Severity N/A
Amiloride (HCl) Interaction of Amiloride (HCl) with Chlorpropamide
Rifampicin Interaction of Rifampicin with Chlorpropamide
Clofibrate Interaction of Clofibrate with Chlorpropamide
Phenobarbitone Interaction of Phenobarbitone with Chlorpropamide
Magnesium Oxides and Hydroxides Interaction of Magnesium Oxides and Hydroxides with Chlorpropamide
Carbamazepine Interaction of Carbamazepine with Chlorpropamide
Desmopressin (Acetate) Interaction of Desmopressin (Acetate) with Chlorpropamide
Sulphadiazine Interaction of Sulphadiazine with Chlorpropamide
Lypressin Interaction of Lypressin with Chlorpropamide
Vasopressin Interaction of Vasopressin with Chlorpropamide
Miconazole (Nitrate) Interaction of Miconazole (Nitrate) with Chlorpropamide
Alcohol Interaction of Alcohol with Chlorpropamide
Salicylic Acid Interaction of Salicylic Acid with Chlorpropamide
Sodium Citrate Interaction of Sodium Citrate with Chlorpropamide
Details: Sodium Citrate may increase the excretion and decrease the serum levels of Chlorpropamide, possibly decreasing their pharmacologic effects.
VORICONAZOLE Interaction of VORICONAZOLE with Chlorpropamide
Details: Additive QTc prolongation may occur.
Management: Consider alternate therapy or monitor for QTc prolongation
Moderate
Chloramphenicol Interaction of Chloramphenicol with Chlorpropamide
Details: Chloramphenicol reduces the hepatic clearence of chlorpropamide or displaces it from binding siteresult in increase plasma concentration of chlorpropamide which may lead to enhanced hypoglycemic effect.
Management: Closely monitor for level of glucose whenever start or discontinuetherapy with chloramphenicol.Adjust the dose of chlorpropamide if necessary.
Phenylbutazone Interaction of Phenylbutazone with Chlorpropamide
Details: Phenylbutazone inhibit the metabolism and renal clearence of chlorpropamide and displace it from plasma protein binding site thus potentiate the hypoglycaemic effect.
Management: Monitor blood sugar regularly. Closely monitor for increased hypoglycemic effect. Reduce the dose of chlorpropamide if necessary.
Phenytoin (Na) Interaction of Phenytoin (Na) with Chlorpropamide
Details: Phenytoin cause hyperlycemia, hypoinsulinemia and glucose intolerance and thus diminishes the hypoglycemic effect of chlorpropamide.While chlorpropamide inhibits the metabolism of phenytoin thus increases its plasma concentration and pharmacological effects.
Management: Closely monitor the level of phenytoin and blood glucose. Patient should notify to physician if experience the symptoms of phenytoin toxiity.
Probenecid Interaction of Probenecid with Chlorpropamide
Details: Probenecid stimulate the secretion of insulin thus potentiate the hypoglycemic effect of chlorpropamide.
Management: Closely monitor the blood glucose level especially in patients of advanced age or renall impairment. Adjust the dose of chlorpropamide if necessary.Patient should notify to physician if experince the signs of hypoglycemia.
Cimetidine (HCl) Interaction of Cimetidine (HCl) with Chlorpropamide
Details: Cimetidine inhibit the hepatic metabolism of chlorpropamide or increase its absorption by altering gastric pH results in increased plasma concentration may lead to enhanced hypoglycemic effect.
Management: Closely monitor blood sugar regularly. Reduce the dose of chlorpropamide if necessary.
Phenelzine Interaction of Phenelzine with Chlorpropamide
Details: Phenelzine inhibits gluconeogenesis thus potentiate the hypoglycemic effect of chlorpropamide.
Management: Adjust the dose of chlorpropamide if necessary. Closely monitor the blood sugar level especially in patients of advance age or renal impairent.
Propranolol (HCl) Interaction of Propranolol (HCl) with Chlorpropamide
Details: Propranolol inhibits the insulin secretion and hepatic glycogenolysis thus potentiate the hypoglycemic effect of chlorpropamide.
Management: Closely monitor the level of blood glucose regularly.
Tranylcypromine (Sulphate) Interaction of Tranylcypromine (Sulphate) with Chlorpropamide
Details: Tranylcypromine stimulate the secretion of insulin thus potentiate the hypoglycemic effect of chlorpropamide.
Management: Closely monitor for blood glucose level especially in patient with advanced age and renal impairement.
Warfarin (Na) Interaction of Warfarin (Na) with Chlorpropamide
Details: Chlorpropamide either enhance or reduce the hypoprothrombinemic effect of warfarin by displacing it from plasma protein binding site. Warfarin also increase the blood level of chlorpropamide by inhibiting hepatic metabolism.
Management: Prothrombin time, INR and blood sugar level should be monitor frequently. Patient should report the sign of bleeding to physician.
Perindopril Interaction of Perindopril with Chlorpropamide
Details: Theoretical potential for Perindopril Erbumine increasing the HYPOGLYCAEMIC effect of CHLORPROPAMIDE.
Management: May need to avoid combination
Fluconazole Interaction of Fluconazole with Chlorpropamide
Details: Fluconazole decrease chlorpropamide clearance by inhibiting CYP450 3A4 thus increases its plasma concentration that leads to marked hypoglycemia.
Management: Regular checking of blood glucose level and chlorpropamide dose adjustment is required when given with fluconazole.
Metipranolol Interaction of Metipranolol with Chlorpropamide
Details: Infrequent reports of METIPRANOLOL [EYE] increasing the HYPOGLYCAEMIC effect of CHLORPROPAMIDE.
Methyltestosterone Interaction of Methyltestosterone with Chlorpropamide
Details: The hypoglycemic effect of insulin secretagogues (e.g., sulfonylureas, meglitinides) may be potentiated by certain drugs, including ACE inhibitors, anabolic steroids, fibrates, monoamine oxidase inhibitors (MAOIs), nonsteroidal anti-inflammatory drugs (NSAIDs), salicylates, selective serotonin reuptake inhibitors (SSRIs), sulfonamides, disopyramide, propoxyphene, quinine, and quinidine. These drugs may increase the risk of hypoglycemia by enhancing insulin sensitivity (ACE inhibitors, fibrates); stimulating insulin secretion (salicylates, NSAIDs, disopyramide, quinine, quinidine, MAOIs); increasing peripheral glucose utilization (SSRIs, insulin-like growth factor); and/or inhibiting gluconeogenesis (SSRIs, MAOIs, insulin-like growth factor). Or, they may increase plasma concentration of insulin secretagogues by displacing them from plasma protein binding sites and/or inhibiting their metabolism (fibrates, NSAIDs, salicylates, sulfonamides). Clinical hypoglycemia has been reported during use of these agents alone or with insulin and/or sulfonylureas. Use of SSRIs has also been associated with loss of awareness of hypoglycemia in isolated cases.
Management: Close monitoring for the development of hypoglycemia is recommended if these drugs are coadministered with insulin secretagogues, particularly in patients with advanced age and/or renal impairment. The oral antidiabetic dosage(s) may require adjustment if an interaction is suspected. Patients should be apprised of the signs and symptoms of hypoglycemia (e.g., headache, dizziness, drowsiness, nausea, hunger, tremor, weakness, sweating, palpitations), how to treat it, and to contact their doctor if it occurs. Patients should be observed for loss of glycemic control when these drugs are withdrawn.