Text 20 Peptic Ulcer Disease

Essentials of Diagnosis

- History of nonspecific epigastric pain present in 80 – 90% of patients with variable relationship to meals.

- Ulcer symptoms characterized by rhythmicity and periodicity.

- Ten to 20 percent of patients present with ulcer complications without antecedent symptoms.

- Most NSAID-induced ulcers are asymptomatic.

- Upper endoscopy with antral biopsy for H pylori is the diagnostic procedure of choice in most patients.

- Gastric ulcer biopsy or documentation of complete healing necessary to exclude gastric malignancy.

General Considerations

Peptic ulcer is a break in the gastric or duodenal mucosa that arises when the normal mucosal defensive factors are impaired or are overwhelmed by aggressive luminal factors such as acid and pepsin. By definition, ulcers extend through the muscularis mucosae and are usually over 5 mm in diameter. In the United States, there are about 500,000 new cases per year of peptic ulcer and 4 million ulcer recurrences; the lifetime prevalence of ulcers in the adult population is approximately 10%. Ulcers occur five times more commonly in the duodenum, where over 95% are in the bulb or pyloric channel. In the stomach, benign ulcers are located most commonly in the antrum (60%) and at the junction of the antrum and body on the lesser curvature (25%). Ulcers occur slightly more commonly in men than in women (1.3:1). Although ulcers can occur in any age group, duodenal ulcers most commonly occur in patients between the ages of 30 and 55 years, whereas gastric ulcers are more common in patients between the ages of 55 and 70 years. Ulcers are more common in smokers and in patients taking NSAIDs on a long-term basis (see below). Alcohol, dietary factors, and stress do not appear to cause ulcer disease. The incidence of duodenal ulcer disease has been declining dramatically for the past

30 years, but the incidence of gastric ulcers appears to be increasing as a result of the widespread use of NSAIDs and low-dose aspirin.

Etiology

Three major causes of peptic ulcer disease are now recognized: NSAIDs, chronic H pylori infection, and acid hypersecretory states such as Zollinger-Ellison syndrome. Evidence of H pylori infection or NSAID ingestion should be sought in all patients with peptic ulcer. NSAID- and H pylori-associated ulcers will be considered in the present section; Zollinger-Ellison syndrome will be discussed subsequently. Uncommon causes of ulcer disease include CMV (especially in transplant recipients), systemic mastocytosis, Crohn’s disease, lymphoma, and medications

(eg. alendronate). Up to 10 % of ulcers are idiopathic.

H pylori – Associated Ulcers

H pylori appears to be a necessary cofactor for the majority of duodenal and gastric ulcers not associated with NSAIDs. Overall, it is estimated that one in six infected patients will develop ulcer disease. The prevalence of H pylori infection in duodenal ulcer patients is 75–90 %. Most H pylori-infected duodenal ulcer patients have infection predominantly in the gastric antrum, which is associated with increased gastric acid secretion and decreased duodenal mucosal bicarbonate secretion. It is hypothesized that increased acid exposure can give rise to small islands of gastric metaplasia in the duodenal bulb. Colonization of these islands by H pylori may lead to duodenitis or duodenal ulcer. The association with gastric ulcers is lower, but H pylori is found in the majority of patients in whom NSAIDs cannot be implicated. H pylori-associated gastric ulcers tend to form at the junction of the gastric body and antrum – the site of transition from oxyntic to pyloric epithelium. Most H pylori-infected gastric ulcer patients have infection that predominates in the gastric body and is associated with decreased acid secretion. It is hypothesized that chronic inflammation overwhelms the gastric mucosal defense mechanisms.

The natural history of H pylori-associated peptic ulcer disease is well defined. In the absence of specific antibiotic treatment to eradicate the organism, 85 % of patients will have an endoscopically visible recurrence within 1 year. Half of these will be symptomatic. After successful eradication of H pylori with antibiotics, ulcer recurrence rates are reduced dramatically to 5–20 % at 1 year. Some of these ulcer recurrences may be due to NSAID use or reinfection with H pylori.

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Учебное издание

Баценко Ирина Владимировна

Игнатова Сталина Адамовна

Мисуно Екатерина Антоновна