Patients who taken or discontinue taking certain other medicines while undergoing treatment with Glimepiride may experience changes in blood glucose control.
The following interactions must be considered; Potentiation of the blood-glucose-lowering effect and, thus, in some instances hypoglycaemia may occur when one of the following drugs is taken, for examples: insulin and other oral antidiabetics, MAO inhibitors, ACE inhibitors, miconazole, anabolic steroids and male sex hormones, para-aminosalicyclic acid, chloramphenicol, pentoxifylline (high dose parenteral), coumarin derivatives, phenylbutazone, azapropazone, oxyphenbutazone, cyclophosphamide, probenecid, disopyramide, quinolones, fenfluramine, salicylates, fenyramidol, sulphinpyrazone, fibrates, sulfonamide antibiotics, fluoxetine, tetracyclines, guanethidine, tritoqualine, ifosfamide, trofosfamide.
Weakening of the blood-glucose-lowering effect and thus raised glucose levels may occur when one of the following drug is taken for example: acetazolamide, laxatives (after protracted use), barbiturates, nicotinic acid (in high doses), corticosteroids, oestrogens and progestogens, diazoxide, phenothiazines, diuretics, phenytoin, epinephrine (adrenaline) and other sympathomimetic agents, rifampicin, glucagons, thyroid hormones.
H2 receptor antagonists, beta-blockers, clonidine and reserpine may lead to either potentiation or weakening of the blood-glucose-lowering effects. Under the influence of sympatholytic drugs such as beta-blockers, clonidine, guanethidine and reserpine, the signs of adrenergic counter-regulation to hypoglycaemia may be reduced or absent. Both acute and chronic alcohol intake may potentiate or weaker the blood-glucose-lowering action of Glimepiride in an unpredictable fashion.
The effect of coumarin derivatives may be potentiated or weakened.