The Internet and the Journal.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R A Barbarash.
Explore the source record for details and available documents.
OBJECTIVE: To document the effects of treatment with famciclovir on the acute signs and symptoms of herpes zoster and postherpetic neuralgia. DESIGN: A randomized, double-blind, placebo-controlled, multicenter trial. SETTING: 36 centers in the United States, Canada, and Australia. PATIENTS: 419 immunocompetent adults with uncomplicated herpes zoster. INTERVENTION: Patients were assigned within 72 hours of rash onset to famciclovir, 500 mg; famciclovir, 750 mg; or placebo, three times daily for 7 days. MEASUREMENTS: Lesions were assessed daily for as long as 14 days until full crusting occurred and then weekly until the lesions healed. Viral cultures were obtained daily while vesicles were present. Pain was assessed at each of the visits at which lesions were examined and then monthly for 5 months after the lesions healed. Safety was assessed throughout the study. RESULTS: Famciclovir was well tolerated, with a safety profile similar to that of placebo. Famciclovir accelerated lesion healing and reduced the duration of viral shedding. Most importantly, famciclovir recipients had faster resolution of postherpetic neuralgia (approximately twofold faster) than placebo recipients; differences between the placebo group and both the 500-mg famciclovir group (hazard ratio, 1.7 [95% CI, 1.1 to 2.7]) and the 750-mg famciclovir group (hazard ratio, 1.9 [CI, 1.2 to 2.9]) were statistically significant (P = 0.02 and 0.01, respectively). The median duration of postherpetic neuralgia was reduced by approximately 2 months. CONCLUSIONS: Oral famciclovir, 500 mg or 750 mg three times daily for 7 days, is an effective and well-tolerated therapy for herpes zoster that decreases the duration of the disease's most debilitating complication, postherpetic neuralgia.
While patient informed consent is an important clinical and legal dimension of specialty medical care, many important issues arise in primary care. Family physicians are in a unique position to implement informed consent discussions in the ethical spirit in which the doctrine was intended. Because of their long-term relationships with patients and sensitivity to psychosocial issues, family physicians can engage patients in collaborative health care decision making. Primary care physicians are optimally suited to assess patients' understanding of medical information and their competence. Instead of viewing the informed consent process simply as a necessary legal requirement, it should be a method for educating patients and allowing them to participate in their health care decision making.
Among the many advances made in intensive care therapeutics in recent years, few have rivaled the impact of mechanical ventilators. Their expanded use affects all who practice in the critical care setting. This article reviews the physiologic basis for mechanical ventilation, how ventilators are classified, the various modes, and specific indications. A basic introduction is made into ventilator set up, weaning techniques, adjunctive drug therapy, and complications. The pharmacotherapy specialist who understands interactions between patients and ventilators, and the effects of mechanical ventilation on cardiopulmonary function will be best equipped to individualize drug therapy.
We measured lidocaine concentrations in bronchoscopic specimens and found that bronchoalveolar lavage (BAL) concentrations (16 +/- 7 micrograms/ml) were lower than those in bronchial washings (967 +/- 379 micrograms/ml [p less than 0.001]). Lidocaine concentrations in bronchial washings obtained "early" (991 +/- 505 micrograms/ml) compared with "late" (943 +/- 580 micrograms/ml) in the procedure did not differ (p = NS). High lidocaine concentrations sufficient to inhibit growth in culture of mycobacterial and fungal pathogens (greater than 5,000 micrograms/ml) occurred in one early and two late bronchial washings but no BAL specimens. No correlation between lidocaine dose and measured concentrations was noted in any specimen category; however, highest bronchial washing concentrations occurred with the use of greater than 250 mg of lidocaine. We conclude that BAL specimens are suitable for culturing pathogens that may be inhibited by lidocaine. Furthermore, collecting bronchial washings late in the procedure or limiting the lidocaine dosage do not reliably decrease measured lidocaine concentrations.
We evaluated the significance of the interaction between rifampin and verapamil in six volunteers who received single doses of verapamil, 10 mg intravenously (IV), then 120 mg orally two days later. Subjects were then given rifampin, 600 mg orally every day for 15 days. After 13 and 15 days of rifampin therapy, the IV and oral doses of verapamil were repeated. Electrocardiograms (ECG) were done and serum verapamil and norverapamil concentrations measured before and for 12 h after each dose. For IV verapamil, there was a small decrease in area under the serum concentration-time curve and an increase in clearance after rifampin therapy (p less than 0.05). There were no changes in elimination half-life, volume of distribution, or AUC for percentage of change in P-R interval-time curve (AUCPR). For oral verapamil, there were marked decreases in peak concentration, AUC, oral bioavailability (all p less than 0.005), and AUCPR (p less than 0.001) after rifampin treatment. There were no changes in time to peak concentration or elimination half-life. For oral verapamil, significant P-R interval prolongation occurred only before treatment with rifampin. The decrease in oral bioavailability and the abolition of ECG response confirm that a highly significant drug interaction exists between rifampin and verapamil given orally but not intravenously.
Seven patients with symptomatic pleural effusions (six) and recurrent pneumothorax (one) underwent attempted pleurodesis using tetracycline. Lidocaine (150 mg), followed immediately by tetracycline (20 mg/kg), was instilled into the pleural space through a chest tube. Venous blood was obtained at 0, 15, 30, 60, and 120 minutes following instillation in order to determine concentrations of lidocaine and tetracycline. The mean peak serum concentration of lidocaine was 1.3 mu/ml +/- 0.4 microgram/ml (mean +/- SE) (range, 0.3 microgram/ml to 3.2 microgram/ml), and the mean time to peak serum concentration of lidocaine was 86 +/- 13 minutes. The mean peak serum concentration of tetracycline was 3.6 microgram/ml +/- 0.9 microgram/ml (range, 1.0 microgram/ml to 5.0 micrograms/ml), and the mean time to peak serum concentration of tetracycline was 96 +/- 16 minutes. Therapeutic serum concentrations of lidocaine were found in four of the seven patients and therapeutic serum levels of tetracycline in four of five patients. With systemic absorption of lidocaine and tetracycline following intrapleural instillation, patients are at risk for potential toxic effects. If lidocaine is used in a dosage of less than 3 mg/kg, toxic levels of the drug are unlikely to occur. Furthermore, use of tetracycline or lidocaine in pleurodesis is contraindicated in patients with known sensitivity to the drugs.
Explore the source record for details and available documents.
Ten patients with symptomatic atrial tachyarrhythmias were treated with an iv verapamil bolus (mean 8.5 mg) followed by a continuous verapamil infusion (mean dose 9.4 mg/h). The infusions were titrated to ventricular rate and continued for an average of 20 h, until oral therapy could be instituted. All patients had a significant, sustained reduction in ventricular rate during the infusion, without a significant reduction in mean arterial pressure. Although one patient complained of dizziness after 8 h of infusion therapy, the regimen was generally well tolerated and no patient had clinical worsening of heart failure. These preliminary data suggest that continuous verapamil infusions can safely and effectively control ventricular rate in patients with rapid atrial tachyarrhythmias, until oral medications can be started.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
A case of verapamil-rifampin interaction is presented in a patient receiving verapamil for supraventricular tachycardia (SVT) and rifampin for pulmonary tuberculosis. The patient experienced recurrent symptomatic SVT, despite receiving verapamil 480 mg po q6h. Serum verapamil concentrations were determined to be extremely low. Discontinuation of rifampin and substitution of ethambutol resulted in an almost four-fold increase in verapamil levels with concurrent control of SVT. Rifampin may have increased the metabolism of verapamil by inducing hepatic microsomal enzymes resulting in low verapamil levels and failure to control SVT.