Pharmacologic Category: Proton Pump Inhibitor.
Pharmacology: Pharmacodynamics and Pharmacokinetics: 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 in the parietal cell. It is rapidly acting and provides control through inhibitor of gastric acid secretion with once daily dosing.
Omeprazole is a weak base and is concentrated and converted to the active form in the highly acidic environment of the intracellular canaliculi within a parietal cell, where it inhibits the enzyme H+/K+-ATPase - the acid pump. This effect on the final step of the gastric acid formulation process is dose-dependent and provides for highly effective inhibition of both basal acid secretion and stimulated acid secretion, irrespective of stimulus.
Omeprazole is rapidly but variably absorbed following oral administration. Absorption is not affected by food. Omeprazole is acid-labile, and pharmacokinetics may vary between the various formulations developed to improve oral bioavailability. The absorption of omeprazole also appears to be dose-dependent. Increasing the dosage above 40 mg has been reported to increase the plasma concentrations in a non-linear fashion because of saturable first pass hepatic metabolism. In addition, absorption is higher after long term administration.
Bioavailability of omeprazole may be increased in elderly patients, in some ethnic groups such as Chinese, and in patients with impaired hepatic function, but it is not markedly affected in patients with renal impairment. Following absorption, omeprazole is almost completely metabolized in the liver, primarily by the cytochrome P450 isoenzyme CYP2C19 to form hydroxyomeprazole, and to a small extent by CYP3A4 to form omeprazole sulfone. The metabolites are inactive, and are excreted mostly in the urine and to a lesser extent in bile. The elimination half-life from plasma is reported to be about 0.5 to 3 hours. Omeprazole is highly bound (about 95%) to plasma proteins.
Omeprazole is a proton pump inhibitor. It inhibits secretions of gastric acid by irreversibly blocking the enzyme system of hydrogen/potassium adenosine triphosphatase, the proton pump of gastric parietal cell. It is used in conditions where inhibition of gastric acid secretion may be beneficial including aspiration syndromes, dyspepsia, gastro-esophageal reflux disease, peptic ulcer disease, and the Zollinger-Ellison Syndrome.
Dyspepsia: Usual dose: 20 mg daily for 2-4 weeks.
Gastro-esophageal reflux disease: Usual dose: 20 mg once daily for 4 weeks followed by a further 4 to 8 weeks if not fully healed.
Refractory esophagitis: 40 mg daily. Maintenance therapy after healing of esophagitis is 20 mg once daily. In children, doses in the range 0.7 to 1.4 mg per kg bodyweight daily, up to a maximum dose of 40 mg, have been given for 4 to 12 weeks.
Peptic ulcer disease: A single dose of 20 mg by mouth, or 40 mg in severe cases, is given. Treatment is continued for 4 weeks for duodenal ulcer and 8 weeks for gastric ulcer. Where appropriate, a dose of 20 mg once daily may be given for maintenance.
NSAID-associated ulceration: A dose of 20 mg daily.
Zollinger-Ellison syndrome: Initial recommended dosage is 60 mg once daily.
Or as prescribed by a physician.
Prophylaxis of acid aspiration during general anesthesia: 40 mg the evening before the surgery and a further 40 mg two to six hours before the procedure. Or as prescribed by a physician.
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 other clinical outcome due to omeprazole has been reported. The rate of elimination was unchanged (first order kinetics) with increased dose and no specific treatment has been needed.
Known hypersensitivity to omeprazole, substituted benzimidazoles or any other constituent of the formulation.
Before giving omeprazole consider the possibility of malignancy in patients with gastric ulcers since this drug may mask symptoms and delay diagnosis. Omeprazole should be used with caution in patients with hepatic impairment.
Results from three prospective epidemiological studies indicate no adverse effect of omeprazole on pregnancy or on the health of the fetus/newborn child. Omeprazole 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 most frequent adverse effects of omeprazole are headache, diarrhea and skin rashes. Other adverse effects include pruritus, dizziness, fatigue, constipation, nausea and vomiting, flatulence, abdominal pain, arthralgia and myalgia, urticaria and dry mouth.
Omeprazole and other proton pump inhibitors are metabolized by the cytochrome P450 system, primarily by isoenzyme CYP2C19 and may alter the metabolism of some other drugs metabolized by these enzymes. Omeprazole may prolong the elimination of diazepam, phenytoin and warfarin. Omeprazole and other proton pump inhibitors can reduce the absorption of drugs such as ketoconazole, and possibly itraconazole, whose absorption is dependent on acid gastric pH. With voriconazole, the plasma concentration of both drugs may be increased. Omeprazole and other proton pump inhibitors should not be used with atazanavir, as it substantially reduces exposure to atazanavir.
A02BC01 - omeprazole ; Belongs to the class of proton pump inhibitors. Used in the treatment of peptic ulcer and gastro-oesophageal reflux disease (GERD).
Wilom cap 40 mg
50's (P51.5/cap, P2,575/pack)
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