Interactions between Quinidex Extentabs and Treosulfan

The quiNIDine in Quinidex Extentabs has a major potential interaction with Glaucoma/Intraocular Hypertension.

The use of quinidine is contraindicated in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as myasthenia gravis, glaucoma, and urinary retention or obstruction.

The quiNIDine in Quinidex Extentabs has a major potential interaction with Heart Block.

The use of quinidine is contraindicated for use in patients without a functioning artificial pacemaker whose cardiac rhythm is dependent upon a junctional or idioventricular pacemaker, including patients with complete AV block. Therapy with quinidine should be administered with caution in patients with severe sinus-node dysfunction such as sick sinus syndrome, bradycardia-tachycardia syndrome, or second- or third-degree heart block.

The quiNIDine in Quinidex Extentabs has a major potential interaction with Heart Failure.

Antiarrhythmic agents can induce severe hypotension (particularly with IV administration) or induce or worsen congestive heart failure (CHF). Patients with primary cardiomyopathy or inadequately compensated CHF are at increased risk. Antiarrhythmic agents should be administered cautiously and dosage and/or frequency of administration modified in patients with hypotension or adequately compensated CHF. Alternative therapy should be considered unless these conditions are secondary to cardiac arrhythmia.

The quiNIDine in Quinidex Extentabs has a moderate potential interaction with Hyperkalemia.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

The quiNIDine in Quinidex Extentabs has a moderate potential interaction with Hypokalemia.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

The quiNIDine in Quinidex Extentabs has a major potential interaction with Hypotension.

Antiarrhythmic agents can induce severe hypotension (particularly with IV administration) or induce or worsen congestive heart failure (CHF). Patients with primary cardiomyopathy or inadequately compensated CHF are at increased risk. Antiarrhythmic agents should be administered cautiously and dosage and/or frequency of administration modified in patients with hypotension or adequately compensated CHF. Alternative therapy should be considered unless these conditions are secondary to cardiac arrhythmia.

The quiNIDine in Quinidex Extentabs has a moderate potential interaction with Liver Disease.

Quinidine is primarily metabolized by the liver to active and inactive forms. Hepatic dysfunction causes a slowed metabolism and elimination of the drug which can lead to quinidine toxicity if dosage is not appropriately reduced. Clinical monitoring of hepatic function is recommended.

Treosulfan has a moderate potential interaction with Liver Disease.

Treosulfan has not been studied in patients with moderate or severe liver and renal dysfunction.

The quiNIDine in Quinidex Extentabs has a moderate potential interaction with Magnesium Imbalance.

Electrolyte imbalance can alter the therapeutic effectiveness of antiarrhythmic agents. Hypokalemia and hypomagnesemia can reduce the effectiveness of antiarrhythmic agents. In some cases, these disorders can exaggerate the degree of QTc prolongation and increase the potential for torsade de pointes. Hyperkalemia can potentiate the toxic effects of antiarrhythmic agents. Electrolyte imbalance should be corrected prior to initiating antiarrhythmic therapy. Clinical monitoring of cardiac function and electrolyte concentrations is recommended.

The quiNIDine in Quinidex Extentabs has a major potential interaction with Myasthenia Gravis.

The use of quinidine is contraindicated in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as myasthenia gravis, glaucoma, and urinary retention or obstruction.

The quiNIDine in Quinidex Extentabs has a moderate potential interaction with Renal Dysfunction.

Renal dysfunction causes a slowed elimination of quinidine which can lead to quinidine toxicity if dosage is not appropriately reduced. Therapy with quinidine should be administered cautiously and dosages reduced in patients with compromised renal function. Quinidine is not appreciably removed by hemodialysis.

Treosulfan has a moderate potential interaction with Renal Dysfunction.

Treosulfan has not been studied in patients with moderate or severe liver and renal dysfunction.

Treosulfan has a moderate potential interaction with Seizures.

There have been reports of seizures in patients following treatment with treosulfan. Patients should be monitored for signs of neurological adverse reactions, and clonazepam prophylaxis may be considered for patients at higher risk for seizures, including infants.

The quiNIDine in Quinidex Extentabs has a major potential interaction with Urinary Retention.

The use of quinidine is contraindicated in patients with preexisting conditions that are likely to be exacerbated by anticholinergic activity, such as myasthenia gravis, glaucoma, and urinary retention or obstruction.