|
This information has been developed and provided by an independent third-party source. Merck & Co., Inc. does not endorse and is not responsible for the accuracy of the content, or for practices or
standards of non-Merck sources.
Special Alerts
Possible Increased Risk of Fractures (Hip, Wrist, and Spine) with Proton Pump Inhibitor (PPI) Use (Update)
March 2011
The U.S. Food and Drug Administration (FDA) has announced that over-the-counter (OTC) labeling for proton pump inhibitors (PPI) will not be required to carry an osteoporosis or fracture warning at this time. In May 2010, the FDA had revised all prescription and OTC labels for PPIs with information regarding an increase in the risk of fractures (hip, wrist, and spine) based on several epidemiologic studies. The greatest risk for these fractures was in patients who received high doses or used them for ≥1 year. The majority of the patients in the epidemiologic studies were ≥50 years of age with the risk of fractures being limited to this age group. The FDA has now concluded that short-term, low dose PPI use is unlikely to increase fracture risk.
The FDA has recommended that healthcare providers continue to prescribe, and patients continue to use these products as described within their labeling. In addition, healthcare providers should consider whether a lower dose or shorter duration of therapy would adequately treat the patient's condition. Patients who continue to receive PPIs and who are at risk for osteoporosis, should receive vitamin D and calcium supplementation and have their bone status monitored and managed according to current practice standards. Patients should not stop taking their proton pump inhibitor unless told to do so by their healthcare provider.
For more information, U.S. healthcare professionals may refer to the following websites:
http://www.fda.gov/Drugs/DrugSafety/PostmarketDrugSafetyInformationforPatientsandProviders/ucm213206.htm
http://www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm213321.htm
Proton Pump Inhibitors (PPIs): Long-term Use May be Associated With Hypomagnesemia
March 2011
The U.S. Food and Drug Administration (FDA) is notifying healthcare providers and patients that long-term use of proton pump inhibitors (PPIs) may be associated with hypomagnesemia. Some of the reported cases of hypomagnesemia occurred after 3 months of use, but most occurred in patients using PPIs for longer than 1 year. The mechanism for this adverse effect is not clearly defined.
Healthcare providers should consider obtaining serum magnesium levels prior to beginning long-term PPI therapy, especially in patients taking concomitant digoxin, diuretics, or other drugs known to cause hypomagnesemia; and periodically thereafter. Although magnesium supplementation may correct hypomagnesemia, discontinuation of the PPI may be necessary to correct and maintain normal magnesium levels. Typically, according to the case reports, magnesium levels returned to normal within 1 week of stopping the PPI. Hypomagnesemia can cause serious adverse events including tetany, tremors, seizures, QT prolongation, and cardiac arrhythmias. Patients should not stop PPI therapy without first discussing with a healthcare professional.
The FDA is requiring all manufacturers of prescription PPI products to update the package labeling to include the potential risk of hypomagnesemia. Since OTC PPIs are only approved for short-term use, the package labeling for these products will not be updated. However, healthcare professionals should be aware of the risk of hypomagnesemia if OTC PPIs are used longer than the approved use.
For additional information, please refer to http://www.fda.gov/Drugs/DrugSafety/ucm245011.htm.
Statement Released Regarding Clopidogrel-Proton Pump Inhibitor (PPI) Interaction
November 2010
The American College of Cardiology Foundation, in conjunction with the American College of Gastroenterology and the American Heart Association, has issued a consensus document regarding the concomitant use of PPIs and thienopyridines, specifically clopidogrel.
The following highlighted recommendations are discussed within this consensus statement:
- Clopidogrel alone, aspirin alone, and their combination are associated with an increased risk of GI bleeding.
- Risk of GI bleeding increases as the number of risk factors increase (eg, prior GI bleeding, advanced age, concurrent use of anticoagulants).
- PPIs are appropriate in patients with multiple risk factors for GI bleeding who are also receiving antiplatelet therapy (eg, clopidogrel).
- Although pharmacokinetic and pharmacodynamic studies have demonstrated varying effects of PPIs on the extent of clopidogrel metabolic conversion to the active metabolite, no evidence has established clinically meaningful differences in outcomes.
- A clinically-significant interaction cannot be excluded in subgroups who are poor metabolizers of clopidogrel.
- Until solid evidence exists to support staggering PPIs with clopidogrel, the dosing of PPIs should not be altered.
Healthcare professionals must evaluate the risks and benefits of concomitant use of PPIs and thienopyridines, considering both the cardiovascular and GI complications. For more information, healthcare professionals may refer to the following website: http://content.onlinejacc.org/cgi/reprint/j.jacc.2010.09.010v1.pdf
Pronunciation
(oh MEP ra zole)
Generic Available (U.S.)
Yes: Excludes granules for suspension
Index Terms
U.S. Brand Names
Canadian Brand Names
Pharmacologic Category
Pharmacologic Category Synonyms
Use: Labeled Indications
Short-term (4-8 weeks) treatment of active duodenal ulcer disease or active benign gastric ulcer; treatment of heartburn and other symptoms associated with gastroesophageal reflux disease (GERD); short-term (4-8 weeks) treatment of endoscopically-diagnosed erosive esophagitis; maintenance healing of erosive esophagitis; long-term treatment of pathological hypersecretory conditions; as part of a multidrug regimen for H. pylori eradication to reduce the risk of duodenal ulcer recurrence
OTC labeling: Short-term treatment of frequent, uncomplicated heartburn occurring ≥2 days/week
Use: Unlabeled/Investigational
Healing NSAID-induced ulcers; prevention of NSAID-induced ulcer; stress-ulcer prophylaxis in the critically-ill
Pregnancy Risk Factor
C
Pregnancy Considerations
Adverse events were observed in some animal reproduction studies. Based on data collected by the Teratogen Information System (TERIS), it was concluded that therapeutic doses used during pregnancy would be unlikely to pose a substantial teratogenic risk (quantity/quality of data: fair). Because the possibility of harm still exists, the manufacturer recommends use during pregnancy only if the potential benefit to the mother outweighs the possible risk to the fetus.
Lactation
Enters breast milk/not recommended
Breast-Feeding Considerations
Following administration of omeprazole 20 mg, peak concentrations detected in the breast milk were <7% of the maternal serum concentration.
Contraindications
Hypersensitivity to omeprazole, substituted benzimidazoles (eg, esomeprazole, lansoprazole), or any component of the formulation
Warnings/Precautions
Concerns related to adverse effects:
• Atrophic gastritis: Long-term omeprazole therapy has caused atrophic gastritis (identified by biopsy).
• Carcinoma: In long-term (2-year) studies in rats, omeprazole produced a dose-related increase in gastric carcinoid tumors. While available endoscopic evaluations and histologic examinations of biopsy specimens from human stomachs have not detected a risk from short-term exposure to omeprazole, further human data on the effect of sustained hypochlorhydria and hypergastrinemia are needed to rule out the possibility of an increased risk for the development of tumors in humans receiving long-term therapy.
• Fractures: Increased incidence of osteoporosis-related bone fractures of the hip, spine, or wrist may occur with proton pump inhibitor therapy. Patients on high-dose (multiple daily doses)or long-term (≥1 year) therapy should be monitored. Use the lowest effective dose for the shortest duration of time, use vitamin D and calcium supplementation, and follow appropriate guidelines to reduce risk of fractures in patients at risk.
Disease-related concerns:
• Gastric malignancy: Relief of symptoms does not preclude the presence of a gastric malignancy.
• Gastrointestinal infection (eg, Salmonella, Campylobacter): Use of proton pump inhibitors may increase risk of these infections.
• Hepatic impairment: Bioavailability may be increased in patients with hepatic dysfunction; consider dosage reductions, especially for maintenance healing of erosive esophagitis.
Concurrent drug therapy issues:
• Clopidogrel: Proton pump inhibitors may diminish the therapeutic effect of clopidogrel, thought to be due to reduced formation of the active metabolite of clopidogrel; an increase in the risk of cardiovascular events may occur. The manufacturer of clopidogrel recommends avoidance of concomitant administration of omeprazole even when scheduled 12 hours apart.
Special populations:
• Asian ethnicity: Bioavailability may be increased in patients of Asian descent; consider dosage reductions, especially for maintenance healing of erosive esophagitis.
• Elderly: Bioavailability may be increased in the elderly.
Other warnings/precautions:
• Appropriate use: Helicobacter pylori eradication: Short-term combination therapy (≤7 days) has been associated with a higher incidence of treatment failure. The American College of Gastroenterology recommends 10-14 days of therapy (triple or quadruple) for eradication of H. pylori (Chey, 2007).
• Self-medication (OTC use): When used for self-medication (OTC), do not use for >14 days; treatment should not be repeated more often than every 4 months.
Adverse Reactions
1% to 10%:
Central nervous system: Headache (7%), dizziness (2%)
Dermatologic: Rash (2%)
Gastrointestinal: Abdominal pain (5%), diarrhea (4%), nausea (4%), vomiting (3%), flatulence (3%), acid regurgitation (2%), constipation (2%)
Neuromuscular & skeletal: Back pain (1%), weakness (1%)
Respiratory: Upper respiratory infection (2%), cough (1%)
≤1%, postmarketing, and/or case reports (adverse event occurrence may vary based on formulation): Abdominal swelling, abnormal dreams, aggression, agitation, agranulocytosis, alkaline phosphatase increased, allergic reactions, alopecia, ALT increased, anaphylaxis, anemia, angina, angioedema, anorexia, anxiety, apathy, AST increased, atrophic gastritis, benign gastric polyps, bilirubin increased, blurred vision, bradycardia, bronchospasm, chest pain, cholestatic hepatitis, confusion, creatinine increased, depression, double vision, dry skin, epistaxis, erythema multiforme, esophageal candidiasis, fatigue, fecal discoloration, fever, fracture, gastroduodenal carcinoids, GGT increased, glycosuria, gynecomastia, hallucinations, hematuria, hemolytic anemia, hepatic encephalopathy, hepatic failure, hepatic necrosis, hepatitis, hepatocellular hepatitis, hyperhidrosis, hypersensitivity, hypertension, hypoglycemia, hyponatremia, insomnia, interstitial nephritis, irritable colon, jaundice, joint pain, leg pain, leukocytosis, leukopenia, liver disease (hepatocellular, cholestatic, mixed), malaise, microscopic pyuria, mucosal atrophy (tongue), muscle cramps, muscle weakness, myalgia, nervousness, neutropenia, ocular irritation, optic atrophy, optic neuritis, optic neuropathy (anterior ischemic), osteoporosis-related fracture, pain, palpitation, pancreatitis, pancytopenia, paresthesia, peripheral edema, petechiae, pharyngeal pain, photosensitivity, proteinuria, pruritus, psychiatric disturbance, purpura, skin inflammation, sleep disturbance, somnolence, Stevens-Johnson syndrome, stomatitis, tachycardia, taste perversion, testicular pain, thrombocytopenia, tinnitus, toxic epidermal necrolysis, tremor, urinary frequency, urinary tract infection, urticaria, vertigo, weight gain, xerophthalmia, xerostomia
Metabolism/Transport Effects
Substrate of CYP2A6 (minor), 2C9 (minor), 2C19 (major), 2D6 (minor), 3A4 (major); Inhibits CYP1A2 (weak), 2C9 (moderate), 2C19 (moderate), 2D6 (weak), 3A4 (weak); Induces CYP1A2 (weak)
Drug Interactions
Amphetamines: Proton Pump Inhibitors may increase the serum concentration of Amphetamines. Specifically, data indicate that Proton Pump Inhibitors may increase the rate at which Amphetamines are absorbed. Total exposure to Amphetamines is not significantly changed. Risk C: Monitor therapy
Atazanavir: Proton Pump Inhibitors may decrease the serum concentration of Atazanavir. Management: Avoid concurrent PPI in HIV treatment-experienced patients. For treatment-naive patients, atazanavir/ritonavir dose should be given approximately 12 hours after the PPI, and the PPI should not exceed the equivalent of 20 mg omeprazole. Risk D: Consider therapy modification
Benzodiazepines (metabolized by oxidation): Proton Pump Inhibitors may increase the serum concentration of Benzodiazepines (metabolized by oxidation). Risk C: Monitor therapy
Bisphosphonate Derivatives: Proton Pump Inhibitors may diminish the therapeutic effect of Bisphosphonate Derivatives. Risk C: Monitor therapy
Carvedilol: CYP2C9 Inhibitors (Moderate) may increase the serum concentration of Carvedilol. Specifically, concentrations of the S-carvedilol enantiomer may be increased. Risk C: Monitor therapy
Cefditoren: Proton Pump Inhibitors may decrease the serum concentration of Cefditoren. Management: 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. Risk D: Consider therapy modification
Cilostazol: Omeprazole may enhance the adverse/toxic effect of Cilostazol. Omeprazole may increase the serum concentration of Cilostazol. Omeprazole may increase the serum concentration of OPC-13015, an active metabolite of Cilostazol. Management: Monitor for increased effects of cilostazol when coadministered with omeprazole. Consider a 50% dose reduction of cilostazol (eg, 100 mg twice daily to 50 mg twice daily) with concomitant use of these agents. Risk D: Consider therapy modification
Clopidogrel: Omeprazole may decrease serum concentrations of the active metabolite(s) of Clopidogrel. Risk X: Avoid combination
CloZAPine: Omeprazole may decrease the serum concentration of CloZAPine. Omeprazole may increase the serum concentration of CloZAPine. Risk C: Monitor therapy
Conivaptan: May increase the serum concentration of CYP3A4 Substrates. Management: Upon completion/discontinuation of conivaptan, allow at least 7 days before initiating therapy with drugs that are CYP3A4 substrates. Risk D: Consider therapy modification
CycloSPORINE: Omeprazole may increase the serum concentration of CycloSPORINE. Risk C: Monitor therapy
CycloSPORINE (Systemic): Omeprazole may increase the serum concentration of CycloSPORINE (Systemic). Risk C: Monitor therapy
CYP2C19 Inducers (Strong): May increase the metabolism of CYP2C19 Substrates. Risk C: Monitor therapy
CYP2C19 Substrates: CYP2C19 Inhibitors (Moderate) may decrease the metabolism of CYP2C19 Substrates. Risk C: Monitor therapy
CYP2C9 Substrates (High risk): CYP2C9 Inhibitors (Moderate) may decrease the metabolism of CYP2C9 Substrates (High risk). Risk C: Monitor therapy
Dabigatran Etexilate: Proton Pump Inhibitors may decrease serum concentrations of the active metabolite(s) of Dabigatran Etexilate. Risk C: Monitor therapy
Dasatinib: Proton Pump Inhibitors may decrease the absorption of Dasatinib. Risk D: Consider therapy modification
Delavirdine: Proton Pump Inhibitors may decrease the serum concentration of Delavirdine. Management: Chronic therapy with proton pump inhibitors (PPIs) should be avoided in patients treated with delavirdine. The clinical significance of short-term PPI therapy with delavirdine is uncertain, but such therapy should be undertaken with caution. Risk X: Avoid combination
Dexmethylphenidate: Proton Pump Inhibitors may increase the absorption of Dexmethylphenidate. Specifically, proton pump inhibitors may interfere with the normal release of drug from the extended-release capsules (Focalin XR brand), which could result in both increased absorption (early) and decreased delayed absorption. Risk C: Monitor therapy
Erlotinib: Proton Pump Inhibitors may decrease the serum concentration of Erlotinib. Risk X: Avoid combination
Fluconazole: May increase the serum concentration of Proton Pump Inhibitors. Risk C: Monitor therapy
Fosphenytoin: Proton Pump Inhibitors may increase the serum concentration of Fosphenytoin. Risk C: Monitor therapy
Gefitinib: Proton Pump Inhibitors may decrease the serum concentration of Gefitinib. Risk C: Monitor therapy
Indinavir: Proton Pump Inhibitors may decrease the serum concentration of Indinavir. Risk C: Monitor therapy
Iron Salts: Proton Pump Inhibitors may decrease the absorption of Iron Salts. Exceptions: Ferric Gluconate; Ferumoxytol; Iron Dextran Complex; Iron Sucrose. Risk C: Monitor therapy
Itraconazole: Proton Pump Inhibitors may decrease the serum concentration of Itraconazole. Risk D: Consider therapy modification
Ketoconazole: Proton Pump Inhibitors may decrease the serum concentration of Ketoconazole. Ketoconazole may increase the serum concentration of Proton Pump Inhibitors. Risk D: Consider therapy modification
Ketoconazole (Systemic): Proton Pump Inhibitors may decrease the serum concentration of Ketoconazole (Systemic). Ketoconazole (Systemic) may increase the serum concentration of Proton Pump Inhibitors. Risk D: Consider therapy modification
Mesalamine: Proton Pump Inhibitors may diminish the therapeutic effect of Mesalamine. Proton pump inhibitor-mediated increases in gastrointestinal pH may cause the premature release of mesalamine from specific sustained-release mesalamine products. Management: Consider avoiding concurrent administration of high-dose proton pump inhibitors (PPIs) with sustained-release mesalamine products. Risk D: Consider therapy modification
Methotrexate: Proton Pump Inhibitors may decrease the excretion of Methotrexate. Antirheumatic doses of methotrexate probably hold minimal risk. Risk C: Monitor therapy
Methylphenidate: Proton Pump Inhibitors may increase the absorption of Methylphenidate. Specifically, proton pump inhibitors may interfere with the normal release of drug from the extended-release capsules (Ritalin LA brand), which could result in both increased absorption (early) and decreased delayed absorption. Risk C: Monitor therapy
Mycophenolate: Proton Pump Inhibitors may decrease the serum concentration of Mycophenolate. Specifically, concentrations of the active mycophenolic acid may be reduced. Risk C: Monitor therapy
Nelfinavir: Proton Pump Inhibitors may decrease serum concentrations of the active metabolite(s) of Nelfinavir. Proton Pump Inhibitors may decrease the serum concentration of Nelfinavir. Risk X: Avoid combination
Peginterferon Alfa-2b: May decrease the serum concentration of CYP2D6 Substrates. Risk C: Monitor therapy
Phenytoin: Proton Pump Inhibitors may increase the serum concentration of Phenytoin. Risk C: Monitor therapy
Posaconazole: Proton Pump Inhibitors may decrease the serum concentration of Posaconazole. Risk X: Avoid combination
Raltegravir: Proton Pump Inhibitors may increase the serum concentration of Raltegravir. Risk C: Monitor therapy
Saquinavir: Proton Pump Inhibitors may increase the serum concentration of Saquinavir. Risk C: Monitor therapy
Tacrolimus: Proton Pump Inhibitors may increase the serum concentration of Tacrolimus. Management: Tacrolimus dose adjustment may be required. Rabeprazole, pantoprazole, or selected H2-receptor antagonists (i.e., ranitidine or famotidine) may be less likely to interact. Genetic testing may predict patients at highest risk. Risk D: Consider therapy modification
Tacrolimus (Systemic): Proton Pump Inhibitors may increase the serum concentration of Tacrolimus (Systemic). Management: Tacrolimus dose adjustment may be required. Rabeprazole, pantoprazole, or selected H2-receptor antagonists (i.e., ranitidine or famotidine) may be less likely to interact. Genetic testing may predict patients at highest risk. Risk D: Consider therapy modification
Tipranavir: May decrease the serum concentration of Proton Pump Inhibitors. These data are derived from studies with Ritonavir-boosted Tipranavir. Risk C: Monitor therapy
Tocilizumab: May decrease the serum concentration of CYP3A4 Substrates. Risk C: Monitor therapy
Vitamin K Antagonists (eg, warfarin): Omeprazole may increase the serum concentration of Vitamin K Antagonists. Risk C: Monitor therapy
Voriconazole: Proton Pump Inhibitors may increase the serum concentration of Voriconazole. Risk C: Monitor therapy
Ethanol/Nutrition/Herb Interactions
Ethanol: Avoid ethanol (may cause gastric mucosal irritation).
Food: Food delays absorption.
Storage
Capsules, tablets: Store at 15°C to 30°C (59°F to 86°F). Protect from light and moisture.
Granules for oral suspension: Store at 25°C (77°F); excursions permitted to 15°C to 30°C (59°F to 86°F).
Reconstitution
Granules for oral suspension: For oral administration, empty the contents of the 2.5 mg packet into 5 mL of water (10 mg packet into 15 mL of water); stir. For NG administration, add 5 mL of water into a catheter-tipped syringe, and then add the contents of a 2.5 mg packet (15 mL water for the 10 mg packet); shake. Note: Regardless of the route of administration, the suspension should be left to thicken for 2-3 minutes prior to administration.
Mechanism of Action
Proton pump inhibitor; suppresses gastric basal and stimulated acid secretion by inhibiting the parietal cell H+/K+ ATP pump
Pharmacodynamics/Kinetics
Onset of action: Antisecretory: ~1 hour
Peak effect: Within 2 hours
Duration: Up to 72 hours; 50% of maximum effect at 24 hours; after stopping treatment, secretory activity gradually returns over 3-5 days
Absorption: Rapid
Protein binding: ~95%
Metabolism: Hepatic via CYP2C19 primarily and (to a lesser extent) via 3A4 to hydroxy, desmethyl, and sulfone metabolites (all inactive); saturable first-pass effect
Bioavailability: Oral: ~30% to 40%; increased in Asian patients, elderly patients, and patients with hepatic dysfunction
Half-life elimination: 0.5-1 hour; hepatic impairment: ~3 hours
Time to peak, plasma: 0.5-3.5 hours
Excretion: Urine (~77% as metabolites, very small amount as unchanged drug); feces
Dosage
Oral:
Children 1-16 years: GERD or other acid-related disorders:
5 kg to <10 kg: 5 mg once daily
10 kg to <20 kg: 10 mg once daily
≥20 kg: 20 mg once daily
Adults:
Active duodenal ulcer: 20 mg once daily for 4-8 weeks
Gastric ulcers: 40 mg once daily for 4-8 weeks
Symptomatic GERD (without esophageal lesions): 20 mg once daily for up to 4 weeks
Erosive esophagitis: 20 mg once daily for 4-8 weeks; maintenance of healing: 20 mg once daily for up to 12 months total therapy (including treatment period of 4-8 weeks)
Helicobacter pylori eradication: Dose varies with regimen:
Manufacturer labeling: 40 mg once daily administered with clarithromycin 500 mg 3 times/day for 14 days or 20 mg twice daily administered with amoxicillin 1000 mg and clarithromycin 500 mg twice daily for 10 days. Note: Presence of ulcer at time of therapy initiation may necessitate an additional 14-18 days of omeprazole 20 mg/day (monotherapy) after completion of combination therapy.
American College of Gastroenterology guidelines (Chey, 2007):
Nonpenicillin allergy: 20 mg twice daily administered with amoxicillin 1000 mg and clarithromycin 500 mg twice daily for 10-14 days
Penicillin allergy: 20 mg twice daily administered with clarithromycin 500 mg and metronidazole 500 mg twice daily for 10-14 days or 20 mg once or twice daily administered with bismuth subsalicylate 525 mg and metronidazole 250 mg plus tetracycline 500 mg 4 times/day for 10-14 days
Pathological hypersecretory conditions: Initial: 60 mg once daily; doses up to 120 mg 3 times/day have been administered; administer daily doses >80 mg in divided doses
Stress-ulcer prophylaxis (ICU patients; unlabeled use): 40 mg once daily; periodically evaluate patient for continued need (Levy, 1997)
Frequent heartburn (OTC labeling): 20 mg once daily for 14 days; treatment may be repeated after 4 months if needed
Dosage adjustment in hepatic impairment: Bioavailability is increased with chronic liver disease. Consider dosage adjustment, especially for maintenance of erosive esophagitis. Specific guidelines are not available.
Administration: Oral
Best if administered before breakfast.
Capsule: Should be swallowed whole; do not chew or crush. Delayed release capsule may be opened and contents added to 1 tablespoon of applesauce (use immediately after adding to applesauce); mixture should not be chewed or warmed.
Oral suspension: Following reconstitution, the suspension should be left to thicken for 2-3 minutes and administered within 30 minutes. If any material remains after administration, add more water, stir, and administer immediately.
Tablet: Should be swallowed whole; do not crush or chew.
Administration: Other
Nasogastric/orogastric (NG/OG) tube administration:
Capsule: When using capsules to extemporaneously prepare a solution for NG/OG administration, the manufacturers of Prilosec® recommend the use of an acidic juice for preparation and administration. Alternative methods have been described as follows:
NG/OG tube administration for the prevention of stress-related mucosal damage in ventilated, critically-ill patients:
Study 1 (Phillips, 1996): Pour the contents of one or two 20 mg omeprazole delayed release capsules (depending on the dose) into a syringe (after removing plunger); withdraw 10-20 mL of an 8.4% sodium bicarbonate solution into the syringe; allow 30 minutes for the enteric-coated omeprazole granules to break down. Shake the resulting milky substance prior to administration. Flush the NG tube with 5-10 mL of water and clamp for at least 1 hour.
Study 2 (Balaban, 1997): Open the omeprazole delayed release capsule (20 mg or 40 mg), then pour the intact granules into a container holding 30 mL of water. Pour one-third to one-half of the granules into a 30 mL syringe (with the plunger removed) attached to a nasogastric tube (NG). Replace the plunger with 1 cm of air between the granules and the plunger top while the plunger is depressed. Repeat this process until all the granules are flushed, then flush a final 15 mL of water through the tube.
Oral suspension: Following reconstitution in a catheter-tipped syringe, shake the suspension well and leave to thicken for 2-3 minutes. Administer within 30 minutes of reconstitution. Use an NG tube or gastric tube that is a size 6 French or larger; flush the syringe and tube with water.
Dietary Considerations
Should be taken on an empty stomach; best if taken before breakfast.
Patient Education
Take before eating. Do not crush or chew capsules. Delayed release capsule may be opened and contents added to applesauce. Avoid alcohol. You may experience anorexia; small frequent meals may help to maintain adequate nutrition. Report severe headache, unresolved severe diarrhea, or abdominal pain.
Geriatric Considerations
In clinical trials, the incidence of side effects in the elderly is no different than that of younger adults (≤65 years) despite slight decrease in elimination and increase in bioavailability. Bioavailability may be increased in the elderly (≥65 years of age), however, dosage adjustments are not necessary.
An increased risk of fractures of the hip, spine, or wrist has been observed in epidemiologic studies with proton pump inhibitor (PPI) use, primarily in older adults ≥50 years of age. The greatest risk was seen in patients receiving high doses or on long-term therapy (≥1 year). Calcium and vitamin D supplementation and close monitoring are recommended to reduce the risk of fracture in high-risk patients.
Anesthesia and Critical Care Concerns/Other Considerations
Evidence-Based Information: The 2008 Surviving Sepsis Campaign guidelines recommend that stress ulcer prophylaxis using an H2 blocker (Grade 1A) or proton pump inhibitor (Grade 1B) be given to patients with severe sepsis to prevent upper GI bleed. Benefit of prevention of upper GI bleed must be weighed against potential effect of increased stomach pH on development of ventilator-associated pneumonia.
Dental Health: Effects on Dental Treatment
Key adverse event(s) related to dental treatment: Taste perversion, dry mouth, esophageal candidiasis, and mucosal atrophy (tongue).
Dental Health: Vasoconstrictor/Local Anesthetic Precautions
No information available to require special precautions
Mental Health: Effects on Mental Status
May cause dizziness, agitation, aggression, depression, confusion, insomnia, nervousness, anxiety, or hallucinations; may rarely cause sedation
Mental Health: Effects on Psychiatric Treatment
May inhibit the metabolism of diazepam; monitor for increased sedation
Nursing: Physical Assessment/Monitoring
For patients at risk of osteoporosis-related fractures, optimize preventive measures and limit high-dose, prolonged therapy if possible.
Dosage Forms
Excipient information presented when available (limited, particularly for generics); consult specific product labeling.
Capsule, delayed release, oral: 10 mg, 20 mg, 40 mg
PriLOSEC®: 10 mg, 20 mg, 40 mg
Granules for suspension, delayed release, oral:
PriLOSEC®: 2.5 mg/packet (30s); 10 mg/packet (30s)
Tablet, delayed release, oral: 20 mg
PriLOSEC OTC®: 20 mg
Pricing: U.S. (www.drugstore.com)
Capsule, delayed release (Omeprazole)
10 mg (30): $34.36
Capsule, delayed release (PriLOSEC)
10 mg (30): $159.99
20 mg (30): $195.99
40 mg (30): $278.98
Tablet, EC (Omeprazole)
20 mg (14): $19.99
20 mg (28): $25.99
Tablet, EC (PriLOSEC OTC)
20 mg (14): $21.99
Extemporaneously Prepared
A 2 mg/mL oral omeprazole solution (Simplified Omeprazole Solution) may be made with five omeprazole 20 mg delayed release capsules and 50 mL sodium bicarbonate 8.4%. Empty capsules into beaker. Add sodium bicarbonate solution. Gently stir (about 15 minutes) until a white suspension forms. Transfer to amber-colored syringe or bottle. Stable for 14 days at room temperature or for 30 days refrigerated.
DiGiacinto JL, Olsen KM, Bergman KL, et al, “Stability of Suspension Formulations of Lansoprazole and Omeprazole Stored in Amber-Colored Plastic Oral Syringes,” Ann Pharmacother, 2000, 34(5):600-5.
Quercia R, Fan C, Liu X, et al, “Stability of Omeprazole in an Extemporaneously Prepared Oral Liquid,” Am J Health Syst Pharm, 1997, 54(16):1833-6.
Sharma V, “Comparison of 24-hour Intragastric pH Using Four Liquid Formulations of Lansoprazole and Omeprazole,” Am J Health Syst Pharm, 1999, 56(23 Suppl 4):18-21.
References
Andersson T, “Omeprazole Drug Interaction Studies,” Clin Pharmacokinet, 1991, 21(3):195-212.
Andersson T, Hasan-Alin M, Hasselgren G, et al, “Drug Interactions Studies With Esomeprazole, the (S)-Isomer of Omeprazole,” Clin Pharmacokinet, 2001, 40(7):523-37.
Balaban DH, Duckworth CW, and Peura DA, "Nasogastric Omeprazole: Effects on Gastric pH in Critically Ill Patients," Am J Gastroenterol, 1997, 92(1):79-83.
Balian JD, Sukhova N, Harris JW, et al, “The Hydroxylation of Omeprazole Correlates With S-Mephenytoin Metabolism: A Population Study,” Clin Pharmacol Ther, 1995, 57(6):662-9.
Berardi RR and Dunn-Kucharski VA, “Omeprazole: Defining Its Role in Gastroesophageal Reflux Disease,” Hosp Formul, 1995, 30:216-25.
Beutler M, Hartmann K, Kuhn M, et al, “Arthralgias on Omeprazole,” BMJ, 1994, 309(6969):1620.
Blume H, Donath F, Warnke A, et al, “Pharmacokinetic Drug Interaction Profiles of Proton Pump Inhibitors,” Drug Saf, 2006, 29(9): 769-84.
Broussard CN and Richter JE, “Treating Gastro-oesophageal Reflux Disease During Pregnancy and Lactation: What Are the Safest Therapy Options?” Drug Saf, 1998, 19(4):325-37.
Carvajal A and Martin Arias LH, “Gynecomastia and Sexual Disorders After the Administration of Omeprazole,” Am J Gastroenterol, 1995, 90(6):1028-9.
Chey WD, Wong BC, et al, “American College of Gastroenterology Guideline on the Management of Helicobacter pylori Infection,” Am J Gastroent, 2007, 102(8):1808-25.
Cockayne SE, Glet RJ, Gawkrodger DJ, et al, “Severe Erythrodermic Reactions to the Proton Pump Inhibitors Omeprazole and Lansoprazole,” Br J Dermatol, 1999, 141(1):173-5.
Dellinger RP, Levy MM, Carlet JM, et al, “Surviving Sepsis Campaign: International Guidelines for Management of Severe Sepsis and Septic Shock: 2008,” [published correction appears in Crit Care Med, 2008, 36(4):1394-6], Crit Care Med, 2008, 36(1):296-327.
Epelde Gonzalo FD, Boada Montagut L, and Tomas Vecina S, “Exfoliative Dermatitis Related to Omeprazole,” Ann Pharmacother, 1995, 29(1):82-3.
Gunasekaran TS and Hassall EG, “Efficacy and Safety of Omeprazole for Severe Gastroesophageal Reflux in Children,” J Pediatr, 1993, 123(1):148-54.
Kahrilas PJ, Shaheen NJ, Vaezi MF, et al, “American Gastroenterological Association Medical Position Statement on the Management of Gastroesophageal Reflux Disease,” Gastroenterology, 2008, 135(4):1383-91.
Kane DL, “Administration of Omeprazole (Prilosec®) in the Atypical Patient,” Int J Pharm Compounding, 1997, 1(1):13.
Kato S, Ebina K, Fujii K, et al, “Effect of Omeprazole in the Treatment of Refractory Acid-Related Diseases in Childhood: Endoscopic Healing and Twenty-Four Hour Intragastric Acidity,” J Pediatr, 1996, 128(3):415-21.
Kraus A and Flores-Suarez LF, “Acute Gout Associated With Omeprazole,” Lancet, 1995, 345(8947):461-2.
Larner AJ and Lendrum R, “Oesophageal Candidiasis After Omeprazole Therapy,” Gut, 1992, 33(6):860-1.
Lau JY, Sung JJ, Lee KK, et al, “Effect of Intravenous Omeprazole on Recurrent Bleeding After Endoscopic Treatment of Bleeding Peptic Ulcers,” N Engl J Med, 2000, 343(5):310-6.
Levy MJ, Seelig CB, Robinson NJ, et al, “Comparison of Omeprazole and Ranitidine for Stress Ulcer Prophylaxis,” Dig Dis Sci, 1997, 42(6):1255-59.
Lindquist M and Edwards IR, “Endocrine Adverse Effects of Omeprazole,” BMJ, 1992, 305(6851):451-2.
Natsch S, Vinks MH, Voogt AK, et al, “Anaphylactic Reactions to Proton-Pump Inhibitors,” Ann Pharmacother, 2000, 34(4):474-6.
Ottervanger JP, Stricker BH, Kappelle JW, et al, “Omeprazole-Associated Agranulocytosis,” Eur J Haematol, 1995, 54(4):279-80.
Paoluzi P, Iacopini F, Crispino P, et al, “2-Week Triple Therapy for Helicobacter pylori Infection is Better Than 1-Week in Clinical Practice: A Large Prospective Single-Center Randomized Study,” Helicobacter, 2006, 11(6):562-8.
Phillips JO, Metzler MH, Palmieri MT, et al, "A Prospective Study of Simplified Omeprazole Suspension for the Prophylaxis of Stress-Related Mucosal Damage," Crit Care Med, 1996, 24(11):1793-800
Soll AH, Weinstein WM, Kurata J, et al, “Nonsteroidal Anti-inflammatory Drugs and Peptic Ulcer Disease,” Ann Intern Med, 1991, 114(4):307-19.
Talley NJ and Vakil N, “Practice Parameters Committee of the American College of Gastroenterology. Guidelines for the Management of Dyspepsia,” Am J Gastroenterol, 2005, 100(10):2324-37.
Wolfe MM and Sachs G, “Acid Suppression: Optimizing Therapy for Gastroduodenal Ulcer Healing, Gastroesophageal Reflux Disease, and Stress-Related Erosive Syndrome,” Gastroenterology, 2000, 118(2 Suppl 1):9-31.
Woods DJ and McClintock AD, “Omeprazole Administration,” Ann Pharmacother, 1993, 27(5):651.
International Brand Names
Lexi-Comp.com
Last full review/revision May 2011
Content last modified May 2011
| 
