American journal of health-system pharmacy : AJHP : official journal of the American Society of Health-System Pharmacists · 2005
Overview of pharmacologic agents for acid suppression in critically ill patients.
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Welage Lynda S
Аннотация
PURPOSE: The physiology of acid secretion, rationale and goals for acid suppression in critically ill patients, and mechanism of action, pharmacokinetics, pharmacodynamics, and safety of histamine H2-receptor antagonists (H2RAs) and proton pump inhibitors (PPIs) are discussed.
SUMMARY: Acid-suppressant therapy may be used in critically ill patients to prevent stress-related mucosal disease or the recurrence of peptic ulcer bleeding. The intragastric pH goal is 3.5-4.5 and 6 or higher, respectively. H2RAs block only one of three pathways in acid secretion and provide less potent acid suppression than PPIs, which block the final common pathway in acid secretion. In addition, tolerance that occurs with H2RAs does not occur with PPIs. All PPIs work in a similar manner, but differences exist in the pharmacokinetic profiles and binding to the proton pump; the clinical relevance of these differences remains debated. The safety profiles of H2RAs and PPIs are similar; however, the H2RA dose, but not the PPI dose, must be adjusted for patients with renal dysfunction. The risk of drug interactions mediated by cytochrome P-450 enzymes is lower with PPIs than with cimetidine, an H2RA. Several new PPI dosage forms have been introduced, facilitating drug administration in the critical care setting.
CONCLUSION: Both H2RAs and PPIs are safe agents to use for providing acid suppression in critically ill patients, but PPIs offer several potential advantages over H2RAs.
SUMMARY: Acid-suppressant therapy may be used in critically ill patients to prevent stress-related mucosal disease or the recurrence of peptic ulcer bleeding. The intragastric pH goal is 3.5-4.5 and 6 or higher, respectively. H2RAs block only one of three pathways in acid secretion and provide less potent acid suppression than PPIs, which block the final common pathway in acid secretion. In addition, tolerance that occurs with H2RAs does not occur with PPIs. All PPIs work in a similar manner, but differences exist in the pharmacokinetic profiles and binding to the proton pump; the clinical relevance of these differences remains debated. The safety profiles of H2RAs and PPIs are similar; however, the H2RA dose, but not the PPI dose, must be adjusted for patients with renal dysfunction. The risk of drug interactions mediated by cytochrome P-450 enzymes is lower with PPIs than with cimetidine, an H2RA. Several new PPI dosage forms have been introduced, facilitating drug administration in the critical care setting.
CONCLUSION: Both H2RAs and PPIs are safe agents to use for providing acid suppression in critically ill patients, but PPIs offer several potential advantages over H2RAs.