Glucotrol XL Drug Interactions

The following products are likely to increase the hypoglycemic effect: Miconazole: Increased in hypoglycemic effect, possibly leading to symptoms of hypoglycemia or even coma.
Fluconazole: There have been reports of hypoglycemia following the co-administration of glipizide and fluconazole, possibly the result an increased half-life of glipizide.
Voriconazole: Although not studied, voriconazole may increase the plasma levels of sulfonylureas, (eg, tolbutamide, glipizide and glyburide), and therefore cause hypoglycemia. Careful monitoring of blood glucose is recommended during co-administration.
Nonsteroidal Anti-Inflammatory Agents (NSAIDS) (eg, Phenylbutazone): Increased hypoglycemic effect of sulfonylureas (displacement of sulfonylurea binding to plasma proteins and/or decrease in sulfonylurea elimination).
Salicylates (Acetylsalicylic Acid): Increased in hypoglycemic effect by high doses of acetylsalicylic acid (hypoglycemic action of the acetylsalicylic acid).
Alcohol: Increased hypoglycemic reaction which can lead to hypoglycemic coma.
Beta-Blockers: All β-blockers mask some of the symptoms of hypoglycemic eg, palpitations and tachycardia. Most noncardioselective β-blockers increase the incidence and severity of hypoglycemia.
Angiotensin-Converting Enzyme Inhibitors: The use of angiotensin-converting enzyme inhibitors may lead to an increased hypoglycemic effect in diabetic patients treated with sulfonylureas, including glipizide GITS. Therefore, a reduction in glipizide dosage may be required.
H₂-Receptor Antagonists: The use of H₂-receptor antagonists (ie, cimetidine) may potentiate the hypoglycemic effects of sulfonylureas, including glipizide.
The hypoglycemic action of sulfonylureas in general may also be potentiated by monoamine oxidase inhibitors and drugs that are highly protein-bound eg, sulfonamides, chloramphenicol, probenecid, coumarins. When such drugs are administered to (or withdrawn from) a patient receiving glipizide GITS, the patient should be observed closely for hypoglycemia (or loss of control). In vitro binding studies with human serum proteins indicate that glipizide binds differently than tolbutamide and does not interact with salicylate or dicoumarol. However, caution must be exercised in extrapolating these findings to the clinical situation and in the use of glipizide with these drugs.
The following products could lead to hyperglycemia: Phenothiazines (eg, chlorpromazine) at high doses (chlorpromazine >100 mg/day): Elevation in blood glucose (reduction in insulin release).
Corticosteroids: Elevation in blood glucose.
Sympathomimetics (eg, Ritodrine, Salbutamol, Terbutaline): Elevation in blood glucose due to β₂-adrenoceptor stimulation.
Other drugs that may be produce hyperglycemia, and lead to a loss of control include the thiazides and other diuretics, thyroid products, estrogens, progestogens, oral contraceptive, phenytoin, nicotinic acid, calcium-channel blocking drugs and isoniazid.
When such drugs are withdrawn from (or administered to) a patient receiving glipizide GITS, the patients should be observed closely for hypoglycemia (or loss control).