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The effective use of quinidine as an antiarrhythmic agent is frequently curtailed by one of its most common side effects-relentless diarrhea. Seven patients are described in whom diarrhea was quickly and completely controlled by the use of cholestyramine resin. To date, this is the only therapy
BACKGROUND
Pseudobulbar affect (PBA) is associated with neurological disorders or injury affecting the brain, and characterized by frequent, uncontrollable episodes of crying and/or laughing that are exaggerated or unrelated to the patient's emotional state. Clinical trials establishing
Seventy-seven horses with atrial fibrillation (AF) were treated orally with quinidine sulfate (QS) at the University of Pennsylvania, School of Veterinary Medicine, Thirty-seven horses (48%) had adverse reactions to QS, the most common of which were nasal mucosal edema, anorexia, colic, and
BACKGROUND
Dextromethorphan (DM) / quinidine (Q) was approved for pseudobulbar affect (PBA) treatment based on efficacy and safety trials in patients with PBA caused by amyotrophic lateral sclerosis or multiple sclerosis. The PRISM II trial evaluated DM/Q as PBA treatment in patients with stroke,
BACKGROUND
Phase 3 trials supporting dextromethorphan/quinidine (DM/Q) use as a treatment for pseudobulbar affect (PBA) were conducted in patients with amyotrophic lateral sclerosis (ALS) or multiple sclerosis (MS). The PRISM II study provides additional DM/Q experience with PBA secondary to
BACKGROUND
Dextromethorphan 20 mg / quinidine 10 mg (DM/Q) was approved to treat pseudobulbar affect (PBA) based on phase 3 trials conducted in participants with amyotrophic lateral sclerosis or multiple sclerosis. PRISM II evaluated DM/Q effectiveness, safety, and tolerability for PBA following
The antiarrhythmic efficacy and safety of oral tocainide hydrochloride and quinidine sulfate were compared in a double-blind, 3-center, parallel trial involving 133 patients with benign and potentially lethal ventricular arrhythmias. Baseline demographic, etiologic, functional and ventricular
Although quinidine has been widely used since the beginning of the century, quinidine-induced hepatotoxicity has been recently reported in the literature. We describe a reversible case of quinidine-induced hepatotoxicity. A 62-y-old male with a past medical history of atrial flutter and adult onset
Quinidine gluconate was administered slowly by intravenous infusion to 20 patients with atrial fibrillation. Nineteen of them had rheumatic heart disease and the other one had Ebstein's disease. The first ten patients received 0.027 mg/kg/min during 6 hs or less if they returned to normal sinus
In an attempt to evaluate the effect of quinidine in the treatment of patients with cirrhosis and muscle cramps, 31 cirrhotic patients with muscle cramps were randomly divided into two groups and given orally 400 mg of quinidine sulfate per day or placebo, respectively. Baseline clinical and
Quinidine gluconate was used to treat arrhythmia induced with maximal exercise testing. Twenty-nine subjects who had previously developed frequent premature contractions on testing were selected for further study. After a control maximal exercise test, quinidine (10 mg. per kilogram) in solution was
Quinidine is suggested as an effective agent to suppress ventricular fibrillation (VF) in the Brugada syndrome by inhibiting transient outward K(+) current (Ito) leading to the reduction and abbreviation of the disparity of repolarization in the right ventricular outflow region and ST segment