Discontinue prophylaxis once critical illness and modifiable risk factors have resolved (Rhodes 2017 Weinhouse 2019). ![]() ![]() Oral or via NG tube: 40 mg once daily (ASHP 1999 Levy 1997) or 40 mg initially, then another 40 mg dose given 6 to 8 hours later, followed by 40 mg once daily (Conrad 2005). Note: For ICU patients with associated risk factors for GI bleeding (including coagulopathy, mechanical ventilation for >48 hours, traumatic brain injury, history of GI ulceration or bleeding within past year, extensive burns) (Rhodes 2017 Weinhouse 2019). Stress ulcer prophylaxis in select critically ill patients (off-label use): Oral: 20 mg once daily (Chan 2001 Feldman 2019b Hawkey 1998 Yeomans 1998). Note: For select high-risk patients (eg, idiopathic ulcers, frequently recurrent ulcers, need for continued NSAID use). Maintenance therapy/secondary prevention (off-label use): The duration of treatment depends on the location and cause of the ulcer. For patients with bleeding, the dose may be decreased to 20 mg once daily 72 hours after endoscopy, provided there is no evidence of recurrent bleeding (Saltzman 2019). Oral (preferably following initial use of an IV PPI): 40 mg twice daily usually continued for 4 weeks, then decreased to 40 mg once daily (Vakil 2019c). In patients with refractory or recurrent disease, may increase the dose to 20 to 40 mg twice daily (Vakil 2019a Vakil 2019b).Ĭomplicated ulcer (bleeding, perforation, penetration, or gastric outlet obstruction) (off-label use): Oral: 20 to 40 mg once daily for 4 weeks for duodenal ulcers and 8 weeks for gastric ulcers. pylori–associated ulcers may not need PPI treatment beyond that included in the eradication regimen (Vakil 2019a). pylori infection should be treated first H. Note: For patients on NSAIDs (including aspirin), the NSAID should be discontinued, if possible (Feldman 2019b). Peptic ulcer disease, treatment and secondary prevention: Oral: 20 mg once daily for the duration of high-risk NSAID use (Bhatt 2010 Cullen 1998 Regula 2006). pylori infection should be treated first (ACG Feldman 2019a). Due to a potential drug-drug interaction with clopidogrel, the manufacturer and some experts recommend avoiding concurrent omeprazole use (Agewall 2013) however, some studies have not identified a clinically meaningful interaction (Bhatt 2010 Hulot 2010). For patients on dual antiplatelet therapy, some experts reserve prophylaxis for those with additional risk factors (ACCF/ACG/AHA ESC ). pylori infection) (Feldman 2019a Holmes 2019). These include patients with a history of GI ulcer, on dual antiplatelet therapy (eg, aspirin plus a P2Y 12 inhibitor), on concurrent anticoagulant therapy, or with multiple additional risk factors (eg, corticosteroid use, high nonsteroidal anti-inflammatory drug dose, H. ![]() Note: For select patients at moderate or high risk for GI toxicity. Nonsteroidal anti-inflammatory drug (including aspirin)–induced ulcers, primary prevention (off-label use): Dose depends on the selected regimen (ACG Crowe 2020 Fallone 2016). Oral: 20 mg or 40 mg twice daily as part of an appropriate combination regimen with antibiotics. Treatment of erosive esophagitis: Short-term treatment of erosive esophagitis (EE) due to acid-mediated gastroesophageal reflux disease (GERD) diagnosed by endoscopy in patients ≥1 year of age short-term treatment (up to 6 weeks) of EE due to acid-mediated GERD in pediatric patients 1 month to 14 days or more often than every 4 months unless directed by a physician (manufacturer's labeling). Gastroesophageal reflux disease, erosive or nonerosive (Rx only): Up to 72 hours 50% of maximum effect at 24 hours after stopping treatment, secretory activity gradually returns over 3 to 5 days Maximum secretory inhibition: 4 days Protein Binding Hepatic via CYP2C19 primarily and (to a lesser extent) via 3A4 to hydroxy, desmethyl, and sulfone metabolites (all inactive) saturable first-pass effect Onset of ActionĪntisecretory: ~1 hour Peak effect: Within 2 hours Duration of Action Proton pump inhibitor suppresses gastric basal and stimulated acid secretion by inhibiting the parietal cell H+/K+ ATP pump Pharmacokinetics/Pharmacodynamics Absorption
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