CEZOL-20 Capsule

Hypersensitivity to any of the ingredients.

Diarrhoea, Nausea, Dry mouth, Dizziness, Headache, Abdominal Colic, Skin rashes.

Since Omeprazole is metabolized by CYP2C19 and CYP3A4, active substances known to inhibit CYP2C19 and CYP3A4 (such as clarithromycin and voriconazole) may lead to increased omeprazole serum levels by decreasing omeprazole’s rate of metabolism. Concomitant voriconazole treatment resulted in more than doubling of the omeprazole exposure. As high doses of omeprazole have been well-tolerated adjustment of the omeprazole dose is not generally required. However, dose adjustment should be considered in patients with severe hepatic impairment and if long-term treatment is indicated.

Pregnancy

The analysis of the results from 3 epidemiological studies has revealed no evidence of adverse events of omeprazole on pregnancy or on the health of the foetus/new-born child.

Omeprazole can be used in pregnancy.

Lactation

Omeprazole is excreted in breast milk but is not likely to influence the child when therapeutic doses are used.

Co-administration of atazanavir with PPI is not recommended. If the combination of atazanavir with a PPI is judged unavoidable, close clinical monitoring (e.g. virus load) is recommended in combination with an increase in the dose of atazanavir to 40mg with 100mg of ritonavir, omeprazole 20mg should not be exceeded.

Omeprazole may reduce the absorption of vitamin B12 (cyanocobalamin) due to hypo-or achlorhydria. This should be considered in patients with reduced body stones or risk factors for reduced vitamin B12 absorption on long-term therapy.

Omeprazole, a racemic mixture of two 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 reversible inhibition 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 the parietal cell, where it inhibits the enzyme H+K+-ATPase- the acid 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.