Gout Study Group: Update on hyperuricemia and gout Robert Terkeltaub a, * , David Zelman b , John Scavulli c , Fernando Perez-Ruiz d , Fre ´de ´ric Liote ´ e,f a Veterans Affairs Medical Center, University of California San Diego, 111K, 3350 La Jolla Village Drive, San Diego, CA 92161, USA b Permanente Medical Group, Rheumatology, 200 Crescent Center Parkway, Tucker, GA 30084, USA c 7905 Avenida Alamar, La Jolla, CA 92037, USA d Rheumatology Division, Hospital de Cruces, Pza Cruces sn 48903 Baracaldo, Spain e Fe ´de ´ration de Rhumatologie, po ˆle appareil locomoteur, ho ˆpital Lariboisie `re (AP-HP), Paris, France f Inserm UMR-S 606, Paris Diderot University, Paris, France Accepted 4 May 2009 Available online 25 June 2009 Keywords: Gout; Comorbidities; Metabolic syndrome; Diet; Allopurinol; Uricosurics; Febuxostat; Uricase; Steroids; Anti-IL-1 antibody The emergence of new therapeutic options for gout has prompted reexamination of the disorder and engendered an understanding that: a) The prevalence of gout is increasing and now includes a more complex case mix characterized by its association with other comorbid conditions (metabolic syndrome, obesity and others) and that hyperuricemia itself may contribute to the co-morbidity (hypertension, chronic kidney disease (CKD), CAD) b) Treatment decisions for both acute attack, prevention of flares and urate-lowering therapy (ULT) should include improved utilization of drugs already available with appropriate adoption of newer modalities c) Simpler approaches such as diet and lifestyle changes as well as increased efforts to educate both patients and healthcare professionals alike will be crucial towards insuring that progress will be made towards gout preven- tion and improving outcomes in established gout. The following is a summary of presentation made at the Euro-American conference addressing these issues: Some recent developments in the basic scientific under- standing of gout and hyperuricemia were first highlighted. New knowledge concern the urate transport mechanism at both borders of the proximal tubular cell in the nephron, and how single nucleotide polymorphisms affecting their function may help explain the genetic influences of gout as well as identify possible sites of future drug development. Also characterized in greater detail was the mechanism for initia- tion of the acute inflammatory response to urate crystals by innate immunity culminating in an IL-1-driven inflammatory response. 1. Which comorbidities should be stressed in gout? It should be recalled the more complex environment in which comorbidities influence the prevalence of hyperuricemia and gout and also complicate the treatment of both acute and chronic disease [1]. Serum urate (SUA) levels (Table 1) should be more commonly included in routine health assessment by primary care MDs involved in the management of diabetes, CKD, obesity, CAD and metabolic syndrome [2]. Similarly, rheumatologists need to be more cognizant of these potential problems when gout patients are referred for management. Ongoing evidence exists concerning whether hyperuricemia itself is an independent risk factor for hypertension, CKD, CAD and overall mortality, whereas interventional trials are still not sufficient to recommend lowering uric acid therapy (LUT) in preventing CKD and CVD. Compiling a risk stratification nomogram integrating comorbidities is an intriguing possibility that warrants investigation. Medications used to treat comor- bidities can raise or lower SUA, and can interact with drugs used in the treatment of gout. Loop diuretics, particularly * Corresponding author. E-mail address: rterkeltaub@ucsd.edu (R. Terkeltaub). 1297-319X/$ - see front matter Ó 2009 Elsevier Masson SAS. All rights reserved. doi:10.1016/j.jbspin.2009.05.006 Available online at www.sciencedirect.com Joint Bone Spine 76 (2009) 444e446