Pharmacist- versus physician-initiated admission medication reconciliation: impact on adverse drug events.

BACKGROUND: Medication reconciliation (MR) has proven to be a problematic task for many hospitals to accomplish. It is important to know the clinical impact of physician- versus pharmacist-initiated MR in the resource-limited hospital environment. METHODS: This quasi-experimental study took place from December 2005 to February 2006 at an urban US Veterans Affairs hospital. MR was implemented on 2 similar general medical units: one received physician-initiated MR and the other received pharmacist-initiated MR. Adverse drug events (ADEs) and a 72-hour medication-prescribing risk score were ascertained by research pharmacists for all admitted patients by structured record review. Multivariable models were tested for intervention effect, accounting for quasi-experimental design and clustered observations, and were adjusted for patient and encounter covariates. RESULTS: Pharmacists completed the MR process in 102 admissions and physicians completed the process in 116 admissions. In completing the MR process, pharmacists documented statistically more admission medication changes than physicians (3.6 vs 0.8; P < 0.001). The adjusted odds of an ADE caused by an admission prescribing change with pharmacist-initiated MR compared with a physician-initiated MR were 1.04 with a 95% CI of 0.53 to 2.0. The adjusted odds of an ADE caused by an admission prescribing change that was a prescribing error with pharmacist-initiated MR compared with a physician-initiated MR were 0.38 with a confidence interval of 0.14 to 1.05. No difference was observed in 72-hour prescribing risk score (coefficient = 0.10; 95% CI, -0.54 to 0.75). CONCLUSION: MR performed by pharmacists versus physicians was more comprehensive and was followed by lower odds of ADEs from admission prescribing errors but with similar odds of all types of ADEs. Further research is warranted to examine how MR tasks may be optimally divided among clinicians and the mechanisms by which MR affects the likelihood of subsequent ADEs.

Ezetimibe 5 and 10 mg for lowering LDL-C: potential billion-dollar savings with improved tolerability.

OBJECTIVE: To compare the clinical efficacy of ezetimibe 5 mg (prescribed as a 10-mg tablet split in half) with a whole 10-mg tablet. STUDY DESIGN: From January 2003 through July 2005, all Bronx Veterans Administration ezetimibe prescriptions were for 10 mg. In August 2005, it was mandated that all new ezetimibe prescriptions be 5 mg, prescribed as a 10-mg tablet split in half. METHODS: The impact of the 2 ezetimibe dosing strategies on percent lowering of low-density lipoprotein cholesterol (LDL-C) and achievement of National Cholesterol Education Program Adult Treatment Panel III (ATP III) goals was assessed in all patients prescribed ezetimibe 5 or 10 mg. RESULTS: A total of 272 patients were prescribed ezetimibe; 86 received 5 mg and 186 received 10 mg. Of those 272 patients, 197 had evaluable baseline and posttreatment LDL-C (55 taking the 5-mg dose and 142 taking the 10-mg dose). The effects of ezetimibe 5 and 10 mg on all lipid parameters were similar. Ezetimibe 10 mg reduced LDL-C by 26.1%, whereas 5 mg reduced LDL-C by 25.8%. The percentages of patients achieving goal LDL-C were similar: 61.8% (5 mg) and 60.5% (10 mg). CONCLUSION: These data strongly suggest that ezetimibe 5 mg and ezetimibe 10 mg are clinically equivalent with respect to LDL-C reduction and achievement of ATP III LDL-C goals. Widespread adoption of this low-dose strategy could result in a potential cost savings of more than a billion dollars annually, with a potential reduction in hepatotoxicity.

Maraviroc: a CCR5-receptor antagonist for the treatment of HIV-1 infection.

BACKGROUND: The emergence of viral resistance is one of the greatest challenges in the treatment of HIV infection. Maraviroc is the first member of a new class of antiretroviral medications, the CCR5-receptor antagonists. It is approved by the US Food and Drug Administration (FDA) for use in combination with other antiretroviral agents in treatment-experienced patients infected with multidrug-resistant, CCR5-tropic HIV-1. OBJECTIVE: This article provides an overview of the pharmacology, efficacy, and tolerability of maraviroc in the treatment of HIV-1 infection. METHODS: Relevant information was identified through a search of MEDLINE (January 2000-May 2008) using the terms maraviroc, UK-427,857, and CCR5-receptor antagonist. Also consulted were abstracts from the International AIDS Society Conference, the Conference on Retroviruses and Opportunistic Infections, and other relevant scientific meetings. Additional publications were found by searching the reference lists of the identified articles and the FDA Web site. RESULTS: Maraviroc is a selective, reversible, small-molecule CCR5-receptor antagonist. In vitro, it has potent anti-HIV-1 activity, with a mean 90% inhibitory concentration of 2.0 nmol/L. It is widely distributed, with a V(d) of approximately 194 L. Maraviroc is moderately metabolized in the liver (65.3%), primarily via the cytochrome P450 3A4 isozyme. It has an elimination t(1/2) of 15.9 to 22.9 hours. Until more data are available, maraviroc should be avoided in patients with severe hepatic insufficiency; dose adjustment does not appear to be necessary on the basis of age, sex, or renal function. In 2 Phase IIb/III studies, maraviroc 300 mg PO QD or BID was found to be more efficacious than placebo in reducing the viral load at 48 weeks in treatment-experienced, CCR5-tropic HIV-1-infected patients receiving an optimized background regimen (difference vs placebo-QD arm: -0.89 log(10) copies/mL [97.5% CI, -1.17 to -0.62]; BID arm: -1.05 log(10) copies/mL [97.5% CI, -1.33 to -0.78]). The proportion of patients with a viral load < 50 copies/mL was 43.2% in the QD arm and 45.5% in the BID arm, compared with 16.7% in the placebo arm (P < 0.001, both treatment arms vs placebo). In treatment-naive patients infected with CCR5-tropic virus only, maraviroc 300 mg PO BID was not noninferior to oral efavirenz 600 mg QD (difference = -4.2%; lower bound of the 1-sided 97.5% CI, -10.9 [predefined statistical cutoff for noninferiority, -10]). Maraviroc was generally well tolerated in clinical trials. The most frequently reported (> or = 5%) adverse events were upper respiratory tract infection (20.0%), cough (12.7%), pyrexia (12.0%), rash (9.6%), musculoskeletal complaints (8.7%), gastrointestinal and abdominal pain (8.2%), dizziness (8.2%), appetite disorders (7.3%), insomnia (7.0%), herpes infection (6.8%), sinusitis (6.3%), joint complaints (6.1%), bronchitis (5.9%), and constipation (5.4%). The recommended dose of maraviroc differs based on concomitant medications, ranging from 150 to 600 mg BID. CONCLUSION: When used in combination with other antiretroviral agents, maraviroc appears to be a promising agent for treatment-experienced patients infected with multidrug-resistant, CCR5-tropic HIV-1.