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      Moxifloxacin in the treatment of skin and skin structure infections

      Therapeutics and Clinical Risk Management

      Dove Medical Press

      moxifloxacin, skin infections, fluoroquinolones, skin ulcers, cellulitis

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          Abstract

          Moxifloxacin is a recent addition to the fluoroquinolone class, differing from ciprofloxacin and other older agents in having much better in vitro activity against Gram-positive aerobes while retaining potent activity against Gram-negative aerobes. It is also active against the pathogens of human and animal bite wounds and those species of atypical mycobacteria associated with dermatologic infections. Its activity against anaerobes is quite variable. Moxifloxacin penetrates well into inflammatory blister fluid and muscle and subcutaneous adipose tissues. Moxifloxacin should thus be a reasonable option for the treatment of skin and skin structure infections (SSSIs). In 3 randomized controlled trials (RCTs), oral moxifloxacin was as effective as cephalexin in the treatment of uncomplicated SSSIs in adults while in 2 RCTs, intravenous/oral moxifloxacin was as effective as intravenous/oral β-lactam/β-lactamase inhibitor therapy in the treatment of complicated SSSIs in adults. Moxifloxacin does not inhibit cytochrome P450 enzymes and thus interact with warfarin or methylxanthines. However, multivalent cations can reduce its oral bioavailability substantially. Dosage adjustment is not required in the presence of renal or hepatic impairment. The clinical relevance of its electrophysiologic effects (QT c prolongation) remains unresolved.

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          Most cited references 121

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          Practice guidelines for the diagnosis and management of skin and soft-tissue infections.

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            Mechanisms of resistance to quinolones: target alterations, decreased accumulation and DNA gyrase protection.

             Joaquim Ruiz (2003)
            Quinolones are broad-spectrum antibacterial agents, commonly used in both clinical and veterinary medicine. Their extensive use has resulted in bacteria rapidly developing resistance to these agents. Two mechanisms of quinolone resistance have been established to date: alterations in the targets of quinolones, and decreased accumulation due to impermeability of the membrane and/or an overexpression of efflux pump systems. Recently, mobile elements have also been described, carrying the qnr gene, which confers resistance to quinolones.
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              Bacterial topoisomerase inhibitors: quinolone and pyridone antibacterial agents.

               L Mitscher (2005)
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                December 2006
                December 2006
                : 2
                : 4
                : 417-434
                Affiliations
                Department of Experimental and Clinical Pharmacology, College of Pharmacy, University of Minnesota Minneapolis, MN, USA
                Author notes
                Correspondence: David RP Guay University of Minnesota, College of Pharmacy, Department of Experimental and Clinical Pharmacology,Weaver-Densford Hall 7–148, 308 Harvard Street SE, Minneapolis, MN 55455, USA Tel +1 612 626 5981 Fax +1 612 625 3927 Email guayx001@ 123456umn.edu
                Article
                1936362
                18360653
                © 2006 Dove Medical Press Limited. All rights reserved
                Categories
                Review

                Medicine

                skin infections, cellulitis, skin ulcers, moxifloxacin, fluoroquinolones

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