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The hypoglycemic action of sulfonylureas may be potentiated by certain drugs including NSAIDs and other drugs that are highly protein bound, eg, salicylates, sulfonamides, chloramphenicol, coumarins, probenecid, MAOIs and β-adrenergic blocking agents. When these drugs are administered to a patient receiving glimepiride, the patient should be observed closely for hypoglycemia.
Certain drugs tend to produce hyperglycemia and may lead to loss of control. These drugs include the thiazides and other diuretics, corticosteroids, phenothiazines, thyroid products, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, and isoniazid. When these drugs are administered to a patient receiving glimepiride, the patient should be closely observed for loss of control.
Glimepiride is metabolized by cytochrome P-450 2C9 (CYP2C9). This should be taken into account when glimepiride is co-administered with inducers, inhibitors or substrate of CYP2C9 (eg, rifampicin, fluconazole, amiodarone, tolbutamide, diclofenac, ibuprofen, naproxen).
H2-receptor antagonists, β-blockers, clonidine and reserpine may lead to either potentiation or weakening of the blood-glucose-lowering effect.
Concomitant treatment with a β-receptor blocker, clonidine, guanethidine or reserpine may mask the warning symptoms of a hypoglycemic attack.
Acute and chronic alcohol intake may either potentiate or attenuate the activity of glimepiride in an unpredictable fashion.
