Galvus Met Drug Interactions

Galvus Met: There have been no formal interaction studies for Galvus Met. The following statements reflect the information available on the individual active substances.
Vildagliptin: Since vildagliptin neither inhibits nor induces CYP450 enzymes, it is not likely to interact with co-medications that are metabolized by CYP450 or that act as inhibitors or inducers of these enzymes.
Drug interaction studies were conducted with commonly co-prescribed medications for patients with type 2 diabetes or medications with a narrow therapeutic window. As a result of these studies, no clinically relevant interactions were observed with other oral antidiabetics (glibenclamide, pioglitazone, metformin), amlodipine, digoxin, ramipril, simvastatin, valsartan or warfarin.
Metformin: Interactions which influence metformin efficacy: Reduction in hypoglycaemic efficacy: Glucocorticoids (systemic and local), beta-2-agonists, diuretics, phenothiazines (e.g. chlorpromazine), thyroid hormones, oestrogens, oral contraceptives, hormone replacement products, phenytoin, nicotinic acid, calcium channel blockers, isoniazid and tetracosactide may increase blood glucose levels.
Potentiation of hypoglycaemic efficacy: Furosemide increases plasma levels of metformin (C_max by 22%, AUC by 15%) with no significant change in renal clearance.
Nifedipine increases plasma levels of metformin (C_max by 20%, AUC by 9-20%) by increasing metformin absorption.
Cimetidine increases metformin C_max by 60% and AUC by 40%. The elimination half-life of metformin is unaffected. Other active substances (amiloride, digoxin, morphine, procainamide, quinidine, quinine, ranitidine, triamterene, trimethoprim, or vancomycin) that are eliminated by active renal tubular secretion have the potential for interaction with metformin. Patients receiving such medicinal products should therefore be closely monitored during treatment with metformin.
ACE inhibitors may lower blood glucose.
Blood glucose may also be lowered by beta-blockers, although cardioselective (beta-1-selective) beta-blockers exhibit such interactions to a much smaller extent than do non-cardioselective agents.
Co-administration of MAO inhibitors and oral antidiabetics may improve glucose tolerance and increase the hypoglycaemic effect.
Concomitant alcohol use may potentiate the hypoglycaemic effect of metformin, and may even cause hypoglycaemic coma.
Increased or reduced hypoglycaemic effect of metformin: H₂-antagonists, clonidine and reserpine may increase or reduce the effect of metformin.
Disturbances of blood glucose control (including hyper- or hypoglycaemia) have been observed following co-administration of quinolones and metformin.
Interactions that increase the adverse effects of metformin: Diuretics: Renal dysfunction due to diuretics (especially loop diuretics) may result in lactic acidosis. Diuretics also cause blood glucose levels to rise.
Iodinated contrast media: See Precautions for information on interactions with iodinated radiocontrast agents and the risk of resultant lactic acidosis. Metformin-containing products (such as Galvus Met) must therefore be discontinued prior to, or at the time of, the test and must not be reinstituted until at least 48 hours afterwards, and only after renal function has been checked and found to be normal.
Alcohol: Acute alcohol intoxication in patients taking metformin poses an increased risk of lactic acidosis, particularly after fasting or in the presence of malnutrition or hepatic impairment.
Other - Some drugs can adversely affect renal function which may increase the risk of lactic acidosis, e.g. NSAIDs [including selective cyclo-oxygenase (COX) II inhibitors], ACE inhibitors, angiotensin II receptor antagonists and diuretics. When starting or using such products in combination with metformin-containing products (such as Galvus Met), close monitoring of renal function is necessary.
Interactions that influence the efficacy of other substances: Metformin lowers plasma levels of furosemide (C_max by 33%, AUC by 12%), and shortens the terminal half-life by 32%, without altering renal clearance of furosemide.
The effect of phenprocoumon may be reduced since its elimination is accelerated by metformin.
Interaction studies with glibenclamide, nifedipine, ibuprofen and propranolol have shown no clinically relevant effects on the pharmacokinetic parameters of these substances.
Other interactions: The warning signs of hypoglycaemia may be rendered less perceptible by the effects of sympatholytics (e.g. beta-blockers, clonidine, guanethidine, reserpine).