On microbes and men: a new era in the treatment of peptic ulcer disease.
Peptic ulcer disease is the name given to a number of disorders all characterized by inflammation and ulceration of the upper GI tract. It afflicts nearly 10% of the U.S. population and, while once a disease primarily in the domain of the male of the species, its occurrence today is almost equally divided between genders. The lesions associated with peptic ulcer disease (PUD) may be acute or chronic and range from mucosal inflammation to perforations of the GI tract. The lesions are thought to be primarily the result of direct or indirect contact of inflamed or exposed GI mucosa to the acid and digestive elements (pancreatic enzymes, bile salts) of the GI tract.
While the inflammation is usually associated with epigastric pain, it is important to note that the symptoms of the disease poorly correlate with actual size or chronicity of the lesions. The tissues involved include those of the esophagus (particularly the junction of the esophagus and the stomach), the stomach and the duodenum.
Prior to the introduction of the [histamine.sub.2] antagonists to the market in 1978, the treatment focus of PUD involved symptomatic medical management followed by what was felt to be definitive surgical management. This generally entailed the removal of the ulcer tissue and the vagal nerves that innervated the region and that stimulated acid production. The medical management involved antacids, anticholinergic agents and was frequently accompanied by a bland and milk-based diet.
With the introduction of the more highly effective and better tolerated [histamine.sub.2] antagonists to therapy regimens, the old medical management, as well as surgical interventions for PUD markedly declined. Morbidity and mortality of the disease similarly was reduced, as was the cost of care since the treatment shifted from an "in-patient" to an outpatient base. Much of the emphasis through the early 1990s in the treatment of PUD centered on that acid-suppression strategy with little concerted thought given to alternative explanations for the disease process.
Today, however, a new framework is being understood as a significant factor for the presence of gastric and duodenal ulcers; that is, a bacteria known as Helicobacter pylori. This organism has been associated with a majority of gastric and duodenal ulcers and therapy directed to its eradication has led to long-term, or durable, remissions (or "cure") of PUD.
Thus, it is now proposed by the American Gastroenterology Association and a National Institutes of Health (NIH) Consensus Panel that treatment of an infectious source, rather than an acid source, be the center of therapy for PUD. This article will explore this new concept, putting it into context with older philosophy, and will present current thought on the appropriate management of PUD.
Strategies that focus on gastric motility and mucosal integrity will also be explored. At the conclusion, the reader should have an appreciation of the key treatment strategies for PUD and the role the pharmacist may play in assuring that therapy is appropriate and that compliance is optimized so that the therapy reaches its intended goal.
RELATED ARTICLE: Objectives:
Upon completing this article, the reader should be able to:
1. Describe the proposed etiologies for the common lesions which comprise the condition known as peptic ulcer disease (PUD).
2. Discuss the rational use of drug therapy in the treatment of PUD.
3. Outline important information to convey to patients to optimize the use and compliance with therapy for the treatment of PUD.
4. Compare/contrast the specific uses and relative risk-benefit ratios for the following agents in the treatment of PUD: antimicrobials, [H.sub.2] antagonists, omeprazole, sucralfate, misoprostol, cisapride, antacids.
Curtis D. Black, R.Ph., Ph.D. is Merck Professor of Clinical Pharmacy and Assistant Dean for Academic Affairs at the College of Pharmacy, the University of Toledo, Ohio.
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|Author:||Black, Curtis D.|
|Publication:||Chain Drug Review|
|Date:||Jun 5, 1995|
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