Update on rifampin and rifabutin drug interactions.

Rifampin is a potent inducer of cytochrome P-450 oxidative enzymes as well as the P-glycoprotein transport system. Several examples of well-documented clinically significant interactions include warfarin, oral contraceptives, cyclosporine, itraconazole, digoxin, verapamil, nifedipine, simvastatin, midazolam, and human immunodeficiency virus-related protease inhibitors. Rifabutin reduces serum concentrations of antiretroviral agents, but less so than rifampin. Examples of clinically relevant interactions demonstrated by recent reports include everolimus, atorvastatin, rosiglitazone/pioglitazone, celecoxib, clarithromycin, caspofungin, and lorazepam. To avoid a decreased therapeutic response, therapeutic failure, or toxic reactions when rifampin is added to or discontinued from medication regimens, clinicians need to be cognizant of these interactions. Studies and cases of rifampin drug interactions continue to increase rapidly. This review is a timely reminder to clinicians to be vigilant.

Intravenous Tissue Plasminogen Activator Administration for Ischemic Stroke 1 Hour After Epidural Catheter Removal: A Case Report.

Anticoagulation after a recent neuraxial procedure poses risk for development of spinal hematoma. Clinical evidence supports prompt IV tissue plasminogen activator administration after onset of ischemic stroke. There is an absence of data regarding emergency fibrinolytic therapy for patients experiencing a stroke with recent neuraxial procedures, resulting in highly disparate, nonevidence-based guidelines. This report describes a patient who developed ischemic stroke when receiving postoperative epidural analgesia. Tissue plasminogen activator was emergently administered 1 hour after epidural catheter removal with a favorable recovery. The patient and his family reviewed the manuscript, and written consent to publish this case report was obtained from the patient.

Rifampin and rifabutin drug interactions: an update.

Rifampin is a potent inducer of cytochrome P-450 oxidative enzymes. A few examples of well-documented clinically significant interactions include interactions with warfarin, oral contraceptives, cyclosporine, glucocorticoids, ketoconazole or itraconazole, theophylline, quinidine sulfate, digitoxin or digoxin, verapamil hydrochloride, human immunodeficiency virus-related protease inhibitors, zidovudine, delavirdine mesylate, nifedipine, and midazolam. Recent reports have demonstrated clinically relevant interactions with numerous other drugs, such as buspirone hydrochloride, zolpidem tartrate, simvastatin, propafenone hydrochloride, tacrolimus, ondansetron hydrochloride, and opiates. Rifabutin reduces serum concentrations of antiretroviral agents, but less so than rifampin. To avoid a reduced therapeutic response, therapeutic failure, or toxic reactions when rifampin is added to or discontinued from medication regimens, clinicians need to be cognizant of these interactions. Enhanced knowledge of known interactions will continue to develop, including research on the induction of specific cytochrome P-450 isoenzymes and on the importance of the P-glycoprotein transport system. New rifampin and rifabutin interactions will be discovered with further investigations.

Update on rifampin, rifabutin, and rifapentine drug interactions.

BACKGROUND: Rifampin is a potent inducer of both cytochrome P-450 oxidative enzymes and the P-glycoprotein transport system. Among numerous well documented, clinically significant interactions, examples include warfarin, oral contraceptives, itraconazole, digoxin, verapamil, simvastatin, and human immunodeficiency virus-related protease inhibitors. Rifabutin reduces serum concentrations of antiretroviral agents, but less so than rifampin. Rifapentine is also an inducer of drug metabolism. METHODS: A literature search of English language journals from 2008 to March 2012 was completed using several databases, including PubMed, EMBASE, and SCOPUS. Search terms included rifampin, rifabutin, rifapentine AND drug interactions. FINDINGS: Examples of clinically relevant interactions with rifampin demonstrated by recent reports include posaconazole, voriconazole, oxycodone, risperidone, mirodenafil, and ebastine. CONCLUSIONS: To avoid a reduced therapeutic response, therapeutic failure, or toxic reactions when rifampin, rifabutin, or rifapentine are added to or discontinued from medication regimens, clinicians need to be aware of these interactions. Recent studies have indicated that other transporter systems play a role in these drug interactions. As reports of rifampin drug interactions continue to grow, this review is a reminder to clinicians to be vigilant.

Aminoglycoside-associated nephrotoxicity in the elderly.

OBJECTIVE: To determine whether there was an increased incidence of nephrotoxicity in elderly patients (> or =65 y) prescribed single-dose (SD) versus multiple-dose (MD) aminoglycosides and whether aminoglycoside-induced nephrotoxicity was associated with length of therapy and other risk factors. METHODS: A prospective, observational audit at a university teaching hospital was conducted. Physician prescribing was used to stratify subjects according to dosing regimen: MD (n = 60) or SD (n = 26). Nephrotoxicity was defined as an increase in the serum creatinine level of 0.5 mg/dL sustained over 2 days. RESULTS: Eighty-six patients were included; 9.3% developed nephrotoxicity, of whom 62.5% received SD therapy. The incidence of nephrotoxicity did not differ between regimens (p = 0.051). There was an increased length of therapy in those who developed nephrotoxicity (mean +/- SD 6.1 +/- 6.2 vs. 3.7 +/- 2.8 d; p = 0.044). Additionally, patients who developed nephrotoxicity had an increased length of hospitalization (20.3 +/- 16.1 vs. 8.4 +/- 5.4 d; p < 0.001). Nephrotoxicity correlated with a diagnosis of diabetes mellitus (OR 15.1; 95% CI 1.11 to 205), concomitant angiotensin-converting enzyme (ACE) inhibitor therapy (OR 28.0; 95% CI 2.15 to 365), and SD therapy (OR 20.7; 95% CI 1.45 to 297). CONCLUSIONS: Our overall incidence of nephrotoxicity is consistent with that reported in the literature. A diagnosis of diabetes mellitus, concomitant use of ACE inhibitors, and SD regimens were risk factors for the development of nephrotoxicity. An adequately powered, randomized trial is needed to assess whether a difference in the incidence of nephrotoxicity exists between SD and MD therapy in the elderly.