Peptic ulcer disease
The term ‘peptic ulcer’ refers to an ulcer in the lower oesophagus, stomach or duodenum, in the jejunum after surgical anastomosis to the stomach or, rarely, in the ileum adjacent to a Meckel’s diverticulum. Ulcers in the stomach or duodenum may be acute or chronic; both penetrate the muscularis mucosae but the acute ulcer shows no evidence of fibrosis. Erosions do not penetrate the muscularis mucosae.
Gastric and duodenal ulcer
The prevalence of peptic ulcer (0.1–0.2%) is decreasing in many Western communities as a result of widespread use of Helicobacter pylori eradication therapy but it remains high in developing countries. The male-to female ratio for duodenal ulcer varies from 5 : 1 to 2 : 1, whilst that for gastric ulcer is 2 : 1 or less. Chronic gastric ulcer is usually single; 90% are situated on the lesser curve within the antrum or at the junction between body and antral mucosa. Chronic duodenal ulcer usually occurs in the first part of the duodenum and 50% are on the anterior wall. Gastric and duodenal ulcers coexist in 10% of patients and more than one peptic ulcer is found in 10–15% of patients.
Peptic ulcer disease is a chronic condition with spontaneous relapses and remissions lasting for decades, if not for life. The most common presentation is with recurrent abdominal pain which has three notable characteristics: localisation to the epigastrium, relationship to food and episodic occurrence. Occasional vomiting occurs in about 40% of ulcer subjects; persistent daily vomiting suggests gastric outlet obstruction. In one-third, the history is less characteristic, especially in elderly people or those taking NSAIDs. In them, pain may be absent or so slight that it is experienced only as a vague sense of epigastric unease. Occasionally, the only symptoms are anorexia and nausea, or early satiety after meals. In some patients, the ulcer is completely ‘silent’, presenting for the first time with anaemia from chronic undetected blood loss, as an abrupt haematemesis or as acute perforation; in others, there is recurrent acute bleeding without ulcer pain. The diagnostic value of individual symptoms for peptic ulcer disease is poor; the history is therefore a poor predictor of the presence of an ulcer.
Endoscopy is the preferred investigation. Gastric ulcers may occasionally be malignant and therefore must always be biopsied and followed up to ensure healing. Patients should be tested for H. pylori infection. The current options available are listed in Some are invasive and require endoscopy; others are noninvasive. They vary in sensitivity and specificity. Breath tests or faecal antigen tests are best because of accuracy,simplicity and non-invasiveness.
The aims of management are to relieve symptoms, induce healing and prevent recurrence. H. pylori eradication is the cornerstone of therapy for peptic ulcers, as this will successfully prevent relapse and eliminate the need for long-term therapy in the majority of patients. H. pylori eradication All patients with proven ulcers who are H. pylori-positive should be offered eradication as primary therapy. Treatment is based upon a PPI taken simultaneously with two
antibiotics (from amoxicillin, clarithromycin and metronidazole) for 7 days High-dose, twice-daily PPI therapy increases efficacy of treatment, as does extending treatment to 10–14 days. Success is achieved in 80–90% of patients, although compliance, side-effects and antibiotic resistance influence this. Resistance to amoxicillin is rare but rates of metronidazole resistance reach 40% in some countries and, recently, rates of clarithromycin resistance of 20–40% have
appeared. Where the latter exceed 15–20%, a quadruple therapy regimen, consisting of omeprazole (or another PPI), bismuth subcitrate, metronidazole and tetracycline (OBMT) for 10–14 days, is recommended. In areas of low clarithromycin resistance, this regimen should also be offered as second-line therapy to those who remain infected after initial therapy, once compliance has been checked. For those who are still colonised after two treatments, the choice lies between a third attempt guided by antimicrobial sensitivity testing, rescue therapy (levofloxacin, PPI and clarithromycin) or long-term acid suppression.