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Nephrology Dialysis Transplantation 2005 20(2):431-433; doi:10.1093/ndt/gfh629
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Nephrol Dial Transplant Vol. 20 No. 2 © ERA–EDTA 2005; all rights reserved


Case Report

Urate oxidase (rasburicase) for treatment of severe tophaceous gout

Bruno Vogt

Division of Nephrology and Hypertension, University Hospital Inselspital, Berne, Switzerland

Correspondence and offprint requests to: Bruno Vogt, MD, Division of Nephrology and Hypertension, Inselspital, University of Berne, Freiburgstrasse 15, 3010, Berne, Switzerland. Email: bruno.vogt@insel.ch

Keywords: cyclosporine; gout; gout tophi; hyperuricaemia; kidney transplant; rasburicase; urate oxidase

The first 10% of the full text of this article appears below.



   Introduction
 
Gout is a clinical disorder caused by deposition of urate crystals in a joint leading to acute inflammatory response with acute pain. In severe and longstanding gout, the crystals accumulate in soft tissues such as cartilage, subcutaneous tissue or even veins leading to the development of tophi responsible for very large deposit formations and disability. Most cases of gout present with the sudden onset of severe acute arthritis in a peripheral joint in the leg.

Urate oxidase, or uricase (EC 1.7.3.3 [EC] ), is a peroxisomal liver enzyme that catalyses the enzymatic oxidation of uric acid into the more water-soluble allantoin (Figure 1). Urate oxidase is an endogenous enzyme found in most mammals but not in humans. During primate evolution, the inactivation of the hominoid urate oxidase gene was caused by independent nonsense or frameshift mutations and has taken a . . . [Full Text of this Article]



   Case report
 


   Discussion
 

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