Pharmacotherapeutics of Peptic Ulcer Disease

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Peptic ulcer is an ulcer of the mucosa in the stomach or proximal duodenum, rarely jejunum. The ulcer develop when the protection of mucosa by mucus, bicarbonate, or prostaglandins fail.1,2

Pathophysiology (including epidemiology, etiology, and pathogenesis)

There is a significant geographical and epidemiological difference for peptic ulcer disease (PUD). Males are more prone for the ulcers in many parts of the world. One of the most convincing reasons for PUD is an infection due to Helicobacter pylori. There are some environmental and genetic factors which contribute to the pathogenesis of peptic ulcer. Smoking is proven to double the chances for peptic ulcer but not the psychological stress or alcohol. Drugs such as non-steroidal anti-inflammatory drugs (NSAIDs) usually cause gastric ulceration rather than duodenal ulcers.1

Epigastric pain is the most common symptom of PUD, which is typically relieved by antacids. Food usually decreases pain in duodenal ulcer but may worsen or leave unaffected in case of gastric ulcers. Duodenal ulcer pain usually occurs at night. Patients shall undergo a screening blood test (breath test) or stool antigen test for H. Pylori, it is found almost always in duodenal ulcers and around 80% in gastric ulcers. Endoscopy is not usually required. Gastroscopy or a barium meal shall be performed in older patients to rule out a gastro-esophageal cancer or obstruction. The rare gastrinoma which causes PUD is Zollinger-Ellison syndrome.1,3

The Complications of PUDs are epigastric pain, anemia, recurrent heamorrhage, perforation, gastric outlet obstruction, secondary infections, pancreatitis, carcinoma etc.1


In H. pylori infected patients, eradication of the organism results in cure of the disease in most of the cases. Recurrence happens if the patient is re-infected with H. pylori.

H. pylori-negative peptic ulcers are usually caused by overproduction of acid in stomach or by the use of NSAIDs. In those cases NSAIDs shall be stopped if possible and use acid-suppressing drugs such as proton pump inhibitors or H2 blockers. If necessary; NSAIDs could be restarted with concomitant use of ulcer prophylactic therapy. A maintenance dose of PPI or use of misoprostol (mucosal protective) could be used as prophylactic therapy.

The rare but serious complications include recurrent heamorrhage, perforation, and gastric outlet obstruction. Surgery shall be used to correct these problems in emergency.

Antacids could not only neutralize gastric acid, but could do further protective actions to gastric mucosa. It shall also inhibit pepsin activity, increase angiogenesis and alginate containing antacids could reduce gastric reflux. But healing of ulcers with the anti-secretary (PPIs and H2 blockers) drugs are much better than in presence of antacids alone. Generally antacids interfere with the absorption of other drugs and food. So the other drugs through oral route shall be given one hour before or 2 hours after taking antacids. Aluminum containing antacids shall cause constipation and magnesium containing antacids shall produce laxative effect. A combination of these two shall nullify those side effects.

H2 blockers reduce acid secretion by blocking histamine2 receptors. Ranitidine or famotidine are the commonly used H2 blockers. In cases of GI bleeding and perforation parenteral PPIs or H2 blockers are preferred over oral therapy. Usual dose of ranitidine is 150 mg twice daily or 300 mg once daily.

Sucralfate could be used to coat the mucosal surface and is equally effective in healing duodenal ulcers in comparison with H2 blockers. It is particularly useful in stress ulcer prophylaxis. But it shall cause constipation.

Proton pump inhibitors (PPIs) block acid secretion by blocking the proton pump of gastric parietal cell. PPIs are more effective in control of acid than H2 blockers or antacids. PPIs are preferred in gastro-esophageal reflux disease (GERD), regimen for eradication of H. pylori and ulcer healing, NSAID induced PUD and in prophylaxis of high risk patients. Omeprazole, pantoprazole, lansoprazole, esmaprazole etc are the commonly used PPIs. PPIs shall cause nausea, vomiting, diarrhea, stomach pain etc. Liver dysfunction and allergic reactions are also noted. There is an increased chance of gastric infections due to decreased acidity. Recent evidences show PPIs increase the chance of osteoporosis and bone fracture. PPIs should be screened for drug-drug interactions. Different PPIs shall produce different drug interactions.

Triple therapy is the basic first line H. pylori eradication regimen with two antimicrobials and a PPI. But there are several regimens are available for the eradication. Clarithromycin, amoxicillin, and metronidazole are the three commonly used antimicrobials. In case of macrolide antibiotic resistance or recurrence to a treatment with clarithromycin; a regimen with antimicrobials other than clarithromycin shall be preferred. In case of penicillin allergy, tetracycline or doxycycline could be used.

Smoking cessation, avoiding re-infection, controlling acidity with properly timed diet, foods containing flavonoids, avoiding consumption of excessive alcohol etc. are some of the non pharmacological measures in management of PUD.1,2,3


1. Ballinger A et al. Pocket Essentials of Clinical Medicine, Elsevier, 2008: 77-80.

2. Fauci AS et al. Harrison's Manual of Medicine, Mc-Graw Hill, 2009: 831-833.

3. Foster C et al. The Washington Manual of Medical Therapeutics, Wolters Kluwer, 2010: 596-600.

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Author: Dixon Thomas

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