indication

For the treatment of acid-reflux disorders (GERD), peptic ulcer disease, H. pylori eradication, and prevention of gastroinetestinal bleeds with NSAID use.

pharmacology

Esomeprazole is a compound that inhibits gastric acid secretion and is indicated in the treatment of gastroesophageal reflux disease (GERD), the healing of erosive esophagitis, and H. pylori eradication to reduce the risk of duodenal ulcer recurrence. Esomeprazole belongs to a new class of antisecretory compounds, the substituted benzimidazoles, that do not exhibit anticholinergic or H2 histamine antagonistic properties, but that suppress gastric acid secretion by specific inhibition of the H⁺/K⁺ ATPase at the secretory surface of the gastric parietal cell. By doing so, it inhibits acid secretion into the gsatric lumen. This effect is dose-related and leads to inhibition of both basal and stimulated acid secretion irrespective of the stimulus.

mechanism of action

Esomeprazole is a proton pump inhibitor that suppresses gastric acid secretion by specific inhibition of the H⁺/K⁺-ATPase in the gastric parietal cell. By acting specifically on the proton pump, Esomeprazole blocks the final step in acid production, thus reducing gastric acidity.

toxicity

Blurred vision, confusion, drowsiness, dry mouth, flushing headache, nausea, rapid heartbeat, sweating

biotransformation

Mainly hepatic. Esomeprazole is completely metabolized by the cytochrome P450 system via CYP2C19 and CYP3A4. Metabolism produces inactive hydroxy and desmethyl metabolites, which have no effect on gastric acid secretion. Less than 1% of the parent drug is excreted in urine.

absorption

90%

half life

1-1.5 hours

route of elimination

Approximately 80% of the administered dose of esomeprazole is excreted as metabolites in urine and the remaining 20% is excreted in feces.

drug interactions

Atazanavir: This gastric pH modifier decreases the levels/effects of atazanavir

Cefditoren: Proton pump inhibitors such as esomeprazole may decrease the serum concentration of cefditoren. If possible, avoid use of cefditoren with proton pump inhibitors (PPIs). Consider alternative methods to minimize/control acid reflux (eg, diet modification) or alternative antimicrobial therapy if use of PPIs can not be avoided.

Clopidogrel: Esomeprazole may decrease serum concentrations of the active metabolite(s) of clopidogrel. Due to the possible risk for impaired clopidogrel effectiveness with this combination, clinicians should carefully consider the need for concurrent esomeprazole therapy in patients receiving clopidogrel. Monitor response to clopidogrel closely when using clopidogrel with esomeprazole. Whether there are differences among individual proton pump inhibitors is unclear. Other acid-lowering therapies (e.g., H2-receptor antagonists, antacids, etc.) do not appear to share this interaction with clopidogrel.

Enoxacin: Esomeprazole may decrease the absorption of enoxacin.

Indinavir: Omeprazole decreases the absorption of indinavir

Itraconazole: The proton pump inhibitor, esomeprazole, may decrease the absorption of itraconazole.

Ketoconazole: The proton pump inhibitor, esomeprazole, may decrease the absorption of ketoconazole.

Tipranavir: Tipranavir, co-administered with Ritonavir, may decrease the plasma concentration of Esomeprazole. Consider alternate therapy or increase the dose of Esomeprazole based on the therapeutic response.