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Hospital de Órbigo, Spain

Perez-Ruiz F.,Hospital Universitario Cruces | Herrero-Beites A.M.,Hospital de Gorliz
Advances in Therapy | Year: 2012

Gout is a disease caused by deposition of monosodium urate crystals in tissues. One of the limitations for successful treatment of gout is to consider it as an intermittent disease rather than a chronic inflammatory disease which, if improperly treated, leads to chronic clinical manifestations. In addition, gout is linked to increased cardiovascular morbidity and mortality. Urate-lowering therapy comprises both nonpharmacologic and pharmacologic interventions, but most patients will need uratelowering drugs to achieve target therapeutic serum urate levels. Reaching target serum urate levels is associated with improvement in clinical outcomes, including a reduction of acute inflammation episodes, resolution of tophi, and improvement in health-related quality of life perception. A number of urate-lowering drugs are available but a number of patients fail to achieve or maintain therapeutic serum urate levels and go on to develop refractory chronic gout. For such patients, efforts have been made to develop new treatments (e.g., febuxostat or pegloticase). This review intends to increase the awareness of gout as a chronic deposition disease, and show that efforts should be made to properly control serum urate levels in order to achieve complete disappearance of urate crystal deposition. © 2012 Springer Healthcare. Source

Perez-Ruiz F.,Hospital Universitario Cruces | Herrero-Beites A.M.,Hospital de Gorliz | Carmona L.,Camilo Jose Cela University
Arthritis and Rheumatism | Year: 2011

Objective It is commonly accepted that the target serum urate level in patients receiving urate-lowering therapy for dissolution of urate crystals in hyperuricemia of gout is <6 mg/dl, and that patients with gout should continue urate-lowering therapy for the rest of their lives. This study was undertaken to reevaluate whether this stringent therapeutic target to dissolve crystals must be maintained lifelong to prevent new crystal formation. Methods In a prospective cohort of 211 patients with gout, urate-lowering therapy was withdrawn after 5 years if no tophus was present at baseline, or 5 years after resolution of the last tophus. Data on recurrence of gout and on serum urate levels and other potentially associated variables were analyzed. Results Multivariate regression analysis of time to crystal-proven recurrence of gout showed that serum urate levels during urate-lowering treatment and after its withdrawal were independently related to gout recurrence. None of the patients who had average serum urate levels of <7 mg/dl after urate-lowering therapy withdrawal developed a crystal-proven recurrence of gout. Post hoc analysis showed that weight loss and use of drugs that lower serum urate, such as losartan or fenofibrate, were associated with serum urate levels of <7 mg/dl during followup after urate-lowering therapy withdrawal; use of diuretics was associated with failure to achieve serum urate levels of <7 mg/dl during followup. Conclusion Our data support the hypothesis that after appropriate long-term treatment of hyperuricemia in gout with urate crystal dissolution being the therapeutic target, lifelong treatment can be targeted to achieve serum urate levels just below the threshold for saturation to avoid new crystal formation, similar to cleaning a dirty dish: more is required to get it clean than to keep it clean. © 2011 by the American College of Rheumatology. Source

Doherty M.,Taipei Medical University Hospital | Jansen T.L.,Radboud University Nijmegen | Nuki G.,University of Edinburgh | Pascual E.,University Miguel Hernandez | And 4 more authors.
Annals of the Rheumatic Diseases | Year: 2012

Gout is the most common inflammatory arthritis and one in which pathogenesis and risk factors are best understood. One of the treatment objectives in current guidelines is 'cure'. However, audits show that only a minority of patients with gout receive adequate advice and treatment. Suboptimal care and outcomes reflect inappropriately negative perceptions of the disease, both in patients and providers. Historically, gout has been portrayed as a benign and even comical condition that is self-in flicted through overeating and alcohol excess. Doctors often focus on managing acute attacks rather than viewing gout as a chronic progressive crystal deposition disease. Urate-lowering treatment is underprescribed and often underdosed. Appropriate education of patients and doctors, catalysed by recent introduction of new urate-lowering treatments after many years with no drug development in the field, may help to overcome these barriers and improve management of this easily diagnosed and curable form of potentially severe arthritis. Source

Richette P.,University Paris Diderot | Perez-Ruiz F.,Hospital Universitario Cruces
Current Medical Research and Opinion | Year: 2013

Objectives: This review presents the information available on the role of uric acid (UA) on metabolic risk and on the link between hyperuricemia and metabolic syndrome. Methods: Key papers for inclusion were identified by a PubMed search and articles were selected according to their relevance for the topic, according to the authors' judgment. Results and conclusions: An elevated UA is both strongly associated and predictive of the metabolic syndrome, and increasing evidence suggests that UA may have a causal role. The classical viewpoint that UA is simply an innocuous marker of metabolic syndrome that should not even be measured will likely have to be modified. Lowering UA may be a novel treatment target for preventing diabetes and justify prospective clinical trials on the possible benefits of the measurement and lowering of serum UA on multiple chronic disease end points. © 2013 Informa UK Ltd. Source

Diaz-Torne C.,Hospital Santa Creu i San Pau | Perez-Herrero N.,Rey Juan Carlos University | Perez-Ruiz F.,Hospital Universitario Cruces
Current Opinion in Rheumatology | Year: 2015

PURPOSE OF REVIEW: To update recent developments in medications targeting hyperuricemia, but not including medications recently labelled in the European Union and the United States. RECENT FINDINGS: A new xanthine oxidase inhibitor, Topiloric (Fujiyakuhin Co., Ltd. Japan) Uriadec (Sanwa Kagaku Kenkyusho Co., Ltd. Japan), has been developed and labelled in Japan. An inhibitor of purine nucleoside phosphorylase, Ulodesine, is in development in combination with allopurinol. The rest of the medications in the pipeline for hyperuricemia are targeting renal transporters of uric acid, mainly URAT1 and OAT4, acting as uricosuric agents. Most of them, such as lesinurad and arhalofenate, are being tested in trials in combination with allopurinol and febuxostat. The most potent RDEA3170 is being tested in monotherapy, but also associated with febuxostat. Recently, medications showing dual activity, inhibiting both xanthine oxidoreductase and URAT1, have been communicated or started exploratory clinical trials. There is no report of medications targeting other transporters such as Glut9 or ABCG2. SUMMARY: There are a number of medications in the pipeline targeting hyperuricemia, mostly uricosurics in combination with xanthine oxidase inhibitors, but some targeting both xanthine oxidoreductase and URAT1. Increasing the number of available medications will ensure proper control of hyperuricemia to target serum urate levels in the near future for most, if not all, patients with hyperuricemia. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. Source

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