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      Cutaneous leukocytoclastic vasculitis associated with levofloxacin therapy

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          Abstract

          Many cases of cutaneous vasculitis are drug-induced with histology revealing leukocytoclastic vasculitis (LCV). We present a case of levofloxacin-associated LCV successfully treated with prednisone and cessation of the offending drug. Although case reports describe a link between LCV and older fluoroquinolones, such as ciprofloxacin and ofloxacin, recent reports have implicated the newer fluoroquinolone levofloxacin. Recognition of fluoroquinolone-induced cutaneous vasculitis is important as continuation or re-exposure of the offending agent may have life-threatening consequences.

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          Most cited references 27

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          Quinolones in 2005: an update.

          Quinolones are one of the largest classes of antimicrobial agents used worldwide. This review considers the quinolones that are available currently and used widely in Europe (norfoxacin, ciprofloxacin, ofloxacin, levofloxacin and moxifloxacin) within their historical perspective, while trying to position them in the context of recent and possible future advances based on an understanding of: (1) their chemical structures and how these impact on activity and toxicity; (2) resistance mechanisms (mutations in target genes, efflux pumps); (3) their pharmacodynamic properties (AUC/MIC and Cmax/MIC ratios; mutant prevention concentration and mutant selection window); and (4) epidemiological considerations (risk of emergence of resistance, clonal spread). Their main indications are examined in relation to their advantages and drawbacks. Overall, it is concluded that these important agents should be used in an educated fashion, based on a careful balance between their ease of use and efficacy vs. the risk of emerging resistance and toxicity. However, there is now substantial evidence to support use of the most potent drug at the appropriate dose whenever this is required.
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            The histological assessment of cutaneous vasculitis.

             Eric Carlson (2009)
            Vasculitis is defined as inflammation directed at vessels, which compromises or destroys the vessel wall leading to haemorrhagic and/or ischaemic events. Skin biopsy is the gold standard for the diagnosis of cutaneous vasculitis, whose manifestations include urticaria, infiltrative erythema, petechiae, purpura, purpuric papules, haemorrhagic vesicles and bullae, nodules, livedo racemosa, deep (punched out) ulcers and digital gangrene. These varied morphologies are a direct reflection of size of the vessels and extent of the vascular bed affected, ranging from a vasculitis affecting few superficial, small vessels in petechial eruptions to extensive pan-dermal small vessel vasculitis in haemorrhagic bullae to muscular vessel vasculitis in lower extremity nodules with livedo racemosa. Skin biopsy, extending to subcutis and taken from the earliest, most symptomatic, reddish or purpuric lesion is crucial for obtaining a high-yielding diagnostic sample. Based on histology, vasculitis can be classified on the size of vessels affected and the dominant immune cell mediating the inflammation (e.g. neutrophilic, granulomatous, lymphocytic, or eosinophilic). Disruption of small vessels by inflammatory cells, deposition of fibrin within the lumen and/or vessel wall coupled with nuclear debris allows for the confident recognition of small vessel, mostly neutrophilic vasculitis (also known as leukocytoclastic vasculitis). In contrast, muscular vessel vasculitis can be identified solely by infiltration of its wall by inflammatory cells. Extravasation of red blood cells (purpura) and necrosis are supportive, but not diagnostic of vasculitis as they are also seen in haemorrhagic and/or vaso-occlusive disorders (pseudovasculitis). Vasculitic foci associated with extravascular granulomas (palisaded neutrophilic and granulomatous dermatitis), tissue eosinophilia, or tissue neutrophilia signal the risk for, or co-existence of systemic disease. This essential histological information coupled with direct immunofluorescence and anti-neutrophil cytoplasmic data and clinical findings enables more precise and accurate diagnosis of localized and systemic vasculitis syndromes.
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              Quinolone generations: natural history or natural selection?

               William Ball (2000)
              The quinolones have evolved from antibacterial agents with a limited spectrum of predominantly anti-gram-negative antimicrobial activity and a restricted number of indications to a class of widely used oral (and, in some cases, intravenous) antibiotics with extensive indications for infections caused by many bacterial pathogens in most body tissues and fluids. This evolutionary pattern has arisen through the development of new core and side-chain structures, with associated improvements in activity, pharmacokinetics and tolerability, and through the selection of molecules that remain useful and well tolerated. This review describes the progress of the quinolones from the first to the third (IIIa and IIIb) generations. Special attention is given to gemifloxacin, currently the most developmentally advanced third-generation quinolone, which has enhanced in vitro gram-positive antimicrobial activity and no troublesome adverse drug reactions. Preliminary data indicate that gemifloxacin should prove to be an important addition to the fluoroquinolone class. Further clinical trial data are awaited with interest.
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                Author and article information

                Journal
                Infect Dis Rep
                IDR
                IDR
                Infectious Disease Reports
                PAGEPress Publications (Pavia, Italy )
                2036-7430
                2036-7449
                30 January 2012
                02 January 2012
                : 4
                : 1
                Affiliations
                [1 ]Department of Internal Medicine and
                [2 ]Infectious Disease Service, San Antonio Military Medical Center, San Antonio, TX, USA
                Author notes
                Correspondence: Dana M. Blyth, MD, Brooke Army Medical Center, 3851 Roger Brooke Drive, Fort Sam Houston, TX 78234-6200, USA. Tel: +1.210.916.4355 - Fax. +1.210.916-5900. E-mail: dana.m.blyth@ 123456us.af.mil

                Contributions: DMB, manuscript preparation, literature research; EM, images providing, case discussion, manuscript review; JFO, manuscript conception, preparation, supervision.

                Conflict of interest: the authors do not declare any potential conflicts of interest with this publication.

                The views expressed in this article are those of the authors and do not reflect the official policy of the Department of the Army, the Department of Defense, or the U. S. Government.

                Article
                idr.2012.e11
                10.4081/idr.2012.e11
                3892663
                ©Copyright D.M. Blyth et al., 2012

                This work is licensed under a Creative Commons Attribution NonCommercial 3.0 License (CC BY-NC 3.0).

                Licensee PAGEPress, Italy

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