Primary Outcome Measures : Time to Maximal Omeprazole Concentration Tmax [ Time Frame: 10, 20, 30, 45, 60, 90, , , , , and min after the study drug was ingested on day 7 of treatment ] Time to max concentration for Immediate release vs. Delayed release omeprazole. Maximal concentration of immediate-release vs. The area under the curve for omeprazole concentration-time curve for immediate release and delayed release omeprazole.
Eligibility Criteria. Information from the National Library of Medicine Choosing to participate in a study is an important personal decision. Contacts and Locations. Information from the National Library of Medicine To learn more about this study, you or your doctor may contact the study research staff using the contact information provided by the sponsor.
Please refer to this study by its ClinicalTrials. More Information. Pharmacokinetic profile of immediate-release omeprazole in patients with gastro-oesophageal reflux associated with gastroparesis.
Aliment Pharmacol Ther. Epub Nov Gastroparesis Gastroesophageal reflux disease heartburn. National Library of Medicine U. National Institutes of Health U. Department of Health and Human Services. The safety and scientific validity of this study is the responsibility of the study sponsor and investigators. Gastroparesis Gastroesophageal Reflux Disease. Drug: Immediate-release omeprazole Drug: Delayed-release omeprazole. Phase 4. Study Type :.
Interventional Clinical Trial. Actual Enrollment :. Study Start Date :. Actual Primary Completion Date :. Actual Study Completion Date :. Experimental: Immediate-release omeprazole release first subjects receive immediate release omeprazole for 7 days then delayed release for 7 days. Drug: Immediate-release omeprazole Immediate-release omeprazole 40 mg qam for 7 days Drug: Delayed-release omeprazole Delayed-release omeprazole 40 mg qam for 7 days. Experimental: Delayed-release omeprazole first subjects receive delayed release omeprazole for 7 days then immediate release for 7 days.
Omeprazole delayed-release capsules, USP are indicated for the long-term treatment of pathological hypersecretory conditions e. Omeprazole delayed-release capsules should be taken before eating. In the clinical trials, antacids were used concomitantly with omeprazole. Patients should be informed that the omeprazole delayed-release capsule should be swallowed whole. For patients unable to swallow an intact capsule, alternative administration options are available [See Dosage and Administration 2.
The recommended adult oral dose of omeprazole delayed-release capsules are 20 mg once daily. The recommended adult oral regimen is omeprazole delayed-release capsules 20 mg plus clarithromycin mg plus amoxicillin mg each given twice daily for 10 days. In patients with an ulcer present at the time of initiation of therapy, an additional 18 days of omeprazole delayed-release capsules 20 mg once daily is recommended for ulcer healing and symptom relief. The recommended adult oral regimen is omeprazoledelayed-release capsules 40 mg once daily plus clarithromycin mg three times daily for 14 days.
In patients with an ulcer present at the time of initiation of therapy, an additional 14 days of omeprazole delayed-release capsules 20 mg once daily is recommended for ulcer healing and symptom relief. The recommended adult oral dose for the treatment of patients with symptomatic GERD and no esophageal lesions is 20 mg daily for up to 4 weeks. The recommended adult oral dose for the treatment of patients with erosive esophagitis and accompanying symptoms due to GERD is 20 mg daily for 4 to 8 weeks.
The dosage of omeprazole delayed-release capsules in patients with pathological hypersecretory conditions varies with the individual patient. The recommended adult oral starting dose is 60 mg once daily. Doses should be adjusted to individual patient needs and should continue for as long as clinically indicated. Doses up to mg three times daily have been administered. Daily dosages of greater than 80 mg should be administered in divided doses.
Some patients with Zollinger-Ellison syndrome have been treated continuously with omeprazole delayed-release capsules for more than 5 years. For the treatment of GERD and maintenance of healing of erosive esophagitis, the recommended daily dose for pediatric patients 2 to 16 years of age is as follows:. On a per kg basis, the doses of omeprazole required to heal erosive esophagitis in pediatric patients are greater than those for adults.
Alternative administrative options can be used for pediatric patients unable to swallow an intact capsule [See Dosage and Administration 2. For patients who have difficulty swallowing capsules, the contents of an omeprazole delayed-release capsule can be added to applesauce. One tablespoon of applesauce should be added to an empty bowl and the capsule should be opened. All of the pellets inside the capsule should be carefully emptied on the applesauce.
The pellets should be mixed with the applesauce and then swallowed immediately with a glass of cool water to ensure complete swallowing of the pellets. The applesauce used should not be hot and should be soft enough to be swallowed without chewing. The pellets should not be chewed or crushed. Omeprazole delayed-release capsules, USP 10 mg are hard gelatin capsules with a pink opaque body and a reddish brown opaque cap. Omeprazole delayed-release capsules, USP 20 mg are hard gelatin capsules with a pink opaque body and a reddish brown opaque cap.
Omeprazole delayed-release capsules, USP 40 mg are hard gelatin capsules with a pink opaque body and a reddish brown opaque cap. Omeprazole delayed-release capsules are contraindicated in patients with known hypersensitivity to substituted benzimidazoles or to any component of the formulation. Hypersensitivity reactions may include anaphylaxis, anaphylactic shock, angioedema, bronchospasm, interstitial nephritis, and urticaria [See Adverse Reactions 6 ].
Symptomatic response to therapy with omeprazole does not preclude the presence of gastric malignancy. Atrophic gastritis has been noted occasionally in gastric corpus biopsies from patients treated long-term with omeprazole. Published observational studies suggest that PPI therapy like omeprazole may be associated with an increased risk of Clostridium difficile associated diarrhea, especially in hospitalized patients.
This diagnosis should be considered for diarrhea that does not improve [see Adverse Reactions 6. Patients should use the lowest dose and shortest duration of PPI therapy appropriate to the condition being treated.
Clostridium difficile associated diarrhea CDAD has been reported with use of nearly all antibacterial agents. Avoid concomitant use of omeprazole with clopidogrel. Clopidogrel is a prodrug. Inhibition of platelet aggregation by clopidogrel is entirely due to an active metabolite. The metabolism of clopidogrel to its active metabolite can be impaired by use with concomitant medications, such as omeprazole, that inhibit CYP2C19 activity. Concomitant use of clopidogrel with 80 mg omeprazole reduces the pharmacological activity of clopidogrel, even when administered 12 hours apart.
When using omeprazole, consider alternative anti-platelet therapy [see Drug Interactions 7. Several published observational studies suggest that proton pump inhibitor PPI therapy may be associated with an increased risk for osteoporosis-related fractures of the hip, wrist, or spine.
The risk of fracture was increased in patients who received high-dose, defined as multiple daily doses, and long-term PPI therapy a year or longer. Patients at risk for osteoporosis-related fractures should be managed according to established treatment guidelines.
Hypomagnesemia, symptomatic and asymptomatic, has been reported rarely in patients treated with PPIs for at least three months, in most cases after a year of therapy. Serious adverse events include tetany, arrhythmias, and seizures.
In most patients, treatment of hypomagnesemia required magnesium replacement and discontinuation of the PPI. For patients expected to be on prolonged treatment or who take PPIs with medications such as digoxin or drugs that may cause hypomagnesemia e. Serum chromogranin A CgA levels increase secondary to drug-induced decreases in gastric acidity. The increased CgA level may cause false positive results in diagnostic investigations for neuroendocrine tumors. Providers should temporarily stop omeprazole treatment before assessing CgA levels and consider repeating the test if initial CgA levels are high.
If serial tests are performed e. In high-dose methotrexate administration a temporary withdrawal of the PPI may be considered in some patients. Because clinical trials are conducted under widely varying conditions, adverse reaction rates observed in the clinical trials of a drug cannot be directly compared to rates in the clinical trials of another drug and may not reflect the rates observed in practice.
The safety data described below reflects exposure to omeprazole delayed-release capsules in patients from worldwide clinical trials patients from US studies and 2, patients from international studies. Indications clinically studied in US trials included duodenal ulcer, resistant ulcer, and Zollinger-Ellison syndrome.
The international clinical trials were double blind and open-label in design. The most common adverse reactions reported i. The clinical trial safety profile in patients greater than 65 years of age was similar to that in patients 65 years of age or less. The clinical trial safety profile in pediatric patients who received omeprazole delayed-release capsules was similar to that in adult patients. Unique to the pediatric population, however, adverse reactions of the respiratory system were most frequently reported in the 2 to 16 year age group Similarly, accidental injuries were reported frequently in the 2 to 16 year age group 3.
In clinical trials using either dual therapy with omeprazole and clarithromycin, or triple therapy with omeprazole, clarithromycin, and amoxicillin, no adverse reactions unique to these drug combinations were observed. Adverse reactions observed were limited to those previously reported with omeprazole, clarithromycin, or amoxicillin alone.
For more information on clarithromycin, refer to the clarithromycin prescribing information, Adverse Reactions section. None of these occurred at a higher frequency than that reported by patients taking antimicrobial agents alone. For more information on clarithromycin or amoxicillin, refer to the respective prescribing information, Adverse Reactions sections. The following adverse reactions have been identified during post-approval use of omeprazole delayed-release capsules.
Because these reactions are voluntarily reported from a population of uncertain size, it is not always possible to reliably estimate their actual frequency or establish a causal relationship to drug exposure. Body As a Whole: Hypersensitivity reactions including anaphylaxis, anaphylactic shock, angioedema, bronchospasm, interstitial nephritis, urticaria, see also Skin below ; fever; pain; fatigue; malaise;.
Cardiovascular: Chest pain or angina, tachycardia, bradycardia, palpitations, elevated blood pressure, peripheral edema. Gastrointestinal: Pancreatitis some fatal , anorexia, irritable colon, fecal discoloration, esophageal candidiasis, mucosal atrophy of the tongue, stomatitis, abdominal swelling, dry mouth, microscopic colitis.
During treatment with omeprazole, gastric fundic gland polyps have been noted rarely. These polyps are benign and appear to be reversible when treatment is discontinued. Gastroduodenal carcinoids have been reported in patients with ZE syndrome on long-term treatment with omeprazole.
This finding is believed to be a manifestation of the underlying condition, which is known to be associated with such tumors.
Hepatic: Liver disease including hepatic failure some fatal , liver necrosis some fatal , hepatic encephalopathy hepatocellular disease, cholestatic disease, mixed hepatitis, jaundice, and elevations of liver function tests [ALT, AST, GGT, alkaline phosphatase, and bilirubin].
Infections and Infestations: Clostridium difficile associated diarrhea. Metabolism and Nutritional disorders: Hypoglycemia, hypomagnesemia, hyponatremia, weight gain. Musculoskeletal: Muscle weakness, myalgia, muscle cramps, joint pain, leg pain, bone fracture. Skin: Severe generalized skin reactions including toxic epidermal necrolysis some fatal , Stevens-Johnson syndrome, and erythema multiforme; photosensitivity; urticaria; rash; skin inflammation; pruritus; petechiae; purpura; alopecia; dry skin; hyperhidrosis.
Special Senses: Tinnitus, taste perversion. Ocular : Optic atrophy, anterior ischemic optic neuropathy, optic neuritis, dry eye syndrome, ocular irritation, blurred vision, double vision.
Urogenital: Interstitial nephritis, hematuria, proteinuria, elevated serum creatinine, microscopic pyuria, urinary tract infection, glycosuria, urinary frequency, testicular pain. Hematologic: Agranulocytosis some fatal , hemolytic anemia, pancytopenia, neutropenia, anemia, thrombocytopenia, leukopenia, leucocytosis. Concomitant use of atazanavir and nelfinavir with proton pump inhibitors is not recommended.
Co-administration of atazanavir with proton pump inhibitors is expected to substantially decrease atazanavir plasma concentrations and may result in a loss of therapeutic effect and the development of drug resistance. 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 2C Reduced concentrations of atazanavir and nelfinavir. 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.
Therefore, clinical and laboratory monitoring for saquinavir toxicity is recommended during concurrent use with omeprazole.
Dose reduction of saquinavir should be considered from the safety perspective for individual patients. There are also some antiretroviral drugs of which unchanged serum levels have been reported when given with omeprazole. Because of its profound and long lasting inhibition of gastric acid secretion, it is theoretically possible that omeprazole may interfere with absorption of drugs where gastric pH is an important determinant of their bioavailability.
Like with other drugs that decrease the intragastric acidity, the absorption of drugs such as ketoconazole, ampicillin esters, iron salts and erlotinib can decrease, while the absorption of drugs such as digoxin can increase during treatment with omeprazole. Therefore, patients may need to be monitored when digoxin is taken concomitantly with omeprazole. In the clinical trials, antacids were used concomitantly with the administration of omeprazole. Omeprazole can prolong the elimination of diazepam, warfarin and phenytoin, drugs that are metabolized by oxidation in the liver.
There have been reports of increased INR and prothrombin time in patients receiving proton pump inhibitors, including omeprazole, and warfarin concomitantly. Increases in INR and prothrombin time may lead to abnormal bleeding and even death. Patients treated with proton pump inhibitors and warfarin may need to be monitored for increases in INR and prothrombin time. Although in normal subjects no interaction with theophylline or propranolol was found, there have been clinical reports of interaction with other drugs metabolized via the cytochrome P system e.
Patients should be monitored to determine if it is necessary to adjust the dosage of these drugs when taken concomitantly with omeprazole. Concomitant administration of omeprazole and voriconazole a combined inhibitor of CYP2C19 and CYP3A4 resulted in more than doubling of the omeprazole exposure.
Dose adjustment of omeprazole is not normally required. Omeprazole acts as an inhibitor of CYP 2C Co-administration of cilostazol with omeprazole is expected to increase concentrations of cilostazol and its above mentioned active metabolite. Therefore a dose reduction of cilostazol from mg twice daily to 50 mg twice daily should be considered. Avoid concomitant use of St. Omeprazole is an inhibitor of CYP2C19 enzyme. Clopidogrel is metabolized to its active metabolite in part by CYP2C Concomitant use of omeprazole 80 mg results in reduced plasma concentrations of the active metabolite of clopidogrel and a reduction in platelet inhibition.
Avoid concomitant administration of omeprazole with clopidogrel. When using omeprazole, consider use of alternative anti-platelet therapy [see Pharmacokinetics There are no adequate combination studies of a lower dose of omeprazole or a higher dose of clopidogrel in comparison with the approved dose of clopidogrel. Concomitant administration of omeprazole and tacrolimus may increase the serum levels of tacrolimus.
Drug-induced decrease in gastric acidity results in enterochromaffin-like cell hyperplasia and increased Chromogranin A levels which may interfere with investigations for neuroendocrine tumors [see Warnings and Precautions 5.
Concomitant administration of clarithromycin with other drugs can lead to serious adverse reactions due to drug interactions [see Warnings and Precautions in prescribing information for clarithromycin]. Because of these drug interactions, clarithromycin is contraindicated for co-administration with certain drugs [see Contraindications in prescribing information for clarithromycin].
However, no formal drug interaction studies of methotrexate with PPIs have been conducted [see Warnings and Precautions 5. There are no adequate and well-controlled studies with omeprazole in pregnant women. Available epidemiologic data fail to demonstrate an increased risk of major congenital malformations or other adverse pregnancy outcomes with first trimester omeprazole use. Reproduction studies in rats and rabbits resulted in dose-dependent embryolethality at omeprazole doses that were approximately 5.
Omeprazole should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Four epidemiological studies compared the frequency of congenital abnormalities among infants born to women who used omeprazole during pregnancy with the frequency of abnormalities among infants of women exposed to H2-receptor antagonists or other controls. The number of infants exposed in utero to omeprazole that had any malformation, low birth weight, low Apgar score, or hospitalization was similar to the number observed 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. A population-based retrospective cohort study covering all live births in Denmark from to , reported on 1, live births whose mothers used omeprazole during the first trimester of pregnancy and , live births whose mothers did not use any proton pump inhibitor.
The overall rate of birth defects in infants born to mothers with first trimester exposure to omeprazole was 2. A retrospective cohort study reported on pregnant women exposed to either H2-blockers or omeprazole in the first trimester exposed to omeprazole and 1, pregnant women unexposed to either during the first trimester.
The overall malformation rate in offspring born to mothers with first trimester exposure to omeprazole, an H2-blocker, or were unexposed was 3. Rates of spontaneous and elective abortions, preterm deliveries, gestational age at delivery, and mean birth weight were similar among the groups.
Several studies have reported no apparent adverse short-term effects on the infant when single dose oral or intravenous omeprazole was administered to over pregnant women as premedication for cesarean section under general anesthesia. In rabbits, omeprazole in a dose range of 6. Omeprazole is present in human milk. Omeprazole concentrations were measured in breast milk of a woman following oral administration of 20 mg. This concentration would correspond to 0. Caution should be exercised when omeprazole is administered to a nursing woman.
Use of omeprazole in pediatric and adolescent patients 2 to 16 years of age for the treatment of GERD and maintenance of healing of erosive esophagitis is supported by a extrapolation of results from adequate and well-controlled studies that supported the approval of omeprazole for adults, and b safety and pharmacokinetic studies performed in pediatric and adolescent patients.
The safety and effectiveness of omeprazole for other pediatric uses have not been established. There were no differences in safety and effectiveness between the elderly and younger subjects. Other reported clinical experience has not identified differences in response between the elderly and younger subjects, but greater sensitivity of some older individuals cannot be ruled out.
Pharmacokinetic studies have shown the elimination rate was somewhat decreased in the elderly and bioavailability was increased. However, no dosage adjustment is necessary in the elderly. Consider dose reduction, particularly for maintenance of healing of erosive esophagitis. Reports have been received of overdosage with omeprazole in humans. Doses ranged up to mg times the usual recommended clinical dose. Manifestations were variable, but included confusion, drowsiness, blurred vision, tachycardia, nausea, vomiting, diaphoresis, flushing, headache, dry mouth, and other adverse reactions similar to those seen in normal clinical experience.
No specific antidote for omeprazole overdosage is known. Omeprazole is extensively protein bound and is, therefore, not readily dialyzable.
In the event of overdosage, treatment should be symptomatic and supportive. As with the management of any overdose, the possibility of multiple drug ingestion should be considered. For current information on treatment of any drug overdose, contact a Poison Control Center at Animals given these doses showed sedation, ptosis, tremors, convulsions, and decreased activity, body temperature, and respiratory rate and increased depth of respiration.
The active ingredient in omeprazole delayed-release capsules is a substituted benzimidazole, 5-methoxy[[ 4-methoxy-3, 5-dimethylpyridinyl methyl] sulfinyl]-1H-benzimidazole, a compound that inhibits gastric acid secretion. The structural formula is:.
It is a weak base, freely soluble in ethanol and methanol, and slightly soluble in acetone and isopropanol and very slightly soluble in water. The stability of omeprazole is a function of pH; it is rapidly degraded in acid media, but has acceptable stability under alkaline conditions.
Omeprazole is supplied as delayed-release capsules for oral administration. Each delayed-release capsule contains either 10 mg, 20 mg or 40 mg of omeprazole in the form of enteric-coated granules with the following inactive ingredients: magnesium hydroxide, mannitol, methacrylic acid copolymer dispersion, povidone and triethyl citrate.
The capsule shells have the following inactive ingredients: gelatin, red iron oxide and titanium dioxide. The capsule imprinting ink contains ammonium hydroxide, black iron oxide, ethyl alcohol, isopropyl alcohol, n-butyl alcohol, potassium hydroxide, propylene glycol and shellac.
Because this enzyme system is regarded as the acid proton pump within the gastric mucosa, omeprazole has been characterized as a gastric acid-pump inhibitor, in that it blocks the final step of acid production.
This effect is dose-related and leads to inhibition of both basal and stimulated acid secretion irrespective of the stimulus. Animal studies indicate that after rapid disappearance from plasma, omeprazole can be found within the gastric mucosa for a day or more. After oral administration, the onset of the antisecretory effect of omeprazole occurs within one hour, with the maximum effect occurring within two hours. When the drug is discontinued, secretory activity returns gradually, over 3 to 5 days.
The inhibitory effect of omeprazole on acid secretion increases with repeated once-daily dosing, reaching a plateau after four days. Results from numerous studies of the antisecretory effect of multiple doses of 20 mg and 40 mg of omeprazole in normal volunteers and patients are shown below. In studies involving more than patients, serum gastrin levels increased during the first 1 to 2 weeks of once-daily administration of therapeutic doses of omeprazole in parallel with inhibition of acid secretion.
No further increase in serum gastrin occurred with continued treatment. In comparison with histamine H2-receptor antagonists, the median increases produced by 20 mg doses of omeprazole were higher 1. Gastrin values returned to pretreatment levels, usually within 1 to 2 weeks after discontinuation of therapy. Increased gastrin causes enterochromaffin-like cell hyperplasia and increased serum Chromogranin A CgA levels. The increased CgA levels may cause false positive results in diagnostic investigations for neuroendocrine tumors.
Human gastric biopsy specimens have been obtained from more than patients treated with omeprazole in long-term clinical trials. The incidence of ECL cell hyperplasia in these studies increased with time; however, no case of ECL cell carcinoids, dysplasia, or neoplasia has been found in these patients. Systemic effects of omeprazole in the CNS, cardiovascular and respiratory systems have not been found to date.
Omeprazole, given in oral doses of 30 or 40 mg for 2 to 4 weeks, had no effect on thyroid function, carbohydrate metabolism, or circulating levels of parathyroid hormone, cortisol, estradiol, testosterone, prolactin, cholecystokinin or secretin.
No effect on gastric emptying of the solid and liquid components of a test meal was demonstrated after a single dose of omeprazole 90 mg. In healthy subjects, a single I. No systematic dose-dependent effect has been observed on basal or stimulated pepsin output in humans. However, when intragastric pH is maintained at 4. As do other agents that elevate intragastric pH, omeprazole administered for 14 days in healthy subjects produced a significant increase in the intragastric concentrations of viable bacteria.
The pattern of the bacterial species was unchanged from that commonly found in saliva. All changes resolved within three days of stopping treatment. No significant differences between treatment groups were observed in development of ECL cell hyperplasia, corpus atrophic gastritis, corpus intestinal metaplasia, or colon polyps exceeding 3 mm in diameter [See Clinical Pharmacology 12 ].
Omeprazole delayed-release capsules contain an enteric-coated granule formulation of omeprazole because omeprazole is acid-labile , so that absorption of omeprazole begins only after the granules leave the stomach. Absorption is rapid, with peak plasma levels of omeprazole occurring within 0. Peak plasma concentrations of omeprazole and AUC are approximately proportional to doses up to 40 mg, but because of a saturable first-pass effect, a greater than linear response in peak plasma concentration and AUC occurs with doses greater than 40 mg.
In healthy subjects the plasma half-life is 0. The bioavailability of omeprazole increases slightly upon repeated administration of omeprazole delayed-release capsules.
Omeprazole delayed-release capsule 40 mg was bioequivalent when administered with and without applesauce. However, omeprazole delayed-release capsule 20 mg was not bioequivalent when administered with and without applesauce.
The clinical relevance of this finding is unknown. Following single dose oral administration of a buffered solution of omeprazole, little if any unchanged drug was excreted in urine.
Two were identified as hydroxyomeprazole and the corresponding carboxylic acid. The remainder of the dose was recoverable in feces. This implies a significant biliary excretion of the metabolites of omeprazole.
Three metabolites have been identified in plasma — the sulfide and sulfone derivatives of omeprazole, and hydroxyomeprazole. These metabolites have very little or no antisecretory activity. Omeprazole 40 mg daily was given in combination with clarithromycin mg every 8 hours to healthy adult male subjects.
The observed increases in omeprazole plasma concentration were associated with the following pharmacological effects. The mean hour gastric pH value was 5.
The plasma levels of clarithromycin and hydroxy-clarithromycin were increased by the concomitant administration of omeprazole. Clarithromycin concentrations in the gastric tissue and mucus were also increased by concomitant administration of omeprazole.
In a crossover clinical study, 72 healthy subjects were administered clopidogrel mg loading dose followed by 75 mg per day alone and with omeprazole 80 mg at the same time as clopidogrel for 5 days. In another study, 72 healthy subjects were given the same doses of clopidogrel and 80 mg omeprazole but the drugs were administered 12 hours apart; the results were similar, indicating that administering clopidogrel and omeprazole at different times does not prevent their interaction.
The elimination rate of omeprazole was somewhat decreased in the elderly, and bioavailability was increased. The pharmacokinetics of omeprazole have been investigated in pediatric patients 2 to 16 years of age:. Dose reduction, particularly where maintenance of healing of erosive esophagitis is indicated, for the hepatically impaired should be considered.
Because urinary excretion is a primary route of excretion of omeprazole metabolites, their elimination slowed in proportion to the decreased creatinine clearance. No dose reduction is necessary in patients with renal impairment. In pharmacokinetic studies of single 20 mg omeprazole doses, an increase in AUC of approximately four-fold was noted in Asian subjects compared with Caucasians.
Dose reduction, particularly where maintenance of healing of erosive esophagitis is indicated, for Asian subjects should be considered. Omeprazole and clarithromycin dual therapy and omeprazole, clarithromycin and amoxicillin triple therapy have been shown to be active against most strains of Helicobacter pylori in vitro and in clinical infections as described in the Indications and Usage section 1. Clarithromycin pretreatment resistance rates were 3.
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