Omeppi (omeprazole/sodium bicarbonate)

Dosage of omeprazole magnesium is expressed in terms of omeprazole.

Antacids are administered orally. The dose of antacids should be expressed in terms of mEq of acid neutralizing capacity. Dose and frequency of administration depend on the acid secretory rate of the stomach, gastric emptying time, and the disorder being treated. The duration of action of antacids is determined principally by gastric emptying time. In fasting subjects, antacids have a duration of action of 20-60 minutes. However, if the drugs are administered 1 hour after meals, acid neutralizing effects may persist up to 3 hours. Sodium bicarbonate generally has a shorter duration of action than other antacids. Antacids should be used for longer than 2-week periods only under the management of a physician and as part of a carefully planned therapeutic regimen.

There is considerable variation in in vivo acid neutralizing capacity of equal volumes of different antacids and antacid products. Since suspensions are more rapidly and effectively solubilized than powders or tablets, antacid suspensions have a greater ability to react with and neutralize gastric acid. Antacid suspensions have a smaller particle size than do tablets and drying of antacid suspensions to prepare powders and tablets causes substantial loss of ability to neutralize acid. In general, an antacid suspension is preferable to a tablet or powder; tablets should be reserved for chronic use in patients who refuse suspensions because they are inconvenient or unpalatable. Tablets should be thoroughly chewed before swallowing.

The US Food and Drug Administration (FDA) requires that antacids have a minimum in vitro acid neutralizing capacity of 5 mEq per dose and that antacid labeling contain the in vitro acid neutralizing capacity; however, this FDA in vitro test does not correlate with in vivo acid neutralizing capacity.

For peptic ulcer disease, dosages of antacids are empirical and various antacid dosages have been used. In patients with uncomplicated duodenal ulcers or gastric ulcers, an antacid is administered 1 and 3 hours postprandially and at bedtime. In patients with duodenal ulcers, antacids are usually given for 4-6 weeks, and in patients with gastric ulcers, antacids are administered until healing is complete. If symptoms of duodenal ulcer recur, some clinicians recommend that antacids be administered 1 and 3 hours postprandially and at bedtime for 1 week and, if pain is relieved, less frequently for an additional 1-2 weeks; these patients should consult their physicians if pain worsens or is not relieved after the first week of therapy. Additional doses of antacids may be administered to relieve ulcer pain which occurs between regularly scheduled doses.

For the acute management of moderate or severe esophageal reflux, an antacid suspension is administered every hour; if symptoms persist, antacids may be given every 30 minutes. For long-term therapy of esophageal reflux, antacids are administered 1 and 3 hours postprandially and at bedtime and whenever symptoms recur.

In the management of GI bleeding and stress ulceration, antacids are usually administered every hour and, for GI bleeding, the antacid dosage should be titrated to maintain the nasogastric aspirate above pH 3.5. For severe symptoms, antacid suspensions may be diluted with water or milk and given by continuous intragastric infusion.

To reduce the risk of anesthesia-induced gastric acid aspiration, an antacid suspension has been given 30 minutes before anesthesia.

In conjunction with dietary phosphate restriction in the management of hyperphosphatemia, 30-40 mL of aluminum hydroxide or aluminum carbonate suspension is administered 3 or 4 times daily.

Omeprazole delayed-release and immediate-release capsules are administered orally; oral suspensions of the drug are administered orally or through a gastric tube. To avoid decomposition of omeprazole in the acidic pH of the stomach, the commercially available delayed-release capsules and delayed-release oral suspension contain enteric-coated granules of the drug. Immediate-release capsules, immediate-release oral suspension, and the kit for oral suspension (Konvomep(R)) all contain sodium bicarbonate to protect the drug from acid degradation.

Omeprazole magnesium is also available in fixed-combination capsules containing amoxicillin and rifabutin (Talicia(R)). A co-packaged product containing delayed-release omeprazole capsules, clarithromycin tablets, and amoxicillin capsules (Omeclamox-Pak(R)) is also commercially available. See the full prescribing information for administration of these combination products.

Antacids may be administered concomitantly with delayed-release preparations of omeprazole.

For patients receiving continuous feedings via a nasogastric or orogastric tube, enteral feeding should be stopped temporarily for 3 hours before and for 1 hour after administration of preparations of omeprazole oral suspension.

Store omeprazole delayed-release capsules in tight containers or the original carton at 20-25degreesC; protect from light and moisture. Store packets of omeprazole powder for delayed-release suspension at 25degreesC (excursions permitted from 15-30degreesC). Store immediate-release capsules in tight, light-resistant containers at 20-25degreesC and protect from moisture. Store packets of omeprazole powder for immediate-release suspension protected from light and moisture at 25degreesC (excursions permitted from 15-30degreesC). Store omeprazole and sodium bicarbonate powder kit for oral suspension (Konvomep(R)) at 2-8degreesC protected from light; do not freeze.

No dosing information is available for this tab.

No dosing information is available for this tab.

All antacids potentially may increase or decrease the rate and/or extent of absorption of concomitantly administered oral drugs by changing GI transit time or by binding or chelating the drug. In vitro studies indicate that magnesium hydroxide or trisilicate has the greatest potential for drug binding and aluminum hydroxide and calcium carbonate are intermediate. Antacid-induced increases in GI pH may affect the disintegration, dissolution, solubility, or ionization of enteric-coated preparations and weakly acidic or basic drugs.

Simultaneous administration of aluminum-, calcium-, or magnesium-containing antacids with orally administered tetracyclines reduces the absorption of the tetracycline, probably because of chelation of these antacids by the tetracycline. Therefore, doses of tetracyclines should be spaced 1-2 hours from doses of antacids.

Concurrent administration of antacids and orally administered digoxin, indomethacin, or iron salts may decrease the absorption of these drugs. Doses of these drugs should be spaced as far apart as possible from doses of antacids. Concurrent administration of isoniazid and aluminum hydroxide gel may decrease the absorption of isoniazid; therefore, isoniazid should be administered at least 1 hour before aluminum-containing antacids. Absorption of buffered or enteric-coated aspirin is increased by simultaneous administration of antacids. Antacid-induced changes in urine pH increase urinary excretion and decrease blood concentrations of salicylates. Concurrent administration of dicumarol and an aluminum and magnesium hydroxides preparation reportedly increases the absorption of dicumarol; patients receiving antacids and oral anticoagulants should probably use warfarin rather than dicumarol. Concurrent administration of aluminum hydroxide and pseudoephedrine or diazepam increases the rate of absorption of the latter drugs. Administration of a magnesium and aluminum hydroxide preparation with chlordiazepoxide decreases the rate of chlordiazepoxide absorption. Administration of sodium bicarbonate with naproxen increases the rate of naproxen absorption, while concurrent administration of magnesium oxide or aluminum hydroxide with naproxen decreases the rate of naproxen absorption.

Antacid-induced increases in urine pH may decrease excretion of weakly basic drugs and increase excretion of weakly acidic drugs. Urinary excretion of amphetamines and quinidine are markedly decreased in patients whose urine is alkalinized with sodium bicarbonate and patients receiving these drugs concomitantly may have increased amphetamine or quinidine effects.

In vivo, omeprazole is a substrate and inhibitor of cytochrome P-450 (CYP) isoenzyme 2C19, and a substrate of CYP3A4. Omeprazole is also an inhibitor of CYP2C19 in vitro.

When co-packaged delayed-release omeprazole capsules, clarithromycin tablets, and amoxicillin capsules (Omeclamox-Pak(R)) are prescribed, drug interactions should be considered for each individual component. Refer to the Omeclamox-Pak(R) prescribing information for drug interaction information.

There are no contraindication interactions for this drug.

There are no severe interactions for this drug.

There are no moderate interactions for this drug.

*Known hypersensitivity reactions (including anaphylaxis) to omeprazole, esomeprazole, or other substituted benzimidazoles (e.g., lansoprazole, pantoprazole, rabeprazole), or any ingredient in the formulation. Hypersensitivity reactions may include anaphylaxis, anaphylactic shock, angioedema, bronchospasm, acute tubulointerstitial nephritis, and urticaria.

*Concomitant use of proton-pump inhibitors (PPIs), including omeprazole, and rilpivirine is contraindicated.

There are no contraindication contraindications for this drug.

There are no severe contraindications for this drug.

There are no moderate contraindications for this drug.

Adverse effects reported in >=2% of adults receiving omeprazole in clinical trials include headache, abdominal pain, nausea, diarrhea, vomiting, and flatulence.

Adverse effects reported in pediatric patients 2--16 years of age receiving omeprazole were similar to those reported in adults, except for more frequently reported respiratory system events and fever.

There are no severe adverse reactions for this drug.

There are no less severe adverse reactions for this drug.

No enhanced messaging available.

Safety and efficacy of omeprazole magnesium delayed-release oral suspension have been established for the treatment of erosive esophagitis due to acid-mediated gastroesophageal reflux disease (GERD) in pediatric patients >=1 month of age. Safety and efficacy of omeprazole magnesium delayed-release oral suspension have also been established for the treatment of symptomatic GERD and maintenance of healing of erosive esophagitis in pediatric patients 1-16 years of age. Safety and efficacy of omeprazole delayed-release capsules have been established for the treatment of symptomatic GERD and maintenance of healing of erosive esophagitis in pediatric patients 2-16 years of age. Use in pediatric patients is supported by adequate and well-controlled studies in adults and uncontrolled safety, efficacy, and pharmacokinetic studies in pediatric and adolescent patients.

Safety and efficacy of omeprazole magnesium delayed-release oral suspension are not established in pediatric patients <1 month of age or for other uses in pediatric patients. Safety and efficacy of omeprazole delayed-release capsules in pediatric patients <1 year of age for the treatment of symptomatic GERD or maintenance of healing of erosive esophagitis have not been established. Safety and efficacy of omeprazole delayed-release capsules have not been established in pediatric patients for the treatment of active duodenal ulcer, H. pylori eradication to reduce the risk of duodenal ulcer recurrence, treatment of active benign gastric ulcer, or pathological hypersecretory conditions. Safety and efficacy of omeprazole immediate-release capsules and oral suspension have not been established in pediatric patients.

Safety and efficacy of omeprazole and sodium bicarbonate powder kit for oral suspension (Konvomep(R)) have not been established in pediatric patients.

Safety and efficacy of co-packaged omeprazole delayed-release capsules, clarithromycin tablets, and amoxicillin capsules (Omeclamox-Pak(R)) have not been established in pediatric patients with H. pylori.

Respiratory adverse reactions and accidental injuries have been reported more frequently in pediatric patients of all ages than in adults. Otitis and fever have been reported more frequently in patients less than one year of age and patients from one month to less one year to less than 2 years of age, respectively, than in other pediatric and adult patients.

Reproductive studies in rats and rabbits using omeprazole dosages during organogenesis of up to 138 and 69.1 mg/kg daily (about 34 times the human dosage of 40 mg daily based on body surface area (BSA)), respectively, have not revealed evidence of teratogenicity. However, in rabbits given omeprazole dosages of 6.9-69.1 mg/kg daily during organogenesis (about 3.4-34 times the human dosage of 40 mg daily based on BSA), dose-related increases in embryolethality, fetal resorptions, and pregnancy loss occurred. In rats, dose-related embryo/fetal toxicity and postnatal developmental toxicity were observed in offspring resulting from administration of omeprazole in dosages of 13.8-138 mg/kg daily (about 3.4-34 times the human dosage of 40 mg daily based on BSA) prior to mating through the lactation period.

Reproductive studies of oral esomeprazole (an enantiomer of omeprazole) in rats and rabbits during organogenesis using dosages approximately 68 and 42 times the usual human dosage of 40 mg daily based on BSA, did not reveal evidence of embryo/fetal toxicity. When administered through most of pregnancy and lactation, effects on bone morphology were observed in rat offspring at dosages approximately 34 times the human dosage of 40 mg daily based on BSA of esomeprazole; however, when confined to administration during the gestational period only, no effects on bone morphology were observed in another study.

There are no adequate and well controlled studies using omeprazole in pregnant women. Available epidemiologic data have not demonstrated an increased risk of major congenital malformations or other adverse pregnancy outcomes with first trimester exposure to omeprazole. Reproductive studies in rats and rabbits using omeprazole dosages approximately 3.4-34 times the human dosage of 40 mg daily (based on BSA) resulted in dose-dependent increases in embryolethality.

A population-based retrospective cohort epidemiologic study using data from the Swedish Medical Birth Registry reported on outcomes in infants whose mothers used omeprazole during pregnancy; most (about 86%) were exposed to omeprazole during the first trimester, 5% during and beyond the first trimester, and about 14% were exposed only after the first trimester of pregnancy. The number of infants exposed to omeprazole in utero with any malformation, low birth weight, low Apgar score, or hospitalization was similar to the number in this population. The number of infants born with ventricular septal defects and the number of stillborn infants was slightly higher in the omeprazole-exposed infants than the expected number in this population.

In a population-based retrospective cohort study in Denmark reporting on 1800 live births whose mothers received omeprazole during the first trimester and 837,317 live births whose mothers did not receive a PPI, the overall rate of birth defects was 2.9% in infants whose mothers received omeprazole during the first trimester and 2.6% in infants born to mothers not exposed to any PPI during the first trimester.

In a retrospective cohort study, the incidence of congenital malformations in 689 women who received omeprazole or histamine H2-antagonists in the first trimester of pregnancy was compared with a control group of women who were not exposed to acid-suppressant drugs. The malformation rate associated with histamine H2-antagonists exposure was 5.5%, the malformation rate for nonexposed women was 4.1%, and the malformation rate associated with omeprazole exposure was 3.6%.

A small prospective cohort study followed women exposed to omeprazole (89% during the first trimester) during pregnancy; major congenital malformations occurred in 4% of live births in omeprazole-exposed women, 2.8% of disease-paired controls, and 2% exposed to non-teratogenic agents. Rates of spontaneous and elective abortions, preterm deliveries, gestational age at delivery, and mean birth weight were similar among the groups.

The manufacturers state that several studies reported that adverse short-term effects were not observed in infants when a single oral or IV dose of omeprazole was administered to pregnant women as premedication for cesarean section under general anesthesia.

Available data on sodium bicarbonate administration during pregnancy have not identified a drug-associated risk of major fetal malformations or miscarriage.

Limited data suggest omeprazole is distributed into human milk. The effects of omeprazole on milk production and on the breast-fed infant are unknown. Consider the developmental and health benefits of breast-feeding along with the mother's clinical need for the drug and any potential adverse effects on the breast-fed infant from omeprazole or from the underlying maternal condition.

Although the elimination rate of omeprazole is somewhat decreased in geriatric patients and the bioavailability increased, no adjustment of the usual recommended dosage is required in geriatric patients.

In US and European clinical trials, more than 2000 patients treated with omeprazole were >=65 years of age. Although no overall differences in efficacy or safety were observed between geriatric and younger patients, and other clinical experience revealed no evidence of age-related differences, the possibility that some older patients may exhibit increased sensitivity to the drug cannot be ruled out.