Glipizide

Colesevelam may decrease sulfonylurea exposure. Administer glipizide 4 hours prior to colesevelam.

Fluconazole increases glipizide AUC by mean 56.9% (range 35-81%), potentially increasing hypoglycemic effect. Close monitoring recommended.

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 leading to severe hypoglycemia has been reported with oral miconazole and oral hypoglycemic agents.

Sulfonamides may potentiate hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia when initiated or withdrawn.

May reduce glucose-lowering effect of glipizide, leading to worsening glycemic control; monitor closely.

May lead to either potentiation or weakening of glucose-lowering effect; increased monitoring required.

May increase the glucose-lowering effect of glipizide, increasing susceptibility to hypoglycemia. Monitor closely.

Tend to produce hyperglycemia and may lead to loss of glipizide control. Monitor for loss of control when administered or withdrawn.

May increase the glucose-lowering effect of glipizide, increasing susceptibility to hypoglycemia. Monitor closely.

Some azoles may potentiate hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia when initiated or withdrawn.

Calcium channel blockers may produce hyperglycemia and lead to loss of glycemic control. Patient should be observed closely for loss of control when initiated or withdrawn.

Chloramphenicol may potentiate hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia when initiated or withdrawn.

May lead to either potentiation or weakening of glucose-lowering effect; may mask hypoglycemia signs.

May reduce glucose-lowering effect of glipizide, leading to worsening glycemic control; monitor closely.

Colesevelam reduces glipizide ER AUC and Cmax by 12-13% when coadministered. Glipizide should be administered at least 4 hours prior to colesevelam.

Corticosteroids may produce hyperglycemia and lead to loss of glycemic control. Patient should be observed closely for loss of control when initiated or withdrawn.

May reduce glucose-lowering effect of glipizide, leading to worsening glycemic control; monitor closely.

In vitro binding studies suggest limited interaction, but caution is advised in clinical use.

May increase glucose-lowering effect of glipizide and susceptibility to hypoglycemia; monitor closely.

Tend to produce hyperglycemia and may lead to loss of control. Patient should be closely observed for loss of control when initiated or hypoglycemia when withdrawn.

TRIKAFTA may increase glipizide exposure via CYP2C9 inhibition. Use with caution and monitor.

May reduce glucose-lowering effect of glipizide, leading to worsening glycemic control; monitor closely.

Estrogens may produce hyperglycemia and lead to loss of glycemic control. Patient should be observed closely for loss of control when initiated or withdrawn.

May increase the glucose-lowering effect of glipizide, increasing susceptibility to hypoglycemia. Monitor closely.

May increase glucose-lowering effect of glipizide and susceptibility to hypoglycemia; monitor closely.

May reduce the glucose-lowering effect of glipizide, leading to worsening glycemic control. Monitor closely.

May mask signs of hypoglycemia in patients taking glipizide.

Isoniazid may produce hyperglycemia and lead to loss of glycemic control. Patient should be observed closely for loss of control when initiated or withdrawn.

Ivacaftor may increase glipizide exposure through CYP2C9 inhibition. Should be used with caution.

May increase the glucose-lowering effect of glipizide, increasing susceptibility to hypoglycemia. Monitor closely.

May increase the glucose-lowering effect of glipizide, increasing susceptibility to hypoglycemia. Monitor closely.

MAOIs may potentiate hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia when initiated or withdrawn.

Nicotinic acid may produce hyperglycemia and lead to loss of glycemic control. Patient should be observed closely for loss of control when initiated or withdrawn.

Beta blockers may potentiate hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia when initiated or withdrawn.

NSAIDs may potentiate hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia when initiated or withdrawn.

May increase glucose-lowering effect of glipizide and susceptibility to hypoglycemia; monitor closely.

May reduce glucose-lowering effect of glipizide, leading to worsening glycemic control; monitor closely.

Coumarins may potentiate hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia when initiated or withdrawn.

Oral contraceptives may produce hyperglycemia and lead to loss of glycemic control. Patient should be observed closely for loss of control when initiated or withdrawn.

May increase glucose-lowering effect of glipizide and susceptibility to hypoglycemia; monitor closely.

Phenothiazines may produce hyperglycemia and lead to loss of glycemic control. Patient should be observed closely for loss of control when initiated or withdrawn.

Phenytoin may produce hyperglycemia and lead to loss of glycemic control. Patient should be observed closely for loss of control when initiated or withdrawn.

May increase glucose-lowering effect of glipizide and susceptibility to hypoglycemia; monitor closely.

Probenecid may potentiate hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia when initiated or withdrawn.

May increase glucose-lowering effect of glipizide and susceptibility to hypoglycemia; monitor closely.

May reduce the glucose-lowering effect of glipizide, leading to worsening glycemic control. Monitor closely.

Quinolones may potentiate hypoglycemic action of glipizide. Patient should be observed closely for hypoglycemia when initiated or withdrawn.

Glipizide exposure increased by 34% following single 150-mg dose of oral ranitidine in diabetic patients. Use appropriate clinical monitoring.

Glipizide exposure increased by 34% following a single 150-mg dose of oral ranitidine. Use appropriate clinical monitoring when initiating or discontinuing ranitidine.

May lead to either potentiation or weakening of glucose-lowering effect; may mask hypoglycemia signs.

Salicylates may potentiate hypoglycemic action of glipizide. Caution should be exercised; in vitro studies suggest glipizide does not interact with salicylate but clinical extrapolation warranted.

May reduce glucose-lowering effect of glipizide, leading to worsening glycemic control; monitor closely.

BACTRIM potentiates oral hypoglycemic effects of glipizide. Additional blood glucose monitoring warranted.

May reduce glucose-lowering effect of glipizide, leading to worsening glycemic control; monitor closely.

Thiazide diuretics may produce hyperglycemia and lead to loss of glycemic control. Patient should be observed closely for loss of control when initiated or withdrawn.

Thyroid products may produce hyperglycemia and lead to loss of glycemic control. Patient should be observed closely for loss of control when initiated or withdrawn.

May reduce the glucose-lowering effect of glipizide, leading to worsening glycemic control. Monitor closely.

May increase glucose-lowering effect of glipizide and susceptibility to hypoglycemia; monitor closely.

In vivo testing showed no clinically significant changes in glipizide exposure when co-administered with LOKELMA.

Glipizide is a CYP2C9 substrate that may interact with desogestrel metabolism. Clinical relevance of this interaction is unknown.

The following are examples of medication that may increase the glucose lowering effect of glipizide extended-release tablets, increase the susceptibility to and/or intensity of hypoglycemia: antidiabetic agents, ACE inhibitors, angiotensin II receptor blocking agents, disopyramide, fibrates, fluoxetine, monoamine oxidase inhibitors, pentoxifylline, pramlintide, propoxyphene, salicylates, somatostatin analogs (e.g., octreotide), sulfonamide antibiotics, nonsteroidal anti-inflammatory agents, chloramphenicol, probenecid, coumarins, voriconazole, H2 receptor antagonists, and quinolones. The following are examples of medication that may increase the glucose lowering effect of glipizide extended-release tablets, increase the susceptibility to and/or intensity of hypoglycemia: antidiabetic agents, ACE inhibitors, angiotensin II receptor blocking agents, disopyramide, fibrates, fluoxetine, monoamine oxidase inhibitors, pentoxifylline, pramlintide, propoxyphene, salicylates, somatostatin analogs (e.g., octreotide), sulfonamide antibiotics, nonsteroidal anti-inflammatory agents, chloramphenicol, probenecid, coumarins, voriconazole, H2 receptor antagonists, and quinolones.

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