). Prevalence is higher in third world countries. Transmission is by food and human contact, sharing food utensils etc.
A minority of cases of Helicobacter infection will eventually lead to an ulcer and a larger proportion of people will get non-specific discomfort, abdominal pain or gastritis.
Treatment
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 antibiotics (Erythromycin, Ampicillin, Tetracycline, Metronidazole) and proton pump inhibitors (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.
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