doi: 10.1093/ajhp/50.4_Suppl_1.S3pmid: N/A
Article PDF first page preview Close This content is only available as a PDF. Copyright © 1993, American Society of Health-System Pharmacists, Inc. All rights reserved.
doi: 10.1093/ajhp/50.4_Suppl_1.S11pmid: N/A
Abstract The phases of therapy for gastroesophageal reflux disease (GERD) and the efficacy, safety, and cost of the various drugs used are discussed. The therapeutic goals for patients with GERD are to relieve pain, promote healing, avoid complications, and prevent recurrence. Sustained inhibition of gastric acid secretion is necessary to facilitate healing of eroded esophageal mucosa. Phase 1 treatment involves lifestyle changes to remove factors that may help to precipitate reflux, such as overeating, alcohol, and tobacco. Phase 2 involves pharmacologic manipulation of the secretion, concentration, and transport of gastric acid. The drugs used are antacids, alginic acid, the histamine H2-receptor antagonists, the prokinetic agents, sucralfate, and omeprazole. While all of these agents may provide symptomatic relief, only the H2 antagonists and omeprazole have been convincingly shown to relieve symptoms and promote healing. The H2 antagonists differ in potency, pharmacodynamic effect, pharmacokinetics in certain patient groups, drug interactions, and adverse effects. The H2 antagonists may not be effective at standard dosages in patients who secrete especially large quantities of gastric acid. Because of its mechanism of action, omeprazole provides greater inhibition of gastric acid than any other antisecretory drug. Omeprazole may also be the most cost-effective treatment. The availability of omeprazole may reduce the number of patients for whom clinicians must resort to phase 3 treatment, surgery. Although many drugs provide symptomatic relief in patients with GERD, the healing that is necessary to break the cycle of damage and symptoms is promoted only by the H2 antagonists and omeprazole. Alginic acid, Antacids, Costs, Drug interactions, Ciastroesophageal reflux, Gastrointestinal drugs, Omeprazole, Pharmacokinetics, Sucralfate, Toxicity This content is only available as a PDF. Copyright © 1993, American Society of Health-System Pharmacists, Inc. All rights reserved.
doi: 10.1093/ajhp/50.4_Suppl_1.S19pmid: N/A
Article PDF first page preview Close This content is only available as a PDF. Copyright © 1993, American Society of Health-System Pharmacists, Inc. All rights reserved.
Schentag, Jfrome, J.;Goss, Thomas, F.
doi: 10.1093/ajhp/50.4_Suppl_1.S7pmid: N/A
Abstract Key pharmacokinetic and pharmacodynamic aspects of gastric acid-suppressive agents in patients with gastroesophageal reflux disease (GERD) are discussed. The acid-suppressive potencies of the histamine H2-receptor antagonists vary widely because of differences in clearance and other factors. The durations of action of cimetidine, ranitidine, and famotidine are similar to the dosage intervals usually chosen (6, 8, and 12 hours, respectively). Single bedtime doses of these drugs will effectively treat duodenal ulcer disease, but GERD requires a different approach since its symptoms are not well controlled by partial (less than 24-hour) suppression of gastric acid. One way to achieve greater efficacy in treating GERD is to administer higher doses more frequently. Another approach is to adjust the dosage upward until symptoms disappear. The improved acid-suppression characteristic of the proton-pump inhibitors was quickly applied to GERD therapy. Unlike the H2 antagonists, omeprazole completely suppresses circadian peaks in acid secretion, and omeprazole performs better than ranitidine in clinical trials. The use of omeprazole is limited, however, by concerns over secondary elevation of serum gastrin and the association between achlorhydria and gastric carcinoma in rats. Omeprazole may offer cost advantages over other agents. Because the effective dosages of all these agents vary, individualized dosage-adjustment strategies are necessary. Pharmacists can help to optimize treatment by monitoring pharmacodynamic markers. With a flexible approach to drug and dosage selection, it should be possible to manage GERD in most patients in a cost-effective manner. Dosage, Dosage schedules, Gastroesophageal reflux, Gastrointestinal drugs, Omeprazole, Pharmacokinetics, loxicity This content is only available as a PDF. Copyright © 1993, American Society of Health-System Pharmacists, Inc. All rights reserved.
doi: 10.1093/ajhp/50.4_Suppl_1.S4pmid: N/A
Abstract The pathophysiology and diagnosis of gastroesophageal reflux disease (GERD) are discussed. GERD is a clinical syndrome involving the reflux of gastric contents into the esophagus. It is distinguished from the reflux that occurs normally in the general population. A low pressure exerted by the lower esophageal sphincter (LES) and inappropriate spontaneous relaxation of the LES may contribute to the development of GERD. Other possible contributory factors are increased intra-abdominal pressure and impaired esophageal clearance. The amount and concentration of refluxed gastric acid, proteolytic enzymes, and bile acids are among the determinants of the extent of esophageal injury. Heartburn is a specific symptom of GERD. Other symptoms include coughing, wheezing, hoarseness, epigastric pain, and regurgitation. Upper-GI roentgenography, endoscopy, biopsy, 24-hour ambulatory pH monitoring, and esophageal manometry have been used to diagnose and evaluate the disease. The complications of GERD are strictures, hemorrhaging, perforation, aspiration, and Barrett esophagus. The causes of GERD are incompletely understood, but low LES pressure seems important. GERD may lead to serious complications. A broad array of diagnostic approaches is available. Diagnosis, Gastroesophageal reflux, Roentgenography This content is only available as a PDF. Copyright © 1993, American Society of Health-System Pharmacists, Inc. All rights reserved.
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