Glipizide And Metformin Hydrochloride

Fluconazole increases glipizide AUC by a mean of 56.9%, potentially increasing hypoglycemic effect. Patient should be observed closely for hypoglycemia.

A potential interaction between oral miconazole and oral hypoglycemic agents leading to severe hypoglycemia has been reported. Whether this interaction also occurs with the intravenous, topical, or vaginal preparations of miconazole is not known.

Potential interaction with oral miconazole leading to severe hypoglycemia has been reported. Effect of intravenous, topical, or vaginal preparations is not known.

Sulfonamides may potentiate the hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia.

Thiazide diuretics tend to produce hyperglycemia and may lead to loss of blood glucose control. Close observation needed for loss of blood glucose control.

Azoles may potentiate the hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia.

Calcium channel blockers may produce hyperglycemia and lead to loss of blood glucose control. Patient should be closely observed for loss of blood glucose control.

Chloramphenicol may potentiate the hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia.

Colesevelam reduces glipizide ER AUC by 12% and Cmax by 13% when coadministered, but not when glipizide ER is given 4 hours prior.

Corticosteroids may produce hyperglycemia and lead to loss of blood glucose control. Patient should be closely observed for loss of blood glucose control.

Estrogens may produce hyperglycemia and lead to loss of blood glucose control. Patient should be closely observed for loss of blood glucose control.

Isoniazid may produce hyperglycemia and lead to loss of blood glucose control. Patient should be closely observed for loss of blood glucose control.

MAOIs may potentiate the hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia.

Nicotinic acid may produce hyperglycemia and lead to loss of blood glucose control. Patient should be closely observed for loss of blood glucose control.

Beta blockers may potentiate the hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia.

NSAIDs may potentiate the hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia.

Coumarins may potentiate the hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia.

Oral contraceptives may produce hyperglycemia and lead to loss of blood glucose control. Patient should be closely observed for loss of blood glucose control.

Diuretics tend to produce hyperglycemia and may lead to loss of blood glucose control. Close observation needed for loss of blood glucose control.

Phenothiazines may produce hyperglycemia and lead to loss of blood glucose control. Patient should be closely observed for loss of blood glucose control.

Phenytoin may produce hyperglycemia and lead to loss of blood glucose control. Patient should be closely observed for loss of blood glucose control.

Probenecid may potentiate the hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia.

Salicylates may potentiate the hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia.

Thiazide diuretics may produce hyperglycemia and lead to loss of blood glucose control. Patient should be closely observed for loss of blood glucose control.

Thyroid products may produce hyperglycemia and lead to loss of blood glucose control. Patient should be closely observed for loss of blood glucose control.

Nifedipine A single-dose, metformin-nifedipine drug interaction study in normal healthy volunteers demonstrated that coadministration of nifedipine increased plasma metformin C max and AUC by 20% and 9%, respectively, and increased the amount excreted in the urine. Nifedipine appears to enhance the absorption of metformin. Metformin had minimal effects on nifedipine.

Other Carbonic Anhydrase Inhibitors Topiramate or other carbonic anhydrase inhibitors (e.g., zonisamide, acetazolamide or dichlorphenamide) frequently causes a decrease in serum bicarbonate and induce non-anion gap, hyperchloremic metabolic acidosis.

Drugs that reduce metformin clearance Concomitant use of drugs that interfere with common renal tubular transport systems involved in the renal elimination of metformin (e.g., organic cationic transporter-2 [OCT2] / multidrug and toxin extrusion [MATE] inhibitors such as ranolazine, vandetanib, dolutegravir, and cimetidine) could increase systemic exposure to metformin and may increase the risk for lactic acidosis.

Metformin Hydrochloride Furosemide A single-dose, metformin-furosemide drug interaction study in healthy subjects demonstrated that pharmacokinetic parameters of both compounds were affected by coadministration. Furosemide increased the metformin plasma and blood C max by 22% and blood AUC by 15%, without any significant change in metformin renal clearance. When administered with metformin, the C max and AUC of furosemide were 31% and 12% smaller, respectively, than when administered alone, and the terminal half-life was decreased by 32%, without any significant change in furosemide renal clearance.

In healthy volunteers, the pharmacokinetics of metformin and propranolol, and metformin and ibuprofen were not affected when coadministered in single-dose interaction studies.

This fetotoxicity has been similarly noted with other sulfonylureas, such as tolbutamide and tolazamide.

In vitro binding studies with human serum proteins indicate that glipizide binds differently than tolbutamide and does not interact with salicylate or dicumarol.

Drugs that reduce metformin clearance Concomitant use of drugs that interfere with common renal tubular transport systems involved in the renal elimination of metformin (e.g., organic cationic transporter-2 [OCT2] / multidrug and toxin extrusion [MATE] inhibitors such as ranolazine, vandetanib, dolutegravir, and cimetidine) could increase systemic exposure to metformin and may increase the risk for lactic acidosis.

Other Carbonic Anhydrase Inhibitors Topiramate or other carbonic anhydrase inhibitors (e.g., zonisamide, acetazolamide or dichlorphenamide) frequently causes a decrease in serum bicarbonate and induce non-anion gap, hyperchloremic metabolic acidosis.