Peptic ulcer

The management of peptic ulcer disease has changed dramatically in the last 20 years as the aetiology of peptic ulceration has become more clearly understood, and more powerful and effective medical treatment has evolved. At the same time there has been a dramatic decrease in both elective and emergency surgery for peptic ulceration. Aetiological factors in peptic ulceration include H. pylori infection, NSAID ingestion, smoking, renal failure, liver disease, and ZollingerEllison (ZE) syndrome. H. pylori is by far the most important, and adequate management of H. pylori is the mainstay of modern ulcer therapy. H. pylori is a spiral, gram-negative bacteria which is spread by direct contact, and infects up to 60% of the population, though only 5-10% of those infected develop ulceration. H. pylori causes increased gastrin levels, a rise in gastric acid production, and also has a direct effect on gastric and duodenal mucosa. NSAIDs have both a localised and systemic effect on gastric and duodenal mucosa, which seems to be through their inhibition of cyclo-oxygenase enzyme (particularly COX-1).

Patients with ulcers have a variety of symptoms, including epigastric pain, anorexia, vomiting, and weight loss. Epigastric pain may be relieved by food, or associated with anorexia, and radiates through to the back. Some patients are asymptomatic. Examination is often unremarkable, except for melaena when there has been bleeding, or a succussion splash with gastric outlet obstruction. The diagnostic investigation is upper GI endoscopy, which allows visualisation of ulcers as well as gastric biopsy. All patients with peptic ulceration must be investigated for H. pylori by, serology, breath testing, CLO test, or histology. The last two are performed on biopsies taken at endoscopy and are the most accurate. All gastric ulcers must be biopsied from their margin to exclude the possibility of malignancy.

Treatment depends on the presumed causal factor. If H. pylori is identified it must be eradicated. If NSAIDs are being used they should be stopped if at all possible and alternative analgesia used. If neither H. pylori is identified or NSAIDs are being used then the initial presumption should be a false-negative result from the H. pylori test, and eradication prescribed - other causes of ulceration are extremely rare. Eradication of H. pylori is achieved by a combination of antibiotics in conjunction with an anti-secretory agent - a common combination would be a PPI, with clarithromycin and amoxycillin, or metronidazole. This 'triple therapy' would be given for one week, and followed by continuing anti-secretory therapy for 8-12 weeks to heal the ulcer, which must also be prescribed for NSAID induced ulcers.

If ulcers fail to heal then repeat testing for H. pylori must be performed, and this is most effective by CLO test and histology at repeat endoscopy. Persistent infection must be treated before alternative diagnoses are sought, and a different combination of antibiotics over a 2-week period is recommended. NSAID ingestion must be re-assessed, and malignancy excluded with endoscopic biopsies. In the absence of other causes ZE syndrome must be considered, where gastrin-secreting tumours result in high-gastric acidity and resistant peptic ulceration. Serum gastrin levels must be measured to diagnose ZE syndrome, and the possibility of multiple endocrine neoplasia (MEN) considered.

Surgery for peptic ulcer disease is now much less common than it used to be. Elective surgery is extremely rare, and consisted of acid-reducing procedures (vagotomy, selective vago-tomy, antrectomy), and gastric resections. Complications from these operations were common, and recurrent ulceration well recognised. It is still occasionally necessary to perform elective surgery for resistant ulcer disease, but only after all medical treatment has been tried thoroughly. Emergency surgery for complications is still common, but less common than 20 years ago. The treatment of bleeding ulcers and perforations has been described already (see Upper GI Bleeding and Perforated Viscus). Gastric outlet obstruction may result from scarring and fibrosis secondary to ulceration in the pyloric region and duodenum, and this often requires surgical intervention. Balloon dilatation at endoscopy is a good first-line treatment, but may result in perforation requiring surgery. Operative treatment of gastric outlet obstruction includes pyloroplasty, gastro-enterostomy, and distal gastrectomy.

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