Losec

Omeprazole (Losec) capsule 10 mg: Hard gelatin capsule with an opaque pink body, marked 10 and an opaque pink cap marked A/OS.
Omeprazole (Losec) capsule 20 mg: Hard gelatin capsule with an opaque pink body, marked 20 and an opaque reddish-brown cap marked A/OM.
Each capsule contains Omeprazole 10 mg or 20 mg as enteric coated pellets.
Excipients/Inactive Ingredients: Disodium hydrogen phosphate dihydrate, low-substituted hydroxypropyl cellulose, hydroxypropyl methylcellulose, lactose anhydrous, magnesium stearate, mannitol, methacrylic acid co-polymer, microcrystalline cellulose, macrogol (polyethylene glycol), sodium lauryl sulphate iron oxide (E 172), titanium dioxide (E 171) and gelatine.

Pharmacology: Pharmacodynamics: Omeprazole, a racemic mixture of two active enantiomers, reduces gastric acid secretion through a highly targeted mechanism of action. It is a specific inhibitor of the acid pump (proton pump) in the parietal cell. It is rapidly acting and provides control through reversible inhibition of gastric acid secretion with once daily dosing.
Site and mechanism of action: Omeprazole is a weak base and is concentrated and converted to the active form in the highly acidic environment of the intracellular canaliculi within the parietal cell, where it inhibits the enzyme H⁺, K⁺-ATPase - the acid pump (proton pump). This effect on the final step of the gastric acid formation process is dose-dependent and provides for highly effective inhibition of both basal acid secretion and stimulated acid secretion, irrespective of stimulus. All pharmacodynamic effects observed can be explained by the effect of omeprazole on acid secretion.
Effect on gastric acid secretion: Oral dosing with Omeprazole (Losec) once daily provides for rapid and effective inhibition of daytime and night-time gastric acid secretion with maximum effect being achieved within 4 days of treatment. With Omeprazole (Losec) 20 mg, a mean decrease of at least 80% in 24-hour intragastric acidity is then maintained in duodenal ulcer patients, with the mean decrease in peak acid output after pentagastrin stimulation being about 70% twenty-four hours after dosing. Oral dosing with Omeprazole (Losec) 20 mg maintains an intragastric pH of ≥3 for a mean time of 17 hours of the 24-hour period in duodenal ulcer patients.
As a consequence of reduced acid secretion and intragastric acidity, omeprazole dose-dependently reduces/normalizes acid exposure of the esophagus in patients with gastro-esophageal reflux disease. The inhibition of acid secretion is related to the area under the plasma concentration-time curve (AUC) of omeprazole and not to the actual plasma concentration at a given time. No tachyphylaxis has been observed during treatment with omeprazole.
Effect on Helicobacter pylori: Helicobacter pylori is associated with peptic ulcer disease, including duodenal and gastric ulcer disease, H. pylori is a major factor in the development of gastritis. H. pylori together with gastric acid are major factors in the development of peptic ulcer disease. H. pylori is a major factor in the development of atrophic gastritis, which is associated with an increased risk of developing gastric cancer.
Eradication of H. pylori with omeprazole and antimicrobials is associated with rapid symptom relief, high rates of healing of any mucosal lesions, and long-term remission of peptic ulcer disease thus reducing complications such as gastrointestinal bleeding as well as the need for prolonged antisecretory treatment.
Other effects related to acid inhibition: During treatment with antisecretory drugs serum gastrin increases in response to the decreased acid secretion. Also chromogranin A (CgA) increases due to decreased gastric acidity. The increased CgA level may interfere with investigations for neuroendocrine tumours. Literature reports indicate that proton pump inhibitor treatment should be stopped 5 to 14 days before CgA measurement.
Measurements should be repeated if levels have not normalised by this time. An increased number of ECL cells possibly related to the increased serum gastrin levels, have been observed in both children and adults during long term treatment with omeprazole. The findings are considered to be of no clinical significance. During long-term treatment, gastric glandular cysts have been reported in a somewhat increased frequency. These changes are a physiological consequence of pronounced inhibition of acid secretion, are benign and appear to be reversible. Decreased gastric acidity due to any means including proton pump inhibitors, increases gastric counts of bacteria normally present in the gastrointestinal tract. Treatment with acid-reducing drugs may lead to slightly increased risk of gastrointestinal infections such as Salmonella and Campylobacter and, in hospitalised patients, possibly also Clostridium difficile.
Pharmacokinetics: Absorption and distribution: Omeprazole and omeprazole magnesium are acid labile and are therefore administered orally as enteric-coated granules in capsules or tablets. Absorption of omeprazole is rapid, with peak plasma levels occurring approximately 1-2 hours after dose. Absorption of omeprazole takes place in the small intestine and is usually completed within 3-6 hours.
Concomitant intake of food has no influence on the bioavailability. The systemic availability (bioavailability) of omeprazole from a single oral dose of Omeprazole (Losec) is approximately 40%. After repeated once-daily administration, the bioavailability increases to about 60%. The apparent volume of distribution in healthy subjects is approximately 0.3 L/kg body weight. Omeprazole is 95% plasma protein bound.
Metabolism and excretion: Omeprazole is completely metabolised by the cytochrome P450 system (CYP). The major part of its metabolism is dependent on the polymorphically expressed CYP2C19, responsible for the formation of hydroxyomeprazole, the major metabolite in plasma. The remaining part is dependent on another specific isoform, CYP3A4, responsible for the formation of omeprazole sulphone. As a consequence of high affinity of omeprazole to CYP2C19, there is a potential for competitive inhibition and metabolic drug-drug interactions with other substrates for CYP2C19. However, due to low affinity to CYP3A4, omeprazole has no potential to inhibit the metabolism of other CYP3A4 substrates. The parameters as follows reflect mainly the pharmacokinetics in individuals with a functional CYP2C19 enzyme, extensive metabolisers.
Total plasma clearance is about 30-40 L/h after a single dose. The plasma elimination half-life of omeprazole is usually shorter than one hour both after single and repeated oral once-daily dosing. The AUC of omeprazole increases with repeated administration. This increase is dose-dependent and results in a non-linear dose-AUC relationship after repeated administration. This time- and dose-dependency is due to a decrease of first pass metabolism and systemic clearance probably caused by an inhibition of the CYP2C19 enzyme by omeprazole and/or its metabolites (eg, the sulphone).
Omeprazole is completely eliminated from plasma between doses with no tendency for accumulation during once-daily administration. No metabolite has been found to have any effect on gastric acid secretion. Almost 80% of an oral dose of omeprazole is excreted as metabolites in the urine, the remainder in the faeces, primarily originating from bile secretion.
Poor metabolisers: Approximately 3% of the Caucasian population and 15-20% of Asian populations lack a functional CYP2C19 enzyme and are called poor metabolisers. In such individuals, the metabolism of omeprazole is probably mainly catalysed by CYP3A4. After repeated once-daily administration of 20 mg omeprazole, the mean AUC was 5 to 10 times higher in poor metabolisers than in subjects having a functional CYP2C19 enzyme (extensive metabolisers). Mean peak plasma concentrations were also higher, by 3 to 5 times. These findings have no implications for the posology of Omeprazole (Losec).
Special patient populations: Impaired hepatic function: The metabolism of omeprazole in patients with liver dysfunction is impaired, resulting in an increased AUC. Omeprazole has not shown any tendency to accumulate with once daily dosing.
Impaired renal function: The pharmacokinetics of omeprazole, including systemic bioavailability and elimination rate, are unchanged in patients with reduced renal function.
Elderly: The metabolism rate of omeprazole is somewhat reduced in elderly subjects (75-79 years of age).
Children: Available data from children (1 year and older) suggests that the pharmacokinetics, within the recommended dosages (see Dosage & Administration), are similar to what has been reported in adults.
Toxicology: Preclinical safety data: Gastric ECL-cell hyperplasia and carcinoids, have been observed in life-long studies in rats treated with omeprazole. These changes are the result of sustained hypergastrinaemia secondary to acid inhibition. Similar findings have been made after treatment with H2-receptor antagonists, proton pump inhibitors and after partial fundectomy. Thus, these changes are not from direct effect of any individual drug.

Omeprazole (Losec) is indicated for the treatment of: Duodenal ulcer; Gastric ulcer; NSAID associated gastric and duodenal ulcers or erosions; Helicobacter pylori eradication in peptic ulcer disease; Reflux esophagitis; Symptomatic gastro-esophageal reflux disease; Acid related dyspepsia; Zollinger-Ellison syndrome; Patients considered to be at risk of aspiration of gastric contents during general anesthesia/Acid aspiration prophylaxis.

Omeprazole (Losec) capsules are recommended to be given in the morning and swallowed whole with half a glass of water. The capsules must not be chewed or crushed.
For patients with swallowing difficulties and for children who can drink or swallow semi-solid food: The capsule can be opened and the contents swallowed directly with half a glass of water or after mixing the contents in a slightly acidic fluid eg, fruit juice or applesauce, or in non-carbonated water. The dispersion should be taken immediately (or within 30 minutes). Always stir just before drinking. Rinse it down with half a glass of water.
Alternatively, patients can suck the capsule and swallow the pellets with half a glass of water.
Ingest without chewing the enteric-coated pellets.
Duodenal ulcer: The recommended dosage in patients with an active duodenal ulcer is Omeprazole (Losec) 20 mg once daily. Symptom resolution is rapid and in most patients healing occurs within 2 weeks. For those patients who may not be fully healed after the initial course, healing usually occurs during a further 2-week treatment period. In patients with poorly responsive duodenal ulcer, 2 capsules of Omeprazole (Losec) 20 mg once daily is recommended and healing is usually achieved within 4 weeks. For the prevention of relapse in patients with duodenal ulcer disease, the recommended dose is Omeprazole (Losec) 10 mg once daily. If needed the dose can be increased to 1 to 2 capsules of Omeprazole (Losec) 20 mg once daily. For NSAID associated duodenal ulcers, see NSAID associated gastroduodenal lesions. For eradication of Helicobacter pylori, see Helicobacter pylori (Hp) eradication regimens in peptic ulcer disease.
Gastric ulcer: The recommended dosage is Omeprazole (Losec) 20 mg once daily. Symptom resolution is rapid and in most patients healing occurs within 4 weeks. For those patients who may not be fully healed after the initial course, healing usually occurs during a further 4-week treatment period.
In patients with poorly responsive gastric ulcer, 2 capsules of Omeprazole (Losec) 20 mg once daily is recommended and healing is usually achieved within 8 weeks. For the prevention of relapse of patients with poorly responsive gastric ulcer, the recommended dose is Omeprazole (Losec) 20 mg once daily. If needed, the dose can be increased to 2 capsules of Omeprazole (Losec) 20 mg once daily. For eradication of Helicobacter pylori, see Helicobacter pylori (Hp) eradication regimens in peptic ulcer disease.
For NSAID associated gastric ulcers, duodenal ulcers or gastroduodenal erosions in patients with or without continued NSAID treatment the recommended dosage of Omeprazole (Losec) is 20 mg once daily. Symptom resolution is rapid and in most patients healing occurs within 4 weeks. For those patients who may not be fully healed after the initial course, healing usually occurs during a further 4-week treatment period. For the prevention of NSAID associated gastric ulcers, duodenal ulcers, gastroduodenal erosions and dyspeptic symptoms the recommended dosage of Omeprazole (Losec) is 20 mg once daily.
Helicobacter pylori (Hp) eradication regimens in peptic ulcer disease: Triple therapy regimens: Omeprazole (Losec) 20 mg, amoxicillin 1 g and clarithromycin 500 mg, all twice a day for one week or Omeprazole (Losec) 20 mg, metronidazole 400 mg (or tinidazole 500 mg) and clarithromycin 250 mg, all twice a day for one week or Omeprazole (Losec) 20 mg 2 capsules once daily with amoxicillin 500 mg and metronidazole 400 mg both three times a day for one week.
Dual therapy regimens: Omeprazole (Losec) 20 mg 2-4 capsules daily with amoxicillin 1.5 g daily in divided doses for two weeks. In clinical studies, daily doses of 1.5-3 g of amoxicillin have been used or Omeprazole (Losec) 20 mg 2 capsules once daily and clarithromycin 500 mg three times a day for two weeks.
To ensure healing in patients with active peptic ulcer disease, see further dosage recommendations for Duodenal and Gastric ulcer. In each regimen if the patient is still Hp positive, therapy may be repeated.
Reflux esophagitis: The recommended dosage is Omeprazole (Losec) 20 mg once daily. Symptom resolution is rapid and in most patients healing occurs within 4 weeks. For those patients who may not be fully healed after the initial course, healing usually occurs during a further 4-week treatment period.
In patients with severe reflux esophagitis 2 capsules of Omeprazole (Losec) 20 mg once daily is recommended and healing is usually achieved within 8 weeks. For the long-term management of patients with healed reflux esophagitis the recommended dose is Omeprazole (Losec) 10 mg once daily. If needed, the dose can be increased to 1-2 capsules of Omeprazole (Losec) 20 mg once daily.
Symptomatic gastro-esophageal reflux disease: The recommended dosage is Omeprazole (Losec) 20 mg daily. Symptom relief is rapid.
Patients may respond adequately to 10 mg daily, and therefore individual dose adjustment should be considered. If symptom control has not been achieved after 4 weeks of treatment with Omeprazole (Losec) 20 mg daily, further investigation is recommended.
Acid-related dyspepsia: In the relief of symptoms in patients with epigastric pain/discomfort with or without heartburn the recommended dosage is Omeprazole (Losec) 20 mg once daily.
Patients may respond adequately to 10 mg daily and therefore this dose could be considered as a starting dose. If symptom control has not been achieved after 4 weeks of treatment with Omeprazole (Losec) 20 mg daily, further investigation is recommended.
Zollinger-Ellison syndrome: In patients with Zollinger-Ellison syndrome, the dosage should be individually adjusted and treatment continued as long as is clinically indicated. The recommended initial dosage is 3 capsules of Omeprazole (Losec) 20 mg daily.
All patients with severe disease and inadequate response to other therapies have been effectively controlled and more than 90% of the patients maintained on doses of Omeprazole (Losec) 20-120 mg daily. When doses exceed Omeprazole (Losec) 80 mg daily, the dose should be divided and given twice daily.
Acid aspiration prophylaxis: The recommended dosage is 2 capsules of Omeprazole (Losec) 20 mg in the evening before surgery, followed by 2 capsules of Omeprazole (Losec) 20 mg on the morning after surgery.
Impaired renal function: Dose adjustment is not needed in patients with impaired renal function.
Impaired hepatic function: As bioavailability and plasma half-life of omeprazole are increased in patients with impaired hepatic function a daily dose of 10-20 mg may be sufficient.
Elderly: Dose adjustment is not needed in the elderly.
Children: For use in children 2 years and older the recommended dose is: See Table 1.

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If needed the dose may be increased to 20 mg and 40 mg respectively.
For use in children 0-24 months the recommended dose is: See Table 2.

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For children 0-3 months a dose of 0.5 mg/kg/day may be sufficient.
Helicobacter pylori eradication for children from 4 years. (See Table 3.)

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Rare reports have been received of overdosage with omeprazole. In the literature doses of up to 560 mg have been described and occasional reports have been received when single oral doses have reached up to 2400 mg omeprazole (120 times the usual recommended clinical dose). Nausea, vomiting, dizziness, abdominal pain, diarrhea and headache have been reported from overdose with omeprazole. Also apathy, depression and confusion have been described in single cases.
The symptoms described in connection to omeprazole overdosage have been transient, and no serious outcome due to omeprazole has been reported. The rate of elimination was unchanged (first order kinetics) with increased doses and no specific treatment has been needed.

Known hypersensitivity to omeprazole, substituted benzimidazoles or any other constituent of the formulation.

In the presence of any alarm symptom (e.g. significant unintentional weight loss, recurrent vomiting, dysphagia, hematemesis or melena) and when gastric ulcer is suspected or present, malignancy should be excluded, as treatment may alleviate symptoms and delay diagnosis.
Concomitant administration with omeprazole and drugs such as atazanavir and nelfinavir is not recommended. (See Interactions).
Results from studies in healthy subjects have shown a pharmacokinetic/pharmacodynamic interaction between clopidogrel (300 mg loading dose/75 mg daily maintenance dose) and omeprazole (80 mg p.o. daily, ie, four times the recommended dose) resulting in decreased exposure to the active metabolite of clopidogrel by an average of 46% and resulting in decreased maximum inhibition of (ADP induced) platelet aggregation by an average of 16%. Based on these data, concomitant use of omeprazole and clopidogrel should be avoided. See also Interactions.
Some published observational studies suggest that proton pump inhibitor (PPI) therapy may be associated with a small increased risk for osteoporosis related fractures. However, in other similar observational studies no such increased risk was found. In AstraZeneca's randomized, double-blind and controlled clinical studies on omeprazole and esomeprazole (including two open long-term studies of up to more than 12 years) there are no indications that PPIs are associated with osteoporotic fractures. Although a causal relationship between omeprazole/esomeprazole and osteoporotic fractures has not been established, patients at risk for developing osteoporosis or osteoporotic fractures are advised to have appropriate clinical monitoring in accordance with current clinical guidelines for these conditions.
Effects on ability to drive and use machines: Omeprazole (Losec) is not likely to affect the ability to drive or use machines.

Results from three prospective epidemiological studies indicate no adverse effects of omeprazole on pregnancy or on the health of the fetus/newborn child. Omeprazole (Losec) can be used during pregnancy.
Omeprazole is excreted in the breast milk but is not likely to influence the child when therapeutic doses are used.

The following adverse drug reactions have been identified or suspected in the clinical trials programme for omeprazole and post-marketing. None was found to be dose-related. The reactions are classified according to frequency (common ≥1/100 to <1/10; uncommon ≥1/1,000 to <1/100; rare ≥1/10,000 to <1/1,000; very rare <1/10,000).
Blood and lymphatic system disorders: Rare: Leukopenia, thrombocytopenia, agranulocytosis, pancytopenia.
Immune system disorders: Rare: Hypersensitivity reactions e.g. fever, angioedema and anaphylactic reaction/shock.
Metabolism and nutrition disorders: Rare: Hyponatraemia. Very Rare: Hypomagnesaemia; severe hypomagnesaemia may result in hypocalcaemia. Hypomagnesaemia may also result in hypokalaemia.
Psychiatric disorders: Uncommon: Insomnia. Rare: Agitation, aggression, confusion, depression, hallucinations.
Nervous system disorders: Common: Headache. Uncommon: Dizziness, paraesthesia, somnolence. Rare: Taste disturbance.
Eye disorders: Rare: Blurred vision.
Ear and labyrinth disorders: Uncommon: Vertigo.
Respiratory, thoracic and mediastinal disorders: Rare: Bronchospasm.
Gastrointestinal disorders: Common: Abdominal pain, constipation, diarrhoea, flatulence, nausea/vomiting. Rare: Dry mouth, stomatitis, gastrointestinal candidiasis, microscopic colitis.
Hepatobiliary disorders: Uncommon: Increased liver enzymes. Rare: Hepatitis with or without jaundice, hepatic failure, encephalopathy in patients with pre-existing liver disease.
Skin and subcutaneous tissue disorders: Uncommon: Dermatitis, pruritus, rash, urticaria. Rare: Alopecia, photosensitivity, erythema multiforme, Stevens-Johnson syndrome, toxic epidermal necrolysis (TEN), acute generalized exanthematous pustulosis (AGEP), drug rash with eosinophilia and systemic symptoms (DRESS)
Musculoskeletal, connective tissue and bone disorders: Rare: Arthralgia, myalgia, muscular weakness.
Renal and urinary disorders: Rare: Interstitial nephritis.
Reproductive system and breast disorders: Rare: Gynaecomastia.
General disorders and administration site conditions: Uncommon: Malaise. Rare: Increased sweating, peripheral oedema.

Effects of omeprazole on the pharmacokinetics of other drugs: Absorption: The gastric acid suppression during treatment with omeprazole and other PPIs might decrease or increase the absorption of drugs with a gastric pH dependent absorption. Like with other drugs that decrease the intragastric acidity, the absorption of drugs, such as ketoconazole, itraconazole and erlotinib can decrease while the absorption of drugs such as digoxin can increase during treatment with omeprazole.
Concomitant treatment with omeprazole (20 mg daily) and digoxin in healthy subjects increased the bioavailability of digoxin by 10% (up to 30% in two out of ten subjects).
Metabolism: Omeprazole inhibits CYP2C19, the major omeprazole metabolising enzyme.
Thus, the metabolism of concomitant drugs also metabolised by CYP2C19, such as diazepam, phenytoin, warfarin (R-warfarin) or other vitamin K antagonists and cilostazol, may be delayed. Monitoring of patients receiving phenytoin is recommended and a reduction of the phenytoin dose may be necessary. However, concomitant treatment with Omeprazole (Losec) 20 mg daily did not change the blood concentration of phenytoin in patients on continuous treatment with this drug. In patients receiving warfarin or other vitamin K antagonists, monitoring of INR is recommended and a reduction of the warfarin (or other vitamin K antagonist) dose may be necessary. Concomitant treatment with Omeprazole (Losec) 20 mg daily did, however, not change coagulation time in patients on continuous treatment with warfarin. Omeprazole, given in doses of 40 mg to healthy subjects in a cross-over study, increased Cmax and AUC for cilostazol by 18% and 26% respectively, and one of its active metabolites by 29% and 69% respectively.
Results from studies in healthy subjects have shown a pharmacokinetic/pharmacodynamic interaction between clopidogrel (300 mg loading dose/75 mg daily maintenance dose) and omeprazole (80 mg p.o. daily, ie, four times the recommended dose) resulting in decreased exposure to the active metabolite of clopidogrel by an average of 46%, and resulting in decreased maximum inhibition of (ADP induced) platelet aggregation by an average of 16%.
It is, however, uncertain to what extent this interaction is clinically important. One prospective, randomized (but incomplete) study (in over 3760 patients comparing placebo with omeprazole 20 mg in patients treated with clopidogrel and Acetylsalicylic Acid/ASA) and non-randomized, post-hoc analyses of data from large, prospective, randomized clinical outcome studies (in over 47000 patients) did not show any evidence of an increased risk for adverse cardiovascular outcome when clopidogrel and PPIs, including omeprazole, were given concomitantly. Results from a number of observational studies are inconsistent with regard to increased risk or no increased risk for CV thromboembolic events when clopidogrel is given together with a PPI. When clopidogrel was given together with a fixed dose combination of esomeprazole 20 mg + ASA 81 mg compared to clopidogrel alone in a study in healthy subjects there was a decreased exposure by almost 40% of the active metabolite of clopidogrel. However, the maximum levels of inhibition of (ADP induced) platelet aggregation in these subjects were the same in the clopidogrel and the clopidogrel + the combined (esomeprazole + ASA) product groups, likely due to the concomitant administration of low dose ASA.
Omeprazole is partly metabolised also by CYP3A4, but omeprazole does not inhibit this enzyme. Thus, omeprazole does not affect the metabolism of drugs metabolised by CYP3A4, such as cyclosporin, lidocaine, quinidine, estradiol, erythromycin, and budesonide. Results from a range of interaction studies with omeprazole versus other drugs demonstrate that omeprazole, 20-40 mg daily, has no significant influence on any other CYP enzymes relevant for drug metabolism, as shown by the lack of metabolic interaction with substrates for CYP1A2 (such as caffeine, theophylline), CYP2C9 (such as S-warfarin, piroxicam, diclofenac, naproxen), CYP2D6 (such as metoprolol, propranolol), CYP2E1 (such as ethanol).
Unknown mechanism: Concomitant administration of omeprazole has been reported to increase the serum levels of tacrolimus.
When given together with proton pump inhibitors, methotrexate levels have been reported to increase in some patients. In high-dose methotrexate administration a temporary withdrawal of omeprazole may need to be considered. Omeprazole has been reported to interact with some antiretroviral drugs. The clinical importance and the mechanisms behind these interactions are not always known. Increased gastric pH during omeprazole treatment may change the absorption of the antiretroviral drug.
Other possible interaction mechanisms are via CYP 2C19. For some antiretroviral drugs, such as atazanavir and nelfinavir, decreased serum levels have been reported when given together with omeprazole.
Concomitant administration with omeprazole and drugs such as atazanavir and nelfinavir is therefore not recommended. For other antiretroviral drugs, such as saquinavir, elevated serum levels have been reported. There are also some antiretroviral drugs of which unchanged serum levels have been reported when given with omeprazole.
Effects of other drugs on the pharmacokinetics of omeprazole: Metabolism: Since omeprazole is metabolised by CYP2C19 and CYP3A4, drugs known to inhibit CYP 2C19 or CYP 3A4 or both (such as clarithromycin and voriconazole) may lead to increased omeprazole serum levels by decreasing the rate of omeprazole's metabolism. Concomitant voriconazole treatment resulted in more than doubling of the omeprazole exposure. Since high doses of omeprazole have been well-tolerated, adjustment of the omeprazole dose is not required during temporary concomitant use. Drugs known to induce CYP 2C19 or CYP 3A4 or both (such as rifampicin and St John's wort) may lead to decreased omeprazole serum levels by increasing omeprazole's rate of metabolism.

Instructions for use, handling and disposal: No special requirements.
Incompatibilities: None known when instructions in Dosage & Administration are followed.

Store at a temperature not exceeding 30°C.

Antacids, Antireflux Agents & Antiulcerants

A02BC01 - omeprazole ; Belongs to the class of proton pump inhibitors. Used in the treatment of peptic ulcer and gastro-oesophageal reflux disease (GERD).

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