Pick Topic
Review Topic
List Experts
Examine Expert
Save Expert
  Site Guide ··   
Gout: HELP
Articles by Dr. Alexander So
Based on 38 articles published since 2010
(Why 38 articles?)
||||

Between 2010 and 2020, A. So wrote the following 38 articles about Gout.
 
+ Citations + Abstracts
Pages: 1 · 2
1 Guideline 2018 updated European League Against Rheumatism evidence-based recommendations for the diagnosis of gout. 2020

Richette, Pascal / Doherty, Michael / Pascual, Eliseo / Barskova, Victoria / Becce, Fabio / Castaneda, Johann / Coyfish, Malcolm / Guillo, Sylvie / Jansen, Tim / Janssens, Hein / Lioté, Frédéric / Mallen, Christian D / Nuki, George / Perez-Ruiz, Fernando / Pimentao, José / Punzi, Leonardo / Pywell, Anthony / So, Alexander K / Tausche, Anne-Kathrin / Uhlig, Till / Zavada, Jakub / Zhang, Weiya / Tubach, Florence / Bardin, Thomas. ·Service de Rhumatologie, Hopital Lariboisiere Centre Viggo Petersen, Paris, France pascal.richette@aphp.fr. · Inserm UMR1132 Bioscar, Universite Paris Diderot UFR de Medecine, Paris, France. · Academic Rheumatology, University of Nottingham, Nottingham, UK. · Rheumatology, Hospital General Universitario de Alicante, Alicante, Spain. · Institute of Rheumatology, RAMS, Moscow, Russian. · Radiology, Lausanne University Hospital, Lausanne, Switzerland. · AP-HP, Hôpital Pitié-Salpêtrière, Département Biostatistique Santé Publique et Information Médicale, Centre de Pharmacoépidémiologie (Cephepi), INSERM, UMR 1123 ECEVE, CIC-1421, Paris, France, Paris, France. · Nottingham, UK. · Département d'Epidémiologie et Recherche Clinique, Paris, France. · Rheumatology, VieCuri, Venlo, Netherlands. · Department of Primary and Community Care, Radboud University Medical Center, Radboud Institute for Health Sciences, Nijmegen, The Netherlands. · Department of Rhumatologie, Hôpital Lariboisière, Paris, France. · INSERM UMR-1132 and Université Paris Diderot, Paris, France. · Arthritis Research UK Primary Care Centre, Keele University, Keele, UK. · Centre Molecular Medicine, University of Edinburgh, Edinburgh, Scotland, UK. · Servicio de Reumatologia, Hospital de Cruces, Baracaldo, Spain. · Rheumatology Unit, Clínica Coração de Jesus, Lisbon, Portugal. · Department of Medicine, University of Padua, Padua, Italy. · Musculoskeletal Medicine, Service de RMR, Lausanne, Switzerland. · Department of Internal Medicine, Section of Rheumatology, University Clinic Carl Gustav Carus, Dresden, Saxonia, Germany. · Rheumatology, Diakonhjemmet Hospital, Oslo, Norway. · Institute of Rheumatology, Prague, Czech Republic, Czech Republic. · Academic Rheumatology, Nottingham University, Nottingham, UK. · Biostatistics and epidemiology, APHP, Hopital Pitié Salpetrière, Paris, France. · Rheumatology, Assistance Publique - Hopitaux de Paris, Paris, France. ·Ann Rheum Dis · Pubmed #31167758.

ABSTRACT: Although gout is the most common inflammatory arthritis, it is still frequently misdiagnosed. New data on imaging and clinical diagnosis have become available since the first EULAR recommendations for the diagnosis of gout in 2006. This prompted a systematic review and update of the 2006 recommendations. A systematic review of the literature concerning all aspects of gout diagnosis was performed. Recommendations were formulated using a Delphi consensus approach. Eight key recommendations were generated. A search for crystals in synovial fluid or tophus aspirates is recommended in every person with suspected gout, because demonstration of monosodium urate (MSU) crystals allows a definite diagnosis of gout. There was consensus that a number of suggestive clinical features support a clinical diagnosis of gout. These are monoarticular involvement of a foot or ankle joint (especially the first metatarsophalangeal joint); previous episodes of similar acute arthritis; rapid onset of severe pain and swelling; erythema; male gender and associated cardiovascular diseases and hyperuricaemia. When crystal identification is not possible, it is recommended that any atypical presentation should be investigated by imaging, in particular with ultrasound to seek features suggestive of MSU crystal deposition (double contour sign and tophi). There was consensus that a diagnosis of gout should not be based on the presence of hyperuricaemia alone. There was also a strong recommendation that all people with gout should be systematically assessed for presence of associated comorbidities and risk factors for cardiovascular disease, as well as for risk factors for chronic hyperuricaemia. Eight updated, evidence-based, expert consensus recommendations for the diagnosis of gout are proposed.

2 Guideline 2016 updated EULAR evidence-based recommendations for the management of gout. 2017

Richette, P / Doherty, M / Pascual, E / Barskova, V / Becce, F / Castañeda-Sanabria, J / Coyfish, M / Guillo, S / Jansen, T L / Janssens, H / Lioté, F / Mallen, C / Nuki, G / Perez-Ruiz, F / Pimentao, J / Punzi, L / Pywell, T / So, A / Tausche, A K / Uhlig, T / Zavada, J / Zhang, W / Tubach, F / Bardin, T. ·AP-HP, hôpital Lariboisière, service de Rhumatologie, F-75010 Paris, France; Inserm, UMR1132, Hôpital Lariboisière, F-75010 Paris, France; Universitè Paris Diderot, Sorbonne Paris Citè, F-75205 Paris, France. · Academic Rheumatology, University of Nottingham, Nottingham, UK. · Department of Rheumatology, Hospital General Universitario de Alicante, Alicante, Spain. · Institute of Rheumatology RAMS, Moscow, Russia. · Department of Diagnostic and Interventional Radiology, Lausanne University Hospital, Lausanne, Switzerland. · AP-HP, Dèpartement d'Epidèmiologie et Recherche Clinique, Hôpital Bichat, Paris, France: APHP, Centre de Pharmacoèpidèmiologie, Paris, France: Univ Paris Diderot, Paris, France: INSERM UMR 1123 ECEVE, Paris, France. · Patient from Nottingham, UK, Paris. · Department of Rheumatology, VieCuri Medical Centre, Venlo, and Scientific IQ HealthCare, Radboud UMC, Nijmegen, The Netherlands. · Department of Primary and Community Care, Radboud University Medical Centre, Nijmegen, Netherlands. · Arthritis Research UK Primary Care Centre University of Keele, Keele, UK. · Osteoarticular Research Group, University of Edinburgh, Edinburgh, UK. · Seccion de Rheumatologia, Hospital de Cruces, Baracaldo, Spain. · Rheumatology Unit, Clínica Coração de Jesus, Lisbon, Portugal. · Rheumatology Unit, University of Padova, Padova, Italy. · Service de Rhumatologie, CHUV and Universitè de Lausanne, Lausanne, Switzerland. · Department of Rheumatology, University Clinic at the Technical University Dresden, Germany. · Department of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway. · Institute of Rheumatology, Prague, and Department of Rheumatology, First Faculty of Medicine, Charles University in Prague, Czech Republic. ·Ann Rheum Dis · Pubmed #27457514.

ABSTRACT: BACKGROUND: New drugs and new evidence concerning the use of established treatments have become available since the publication of the first European League Against Rheumatism (EULAR) recommendations for the management of gout, in 2006. This situation has prompted a systematic review and update of the 2006 recommendations. METHODS: The EULAR task force consisted of 15 rheumatologists, 1 radiologist, 2 general practitioners, 1 research fellow, 2 patients and 3 experts in epidemiology/methodology from 12 European countries. A systematic review of the literature concerning all aspects of gout treatments was performed. Subsequently, recommendations were formulated by use of a Delphi consensus approach. RESULTS: Three overarching principles and 11 key recommendations were generated. For the treatment of flare, colchicine, non-steroidal anti-inflammatory drugs (NSAIDs), oral or intra-articular steroids or a combination are recommended. In patients with frequent flare and contraindications to colchicine, NSAIDs and corticosteroids, an interleukin-1 blocker should be considered. In addition to education and a non-pharmacological management approach, urate-lowering therapy (ULT) should be considered from the first presentation of the disease, and serum uric acid (SUA) levels should be maintained at<6 mg/dL (360 µmol/L) and <5 mg/dL (300 µmol/L) in those with severe gout. Allopurinol is recommended as first-line ULT and its dosage should be adjusted according to renal function. If the SUA target cannot be achieved with allopurinol, then febuxostat, a uricosuric or combining a xanthine oxidase inhibitor with a uricosuric should be considered. For patients with refractory gout, pegloticase is recommended. CONCLUSIONS: These recommendations aim to inform physicians and patients about the non-pharmacological and pharmacological treatments for gout and to provide the best strategies to achieve the predefined urate target to cure the disease.

3 Editorial How to regulate neutrophils in gout. 2013

So, Alexander. · ·Arthritis Res Ther · Pubmed #24063679.

ABSTRACT: Most research in gout has concentrated on the proinflammatory mechanisms to explain the inflammation that is generated when leucocytes are in contact with monosodium urate crystals. However, the episodic nature of gout and the absence of inflammation even when crystals are present suggest that there are natural counter-regulatory mechanisms to limit the inflammatory response. Gagné and colleagues showed that myeloid inhibitory C-type lectin, a C-type lectin inhibitory receptor expressed on neutrophils, modulates monosodium urate-induced neutrophil responses in vitro.

4 Review The role of IL-1 in gout: from bench to bedside. 2018

So, Alexander / Dumusc, Alexandre / Nasi, Sonia. ·Service de Rhumatologie, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland. ·Rheumatology (Oxford) · Pubmed #29272514.

ABSTRACT: The translation of our knowledge of the biology of MSU crystal-induced IL-1 secretion gives rise to new targets and therapeutic strategies in the treatment of acute gout. The NACHT, LRR and PYD domains-containing protein 3 inflammasome is key to this, and is the subject of intense research. Novel pathways that modulate inflammasome activation, reactive oxygen species generation and extracellular processing of IL-1 have been described and show promise in in vitro and animal studies. Meanwhile, blocking IL-1 by various IL-1 inhibitors has shown the validity of this concept. Patients with acute gout treated with these inhibitors showed positive clinical and biological responses. More work needs to be performed to assess the risk/benefit profile of anti-IL-1 therapies as well as to identify those who will benefit the most from this novel approach to the treatment of gout.

5 Review Inflammation in gout: mechanisms and therapeutic targets. 2017

So, Alexander K / Martinon, Fabio. ·Service of Rheumatology, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Avenue Pierre Decker 4, 1011 Lausanne, Switzerland. · Department of Biochemistry, University of Lausanne, 155 Chemin des Boveresses, 1066 Epalinges, Switzerland. ·Nat Rev Rheumatol · Pubmed #28959043.

ABSTRACT: The acute symptoms of gout are triggered by the inflammatory response to monosodium urate crystals, mediated principally by macrophages and neutrophils. Innate immune pathways are of key importance in the pathogenesis of gout, in particular the activation of the NLRP3 inflammasome, which leads to the release of IL-1β and other pro-inflammatory cytokines. The orchestration of this pro-inflammatory cascade involves multiple intracellular and extracellular receptors and enzymes interacting with environmental influences that modulate the inflammatory state. Furthermore, the resolution of inflammation in gout is becoming better understood. This Review highlights recent advances in our understanding of both positive and negative regulatory pathways, as well as the genetic and environmental factors that modulate the inflammatory response. Some of these pathways can be manipulated and present novel therapeutic opportunities for the treatment of acute gout attacks.

6 Review Discordant American College of Physicians and international rheumatology guidelines for gout management: consensus statement of the Gout, Hyperuricemia and Crystal-Associated Disease Network (G-CAN). 2017

Dalbeth, Nicola / Bardin, Thomas / Doherty, Michael / Lioté, Frédéric / Richette, Pascal / Saag, Kenneth G / So, Alexander K / Stamp, Lisa K / Choi, Hyon K / Terkeltaub, Robert. ·Department of Medicine, University of Auckland, 85 Park Road, Grafton, Auckland 1023, New Zealand. · University Paris Diderot Cité Sorbonne, Service de Rhumatologie, Centre Viggo Petersen, Lariboisière Hospital, INSERM U1132, Paris, France. · Division of Rheumatology, Orthopaedics and Dermatology, School of Medicine, University of Nottingham, Clinical Sciences Building, City Hospital, Nottingham NG5 1PB, UK. · Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham (UAB), 820 Faculty Office Tower, 510 20th Street, Birmingham, Alabama 35294-3408, USA. · Service of Rheumatology, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Avenue Pierre Decker 4, 1011 Lausanne, Switzerland. · Department of Medicine, University of Otago, Christchurch, P.O. BOX 4345, Christchurch 8140, New Zealand. · Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, 55 Fruit Street, Harvard Medical School, Boston, Massachusetts 02114, USA. · VA San Diego Healthcare System, 111K, 3350 La Jolla Village Drive, San Diego, California 92161, USA. ·Nat Rev Rheumatol · Pubmed #28794514.

ABSTRACT: In November 2016, the American College of Physicians (ACP) published a clinical practice guideline on the management of acute and recurrent gout. This guideline differs substantially from the latest guidelines generated by the American College of Rheumatology (ACR), European League Against Rheumatism (EULAR) and 3e (Evidence, Expertise, Exchange) Initiative, despite reviewing largely the same body of evidence. The Gout, Hyperuricemia and Crystal-Associated Disease Network (G-CAN) convened an expert panel to review the methodology and conclusions of these four sets of guidelines and examine possible reasons for discordance between them. The G-CAN position, presented here, is that the fundamental pathophysiological knowledge underlying gout care, and evidence from clinical experience and clinical trials, supports a treat-to-target approach for gout aimed at lowering serum urate levels to below the saturation threshold at which monosodium urate crystals form. This practice, which is truly evidence-based and promotes the steady reduction in tissue urate crystal deposits, is promoted by the ACR, EULAR and 3e Initiative recommendations. By contrast, the ACP does not provide a clear recommendation for urate-lowering therapy (ULT) for patients with frequent, recurrent flares or those with tophi, nor does it recommend monitoring serum urate levels of patients prescribed ULT. Results from emerging clinical trials that have gout symptoms as the primary end point are expected to resolve this debate for all clinicians in the near term future.

7 Review Imaging in Gout and Other Crystal-Related Arthropathies. 2016

Omoumi, Patrick / Zufferey, Pascal / Malghem, Jacques / So, Alexander. ·Department of Diagnostic and Interventional Radiology, Lausanne University Hospital, Rue du Bugnon 46, Lausanne 1011, Switzerland. Electronic address: patrick.omoumi@chuv.ch. · Department of Rheumatology, Lausanne University Hospital, Av Pierre Decker 5, Lausanne 1011, Switzerland. · Department of Radiology, Saint Luc University Hospital, UC Louvain, Av Hippocrate 10, Brussels 1200, Belgium. ·Rheum Dis Clin North Am · Pubmed #27742018.

ABSTRACT: In this article, the authors consider the manifestations of intraarticular and periarticular crystal deposits. Most cases of crystal deposits are asymptomatic and represent incidental findings at imaging. In symptomatic arthropathies, imaging can play an important role in the diagnosis and assessment of disease progression and the extent of crystal deposits. Conventional radiography is the most common imaging modality. But ultrasound, conventional computerized tomography (CT), dual-energy CT, and MRI play an increasing role. The authors review typical radiographic features of crystal-induced arthropathies and findings that help to differentiate them. The authors also emphasize the increasing role of complementary imaging techniques.

8 Review Why better treatment of gout is needed. 2016

So, Alexander K. ·Service de Rhumatologie, CHUV and University of Lausanne, Switzerland. alexanderkai-lik.so@chuv.ch. ·Clin Exp Rheumatol · Pubmed #27586807.

ABSTRACT: The treatment of gout is thought to be simple, but in reality we are confronted regularly with patients who do not adhere to treatment and patients who have other medical conditions that render the choice of therapy difficult. A treat-to-target approach is essential in order to manage hyperuricaemia effectively and this, combined with a better use of existing treatments, offers the best way forward.

9 Review Interleukin-1 as a therapeutic target in gout. 2015

Dumusc, Alexandre / So, Alexander. ·Department of Rheumatology, Lausanne University Hospital, CHUV, Lausanne, Switzerland. ·Curr Opin Rheumatol · Pubmed #25633244.

ABSTRACT: PURPOSE OF REVIEW: To give an overview of current evidence for interleukin (IL)-1 blockade in the management of gout. RECENT FINDINGS: Three IL-1 blockers are currently available for clinical use: anakinra, rilonacept and canakinumab. Recent studies have focused on drugs with a long half-life: rilonacept and canakinumab. For treatment of acute gouty arthritis, three randomized controlled trials (RCTs) showed efficacy of canakinumab with some safety concerns and one RCT failed to show efficacy of rilonacept. For prevention of gout flare when starting uric acid lowering therapy (ULT), four RCTs showed efficacy of rilonacept and one RCT showed efficacy of canakinumab. SUMMARY: There is sufficient evidence supporting the use of IL-1 blockers for treatment of acute gouty arthritis or for prevention of gout flares when starting ULT in selected patients, with contraindications or intolerance to conventional therapy. More data are needed to assess safety and to specify their use in routine practice.

10 Review Improving cardiovascular and renal outcomes in gout: what should we target? 2014

Richette, Pascal / Perez-Ruiz, Fernando / Doherty, Michael / Jansen, Tim L / Nuki, George / Pascual, Eliseo / Punzi, Leonardo / So, Alexander K / Bardin, Thomas. ·Hôpital Lariboisière, Fédération de Rhumatologie, Centre Viggo Petersen 2, rue Ambroise Parè 75475 Cedex 10, Paris, France. · Servicio de Reumatología and BioCruces Health Research Institute, Cruces University Hospital, Plaza Cruces S/N, 48903 Barakaldo, Spain. · Division of Academic Rheumatology, University of Nottingham, Clinical Sciences Building, City Hospital Nottingham, Hucknall Road, Nottingham NG5 1PB, UK. · Department of Rheumatology, Radboud University Medical Center, Geert Grooteplein Zuid 8, 6525 GA Nijmegen, Netherlands. · Department of Rheumatology, University of Edinburgh, Western General Hospital, Crewe Road South, Edinburgh EH4 2XU, UK. · Department of Medicine, Rheumatology Section, Alicante University and General Hospital, University Miguel Hernández, Av. Pintor Baeza 12, Alicante 03010, Spain. · Department of Rheumatology, Rheumatology Unit, University of Padova, Via Giustiniani 2, 35128 Padova, Italy. · Service of Rheumatology, Centre Hospitalier Universitaire Vaudois, Avenue Pierre Decker 4, 1011 Lausanne, Switzerland. ·Nat Rev Rheumatol · Pubmed #25136785.

ABSTRACT: Epidemiological and experimental studies have shown that hyperuricaemia and gout are intricately linked with hypertension, metabolic syndrome, chronic kidney disease and cardiovascular disease. A number of studies suggest that hyperuricaemia and gout are independent risk factors for the development of these conditions and that these conditions account, in part, for the increased mortality rate of patients with gout. In this Review, we first discuss the links between hyperuricaemia, gout and these comorbidities, and present the mechanisms by which uric acid production and gout might favour the development of cardiovascular and renal diseases. We then emphasize the potential benefit of urate-lowering therapies on cardiovascular and renal outcomes in patients with hyperuricaemia. The mechanisms that link elevated serum uric acid levels and gout with these comorbidities seem to be multifactorial, implicating low-grade systemic inflammation and xanthine oxidase (XO) activity, as well as the deleterious effects of hyperuricaemia itself. Patients with asymptomatic hyperuricaemia should be treated by nonpharmacological means to lower their SUA levels. In patients with gout, long-term pharmacological inhibition of XO is a treatment strategy that might also reduce cardiovascular and renal comorbidities, because of its dual effect of lowering SUA levels as well as reducing free-radical production during uric acid formation.

11 Review The concept of the inflammasome and its rheumatologic implications. 2014

So, Alexander / Busso, Nathalie. ·Service de rhumatologie, université de Lausanne, CHU Vaudois, avenue Pierre-Decker 4, 1011 Lausanne, Suisse. Electronic address: alexanderkai-lik.so@chuv.ch. · Service de rhumatologie, université de Lausanne, CHU Vaudois, avenue Pierre-Decker 4, 1011 Lausanne, Suisse. ·Joint Bone Spine · Pubmed #24703401.

ABSTRACT: The inflammasome is a proteolytic complex that regulates IL1β and IL-18 secretion in macrophages and dendritic cells. Its plays a vital role in the control of the inflammatory and cellular responses to infectious and danger signals and is an essential part of the innate immune system. Four different inflammasomes have been identified so far, and the NLRP3-inflammasome has been the best-studied in relation to human disease. Activation of the NLRP3-inflammasome by microcrystals, such as monosodium urate (MSU) and basic calcium phosphate (BCP) crystals, leads to IL1β release, which in turn triggers local inflammation. Dysfunction of the NLRP3-inflammasome due to mutations of the NLRP3 gene is the cause of the auto-inflammatory syndrome CAPS. The symptoms and signs of inflammation in both conditions respond to IL1 blockade. IL1 inhibitors have also been used successfully in other idiopathic inflammatory diseases, suggesting that dysregulated inflammasome activity contributes to the pathogenesis of multiple diseases, but the precise underlying mechanisms remain to be identified.

12 Review Emerging therapies for gout. 2014

Edwards, N Lawrence / So, Alexander. ·Department of Medicine, University of Florida College of Medicine, 1600 South West Archer Road, Gainesville, FL 32610-0277, USA. Electronic address: edwarnl@medicine.ufl.edu. · Service de Rhumatologie, CHUV, Avenue Pierre Decker, Lausanne 1011, Switzerland. ·Rheum Dis Clin North Am · Pubmed #24703353.

ABSTRACT: Over the past decade much has been learned about the mechanisms of crystal-induced inflammation and renal excretion of uric acid, which has led to more specific targeting of gout therapies and a more potent approach to future management of gout. This article outlines agents being developed for more aggressive lowering of urate and more specific anti-inflammatory activity. The emerging urate-lowering therapies include lesinurad, arhalofenate, ulodesine, and levotofisopam. Novel gout-specific anti-inflammatories include the interleukin-1β inhibitors anakinra, canakinumab, and rilonacept, the melanocortins, and caspase inhibitors. The historic shortcomings of current gout treatment may, in part, be overcome by these novel approaches.

13 Review Recommendations for the use of ultrasound in rheumatoid arthritis: literature review and SONAR score experience. 2013

Zufferey, Pascal / Tamborrini, Giorgio / Gabay, Cem / Krebs, Andreas / Kyburz, Diego / Michel, Beat / Moser, Urs / Villiger, Peter M / So, Alexander / Ziswiler, Hans Rudolf. ·CHUV, av Pirre decker 4, 1005, Lausanne (vd), SWITZERLAND; pascal.zufferey@chuv.ch. ·Swiss Med Wkly · Pubmed #24363082.

ABSTRACT: Ultrasound (US) has become a useful tool in the detection of early disease, differential diagnosis, guidance of treatment decisions and treatment monitoring of rheumatoid arthritis (RA). In 2008, the Swiss Sonography in Arthritis and Rheumatism (SONAR) group was established to promote the use of US in inflammatory arthritis in clinical practice. A scoring system was developed and taught to a large number of Swiss rheumatologists who already contributed to the Swiss Clinical Quality Management (SCQM) database, a national patient register. This paper intends to give a Swiss consensus about best clinical practice recommendations for the use of US in RA on the basis of the current literature knowledge and experience with the Swiss SONAR score. Literature research was performed to collect data on current evidence. The results were discussed among specialists of the Swiss university centres and private practice, following a structured procedure. Musculoskelatal US was found to be very helpful in establishing the diagnosis and monitoring the evolution of RA, and to be a reliable tool if used by experienced examiners. It influences treatment decisions such as continuing, intensifying or stepping down therapy. The definite modalities of integrating US into the diagnosis and monitoring of RA treatments will be defined within a few years. There are, however, strong arguments to use US findings as of today in daily clinical care. Some practical recommendations about the use of US in RA, focusing on the diagnosis and the use of the SONAR score, are proposed.

14 Review Serum uric acid and gout: from the past to molecular biology. 2013

Punzi, L / So, A. ·Rheumatology Unit, Department of Medicine DIMED, University of Padua, Italy. punzireu@unipd.it ·Curr Med Res Opin · Pubmed #23621555.

ABSTRACT: OBJECTIVES: This review will briefly present the epidemiology and risk factors of gout, with a focus on recent advances. METHODS: Key papers for inclusion were identified by a PubMed search, and articles were selected according to their relevance for the topic, according to authors' judgment. RESULTS AND CONCLUSIONS: Gout therapy has remained very much unchanged for the last 50 years, but recently we have seen the approval of another gout treatment: the xanthine oxidase inhibitor febuxostat, and several new drugs are now in the late stages of clinical testing. Together with our enhanced level of understanding of the pathophysiology of the inflammatory process involved, we are entering a new era for the treatment of gout.

15 Review Update on gout 2012. 2012

So, Alexander / Busso, Nathalie. ·Service de Rhumatologie, Département de l'Appareil Locomoteur, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland. alexanderkai-lik.so@chuv.ch ·Joint Bone Spine · Pubmed #23165182.

ABSTRACT: Significant scientific advances have been made over the last five years in the pathogenesis of hyperuricemia and understanding how monosodium urate (MSU) crystals provoke gout. New detection methods using ultrasound (US) have been evaluated and may become part of our routine diagnostic approach in a patient presenting with gout. This review will concentrate on the latest developments in the field, and discuss how these data may impact on clinical practice. Finally, a brief review of the therapeutic implications and new therapies that have become available will be presented.

16 Review Gout: why is this curable disease so seldom cured? 2012

Doherty, Michael / Jansen, Tim L / Nuki, George / Pascual, Eliseo / Perez-Ruiz, Fernando / Punzi, Leonardo / So, Alexander K / Bardin, Thomas. ·Department of Rheumatology, City Hospital, Nottingham, UK. Michael.Doherty@nottingham.ac.uk ·Ann Rheum Dis · Pubmed #22863577.

ABSTRACT: 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-inflicted 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.

17 Review [The etiology and management of gout]. 2012

Pazár Maldonado, B / So, A. ·Department of Rheumatology, Centre Hospitalier Universitaire Vaudois, 1011, Lausanne, Suisse. ·Z Rheumatol · Pubmed #22370804.

ABSTRACT: Gout is an inflammatory arthritis caused by monosodium urate (MSU) crystal deposits in and around the joint. The formation of urinary calculi can also occur in gout, but are less common than arthritis. Gout usually presents with recurrent episodes of joint inflammation, which over time lead to tophus formation and joint destruction. In the last decade, significant advances have been made regarding not only the epidemiology and genetics of gout and hyperuricemia but also the mechanisms of inflammation and treatment of gout. In addition, knowledge concerning the key role of interleukin 1 (IL-1) has provided new therapeutic perspectives. However, the current management of gout is often suboptimal, with many Patienten either not receiving adequate treatment or being unable to tolerate existing treatments. New therapeutic agents provide interesting new options for Patienten with difficult-to-treat gouty arthritis.The English full-text version of this is available at SpringerLink (under "Supplemental").

18 Review Hyperuricaemia and gout: state of the art and future perspectives. 2010

Dalbeth, Nicola / So, Alexander. ·Bone and Joint Research Group, Department of Medicine, University of Auckland, Auckland, New Zealand. ·Ann Rheum Dis · Pubmed #20858623.

ABSTRACT: Major progress has been made in the past decade in understanding the pathogenesis and treatment of gout. These advances include identification of the genetic and environmental risk factors for gout, recognition that gout is an important risk factor for cardiovascular disease, elucidation of the pathways regulating the acute gout attack and the development of novel therapeutic agents to treat both the acute and chronic phases of the disease. This review summarises these advances and highlights the research agenda for the next decade.

19 Review Uric acid transport and disease. 2010

So, Alexander / Thorens, Bernard. ·Service de Rhumatologie, Department of Musculoskeletal Medicine, University of Lausanne, Lausanne, Switzerland. ·J Clin Invest · Pubmed #20516647.

ABSTRACT: Uric acid is the metabolic end product of purine metabolism in humans. It has antioxidant properties that may be protective but can also be pro-oxidant, depending on its chemical microenvironment. Hyperuricemia predisposes to disease through the formation of urate crystals that cause gout, but hyperuricemia, independent of crystal formation, has also been linked with hypertension, atherosclerosis, insulin resistance, and diabetes. We discuss here the biology of urate metabolism and its role in disease. We also cover the genetics of urate transport, including URAT1, and recent studies identifying SLC2A9, which encodes the glucose transporter family isoform Glut9, as a major determinant of plasma uric acid levels and of gout development.

20 Review Mechanisms of inflammation in gout. 2010

Busso, Nathalie / So, Alexander. ·Service de Rheumatologie, Centre Hospitalier Universitaire Vaudois, Université de Lausanne, Avenue Pierre Decker, 1011 Lausanne, Suisse. ·Arthritis Res Ther · Pubmed #20441605.

ABSTRACT: An acute attack of gout is a paradigm of acute sterile inflammation, as opposed to pyogenic inflammation. Recent studies suggest that the triggering of IL-1beta release from leucocytes lies at the heart of a cascade of processes that involves multiple cytokines and mediators. The NLRP3 inflammasome appears to have a specific role in this regard, but the biochemical events leading to its activation are still not well understood. We review the known mechanisms that underlie the inflammatory process triggered by urate crystals and suggest areas that require further research.

21 Clinical Trial Lesinurad in combination with allopurinol: a randomised, double-blind, placebo-controlled study in patients with gout with inadequate response to standard of care (the multinational CLEAR 2 study). 2017

Bardin, Thomas / Keenan, Robert T / Khanna, Puja P / Kopicko, Jeff / Fung, Maple / Bhakta, Nihar / Adler, Scott / Storgard, Chris / Baumgartner, Scott / So, Alexander. ·Rhumatologie, Lariboisière Hospital, and Université Paris Diderot Sorbonne Cité, Paris, France. · Division of Rheumatology, Duke University School of Medicine, Durham, North Carolina, USA. · Division of Rheumatology, University of Michigan, Ann Arbor, Michigan, USA. · Biometrics, Ardea Biosciences, Inc., San Diego, California, USA. · Research & Development, Ardea Biosciences, Inc., San Diego, California, USA. · Research & Development, AstraZeneca Pharmaceuticals, Gaithersburg, Maryland, USA. · Medical Affairs, Ardea Biosciences, Inc., San Diego, California, USA. · Service de rhumatologie, Université de Lausanne, Lausanne, Switzerland. ·Ann Rheum Dis · Pubmed #27821644.

ABSTRACT: OBJECTIVES: Determine the efficacy and safety of daily lesinurad (200 or 400 mg orally) added to allopurinol in patients with serum uric acid (sUA) above target in a 12-month, randomised, phase III trial. METHODS: Patients on allopurinol ≥300 mg (≥200 mg in moderate renal impairment) had sUA level of ≥6.5 mg/dL (≥387 µmol/L) at screening and two or more gout flares in the prior year. Primary end point was the proportion of patients achieving sUA level of <6.0 mg/dL (<357 µmol/L) (month 6). Key secondary end points were mean gout flare rate requiring treatment (months 7 through 12) and proportions of patients with complete resolution of one or more target tophi (month 12). Safety assessments included adverse events and laboratory data. RESULTS: Patients (n=610) were predominantly male, with mean (±SD) age 51.2±10.90 years, gout duration 11.5±9.26 years and baseline sUA of 6.9±1.2 mg/dL (410±71 µmol/L). Lesinurad at 200 and 400 mg doses, added to allopurinol, significantly increased proportions of patients achieving sUA target versus allopurinol-alone therapy by month 6 (55.4%, 66.5% and 23.3%, respectively, p<0.0001 both lesinurad+allopurinol groups). In key secondary end points, there were no statistically significant treatment-group differences favouring lesinurad. Lesinurad was generally well tolerated; the 200 mg dose had a safety profile comparable with allopurinol-alone therapy. Renal-related adverse events occurred in 5.9% of lesinurad 200 mg+allopurinol, 15.0% of lesinurad 400 mg+allopurinol and 4.9% of allopurinol-alone groups, with serum creatinine elevation of ≥1.5× baseline in 5.9%, 15.0% and 3.4%, respectively. Serious treatment-emergent adverse events occurred in 4.4% of lesinurad 200 mg+allopurinol, in 9.5% of lesinurad 400 mg+allopurinol and in 3.9% of allopurinol-alone groups, respectively. CONCLUSION: Lesinurad added to allopurinol demonstrated superior sUA lowering versus allopurinol-alone therapy and lesinurad 200 mg was generally well tolerated in patients with gout warranting additional therapy. TRIAL REGISTRATION NUMBER: NCT01493531.

22 Clinical Trial Canakinumab for the treatment of acute flares in difficult-to-treat gouty arthritis: Results of a multicenter, phase II, dose-ranging study. 2010

So, Alexander / De Meulemeester, Marc / Pikhlak, Andrey / Yücel, A Eftal / Richard, Dominik / Murphy, Valda / Arulmani, Udayasankar / Sallstig, Peter / Schlesinger, Naomi. ·University Hospital of Lausanne, Lausanne, Switzerland. AlexanderKai-Lik.So@chuv.ch ·Arthritis Rheum · Pubmed #20533546.

ABSTRACT: OBJECTIVE: To assess the efficacy and tolerability of canakinumab, a fully human anti-interleukin-1β monoclonal antibody, for the treatment of acute gouty arthritis. METHODS: In this 8-week, single-blind, double-dummy, dose-ranging study, patients with acute gouty arthritis whose disease was refractory to or who had contraindications to nonsteroidal antiinflammatory drugs and/or colchicine were randomized to receive a single subcutaneous dose of canakinumab (10, 25, 50, 90, or 150 mg; n = 143) or an intramuscular dose of triamcinolone acetonide (40 mg; n = 57). Patients assessed pain using a 100-mm visual analog scale. RESULTS: Seventy-two hours after treatment, a statistically significant dose response was observed for canakinumab. All canakinumab doses were associated with numerically less pain than triamcinolone acetonide; thus, a dose with equivalent efficacy to triamcinolone acetonide 72 hours after treatment could not be determined. The reduction from baseline in pain intensity with canakinumab 150 mg was greater than with triamcinolone acetonide 24, 48, and 72 hours after treatment (differences of -11.5 mm [P = 0.04], -18.2 mm [P = 0.002], and -19.2 mm [P < 0.001], respectively), and 4, 5, and 7 days after treatment (all P < 0.05). Canakinumab significantly reduced the risk of recurrent flares versus triamcinolone acetonide (P ≤ 0.01 for all doses) (relative risk reduction 94% for canakinumab 150 mg versus triamcinolone acetonide). The overall incidence of adverse events was similar for canakinumab (41%) and triamcinolone acetonide (42%); most were mild or moderate in severity. CONCLUSION: Our findings indicate that canakinumab 150 mg provides rapid and sustained pain relief in patients with acute gouty arthritis, and significantly reduces the risk of recurrent flares compared with triamcinolone acetonide.

23 Article Pleiotropic effect of the ABCG2 gene in gout: involvement in serum urate levels and progression from hyperuricemia to gout. 2020

Wrigley, Rebekah / Phipps-Green, Amanda J / Topless, Ruth K / Major, Tanya J / Cadzow, Murray / Riches, Philip / Tausche, Anne-Kathrin / Janssen, Matthijs / Joosten, Leo A B / Jansen, Tim L / So, Alexander / Harré Hindmarsh, Jennie / Stamp, Lisa K / Dalbeth, Nicola / Merriman, Tony R. ·Department of Biochemistry, University of Otago, Box 56, Dunedin, New Zealand. · Rheumatic Diseases Unit, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK. · Department of Rheumatology, University Clinic "Carl-Gustav-Carus", Dresden, Germany. · Department of Rheumatology, VieCuri Medical Center, Venlo, The Netherlands. · Department of Internal Medicine and Radboud Institute of Molecular Life Science, Radboud University Medical Center, Nijmegen, The Netherlands. · Department of Medical Genetics, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania. · Laboratory of Rheumatology, University of Lausanne, CHUV, Nestlé 05-5029, 1011, Lausanne, Switzerland. · Ngāti Porou Hauora Charitable Trust, Te Puia Springs, Tairāwhiti, New Zealand. · Department of Medicine, University of Otago, Christchurch, PO Box 4345, Christchurch, New Zealand. · Department of Medicine, University of Auckland, Auckland, New Zealand. · Department of Biochemistry, University of Otago, Box 56, Dunedin, New Zealand. tony.merriman@otago.ac.nz. ·Arthritis Res Ther · Pubmed #32164793.

ABSTRACT: BACKGROUND: The ABCG2 Q141K (rs2231142) and rs10011796 variants associate with hyperuricaemia (HU). The effect size of ABCG2 rs2231142 on urate is ~ 60% that of SLC2A9, yet the effect size on gout is greater. We tested the hypothesis that ABCG2 plays a role in the progression from HU to gout by testing for association of ABCG2 rs2231142 and rs10011796 with gout using HU controls. METHODS: We analysed 1699 European gout cases and 14,350 normouricemic (NU) and HU controls, and 912 New Zealand (NZ) Polynesian (divided into Eastern and Western Polynesian) gout cases and 696 controls. Association testing was performed using logistic and linear regression with multivariate adjusting for confounding variables. RESULTS: In Europeans and Polynesians, the ABCG2 141K (T) allele was associated with gout using HU controls (OR = 1.85, P = 3.8E CONCLUSION: These data are consistent with a role for ABCG2 141K in gout in the presence of established HU.

24 Article Systematic genetic analysis of early-onset gout: ABCG2 is the only associated locus. 2020

Zaidi, Faseeh / Narang, Ravi K / Phipps-Green, Amanda / Gamble, Greg G / Tausche, Anne-Katherin / So, Alexander / Riches, Philip / Andres, Mariano / Perez-Ruiz, Fernando / Doherty, Michael / Janssen, Matthijs / Joosten, Leo A B / Jansen, Tim L / Kurreeman, Fina / Torres, Rosa J / McCarthy, Geraldine M / Miner, Jeffrey N / Stamp, Lisa K / Merriman, Tony R / Dalbeth, Nicola. ·Department of Medicine, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand. · Department of Biochemistry, University of Otago, Dunedin, New Zealand. · Department of Rheumatology, Technical University Dresden, Dresden, Germany. · Department of Medicine, Service of Rheumatology, Centre Hospitalier Universitaire Vaudois and University of Lausanne, Lausanne, Switzerland. · Rheumatology and Bone Disease Unit, Centre for Genomic and Experimental Medicine, Institute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK. · Department of Medicine, Sección de Reumatología, Hospital General Universitario de Alicante, Alicante, Spain. · Rheumatology Division, Hospital Universitario Cruces, Baracaldo, Biscay, Spain. · Division of Rheumatology, Orthopaedics and Dermatology, School of Medicine, University of Nottingham, Nottingham, UK. · Department of Rheumatology, VieCuri Medical Center, Venlo, The Netherlands. · Department of Internal Medicine, Radboud University Medical Center, Nijmegen, The Netherlands. · Department of Medical Genetics, Iuliu Hatieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania. · Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands. · Department of Biochemistry, La Paz University Hospital Health Research Institute (FIBHULP), IdiPaz, Madrid, Spain. · Center for Biomedical Network Research on Rare Diseases (CIBERER), ISCIII, Madrid, Spain. · Department of Rheumatology, School of Medicine and Medical Science, University College Dublin, Dublin, Ireland. · Ardea Biosciences, Inc., San Diego, CA, USA. · Department of Medicine, University of Otago, Christchurch, New Zealand. ·Rheumatology (Oxford) · Pubmed #31998961.

ABSTRACT: OBJECTIVE: The aim of this study was to examine whether serum urate-associated genetic variants are associated with early-onset gout. METHODS: Participants with gout in the Genetics of Gout in Aotearoa study with available genotyping were included (n = 1648). Early-onset gout was defined as the first presentation of gout <40 years of age. Single nucleotide polymorphisms (SNPs) for the 10 loci most strongly associated with serum urate were genotyped. Allelic association of the SNPs with early-onset gout was tested using logistic regression in an unadjusted model and in a model adjusted for sex, body mass index, tophus presence, flare frequency, serum creatinine and highest serum urate. The analysis was also done in two replication cohorts: Eurogout (n = 704) and Ardea (n = 755), and data were meta-analysed. RESULTS: In the Genetics of Gout in Aotearoa study, there were 638 (42.4%) participants with early-onset gout. The ABCG2 rs2231142 gout risk T-allele was present more frequently in participants with early-onset gout compared with the later-onset group. For the other SNPs tested, no differences in risk allele number were observed. In the allelic association analysis, the ABCG2 rs2231142 T-allele was associated with early-onset gout in unadjusted and adjusted models. Analysis of the replication cohorts confirmed the association of early-onset gout with the ABCG2 rs2231142 T-allele, but not with other serum urate-associated SNPs. In the meta-analysis, the odds ratio (95% CI) for early-onset gout for the ABCG2 rs2231142 T-allele was 1.60 (1.41, 1.83). CONCLUSION: In contrast to other serum urate-raising variants, the ABCG2 rs2231142 T-allele is strongly associated with early-onset gout.

25 Article Gout, Hyperuricaemia and Crystal-Associated Disease Network (G-CAN) consensus statement regarding labels and definitions of disease states of gout. 2019

Bursill, David / Taylor, William J / Terkeltaub, Robert / Abhishek, Abhishek / So, Alexander K / Vargas-Santos, Ana Beatriz / Gaffo, Angelo Lino / Rosenthal, Ann / Tausche, Anne-Kathrin / Reginato, Anthony / Manger, Bernhard / Sciré, Carlo / Pineda, Carlos / van Durme, Caroline / Lin, Ching-Tsai / Yin, Congcong / Albert, Daniel Arthur / Biernat-Kaluza, Edyta / Roddy, Edward / Pascual, Eliseo / Becce, Fabio / Perez-Ruiz, Fernando / Sivera, Francisca / Lioté, Frédéric / Schett, Georg / Nuki, George / Filippou, Georgios / McCarthy, Geraldine / da Rocha Castelar Pinheiro, Geraldo / Ea, Hang-Korng / Tupinambá, Helena De Almeida / Yamanaka, Hisashi / Choi, Hyon K / Mackay, James / ODell, James R / Vázquez Mellado, Janitzia / Singh, Jasvinder A / Fitzgerald, John D / Jacobsson, Lennart T H / Joosten, Leo / Harrold, Leslie R / Stamp, Lisa / Andrés, Mariano / Gutierrez, Marwin / Kuwabara, Masanari / Dehlin, Mats / Janssen, Matthijs / Doherty, Michael / Hershfield, Michael S / Pillinger, Michael / Edwards, N Lawrence / Schlesinger, Naomi / Kumar, Nitin / Slot, Ole / Ottaviani, Sebastien / Richette, Pascal / MacMullan, Paul A / Chapman, Peter T / Lipsky, Peter E / Robinson, Philip / Khanna, Puja P / Gancheva, Rada N / Grainger, Rebecca / Johnson, Richard J / Te Kampe, Ritch / Keenan, Robert T / Tedeschi, Sara K / Kim, Seoyoung / Choi, Sung Jae / Fields, Theodore R / Bardin, Thomas / Uhlig, Till / Jansen, Tim / Merriman, Tony / Pascart, Tristan / Neogi, Tuhina / Klück, Viola / Louthrenoo, Worawit / Dalbeth, Nicola. ·Department of Health and Medical Sciences, The University of Adelaide, Adelaide, South Australia, Australia davebursill@bigpond.com. · Department of Medicine, University of Otago, Wellington, New Zealand. · Wellington Regional Rheumatology Unit, Hutt Valley District Health Board, Lower Hutt, New Zealand. · Department of Rheumatology, UCSD/ VA Medical Center, San Diego, California, USA. · Department of Academic Rheumatology, University of Nottingham, Nottingham, UK. · Department of Musculoskeletal Medicine, Service de RMR, Lausanne, Switzerland. · Department of Internal Medicine, Rheumatology Unit, State University of Rio de Janeiro, Rio de Janeiro, Brazil. · Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA. · Division of Rheumatology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA. · Translational Research Unit, Clement J Zablocki VA Medical Center, Milwaukee, Wisconsin, USA. · Department of Rheumatology, University Hospital 'Carl Gustav Carus' of the Technical University Dresden, Dresden, Germany. · Division of Rheumatology, The Warren Alpert School of Medicine at Brown University, Providence, Rhode Island, USA. · Rheumatology and Immunology, Universität Erlangen-Nürnberg, Erlangen, Germany. · Section of Rheumatology, Department of Medical Sciences, University of Ferrara, Ferrara, Italy. · Epidemiology Unit, Italian Society for Rheumatology, Milan, Italy. · Department of Rheumatology, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, Mexico City, Mexico. · Department of Internal Medicine, Division of Rheumatology, Maastricht University Medical Centre, Maastricht, The Netherlands. · Division of Allergy, Immunology and Rheumatology, Taichung Veterans General Hospital, Taichung, Taiwan. · Department of Immunology and Dermatology, Henry Ford Health System, Detroit, Michigan, USA. · Department of Rheumatology, Dartmouth-Hitchcock Medical Center, Hanover, New Hampshire, USA. · Outpatient Rheumatology Clinic, Nutritional and Lifestyle Medicine Centre, ORLIK, Warsaw, Poland. · Research Institute for Primary Care and Health Sciences, Keele University, Keele, UK. · Department of Rheumatology, Hospital General Universitario de Alicante, Alicante, Spain. · Departamento de Medicina Clínica, Universidad Miguel Hernández, Alicante, Spain. · Department of Diagnostic and Interventional Radiology, University of Lausanne, Lausanne, Switzerland. · Rheumatology Division, Cruces University Hospital, Baracaldo, Spain. · Department of Medicine, University of the Basque Country, Biscay, Spain. · Investigation Group for Arthritis, Biocruces Health Research Institute, Baracaldo, Spain. · Department of Rheumatology, Hospital General Universitario Elda, Elda, Spain. · Department of Rhumatologie, Hôpital Lariboisière, Assistance Publique-Hopitaux de Paris, Paris, France. · Department of Rhumatologie, INSERM UMR-1132 and Université Paris Diderot, Paris, France. · Department of Internal Medicine III, Friedrich-Alexander University Erlangen-Nürnberg and Universitatsklinikum Erlangen, Erlangen, Germany. · Insititute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK. · Department of Rheumatology, Mater Misericordiae University Hospital, Dublin, Ireland. · School of Medicine and Medical Science, University College Dublin, Dublin, Ireland. · Department of Rheumatology, Hôpital Lariboisière, Paris, France. · Rheumatology, State University of Rio de Janeiro, Rio de Janeiro, Brazil. · Institute of Rheumatology, Tokyo Women's Medical University Hospital, Tokyo, Japan. · School of Medicine, Tokyo Women's Medical University, Tokyo, Japan. · Section of Rheumatology and Clinical Epidemiology, Harvard Medical School and Massachusetts General Hospital, Boston, Massachusetts, USA. · President and CEO, Aristea Therapeutics, San Diego, California, USA. · Division of Rheumatology, University of Nebraska Medical Center, Omaha, Nebraska, USA. · Department of Rheumatology, Hospital General de Mexico and Universidad Nacional Autónoma de México, Mexico City, Mexico. · Department of Medicine at School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA. · Medicine Service, Birmingham Veterans Affairs Medical Center, Birmingham, Alabama, USA. · Division of Epidemiology at School of Public Health, University of Alabama at Birmingham, Birmingham, Alabama, USA. · Department of Medicine/Rheumatology, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, California, USA. · Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. · Department of Internal Medicine, Radboud University Medical Center Nijmegen, Nijmegen, The Netherlands. · Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA. · Chief Scientific Officer, Corrona, LLC, Southborough, Massachusetts, USA. · Department of Medicine, Otago University, Christchurch, New Zealand. · Department of Rheumatology, Hospital Universitario de Alicante, Alicante, Spain. · Division of Musculoskeletal and Rheumatic Diseases, Instituto Nacional Rehabilitación, México City, México. · Division of Renal Diseases and Hypertension, University of Colorado Denver School of Medicine, Aurora, Colorado, USA. · Department of Cardiology, Toranomon Hospital, Minato-ku, Japan. · Department of Rheumatology and Inflammation Research, Sahlgrenska Academy, University of Göteborg, Göteborg, Sweden. · Department of Rheumatology, VieCuri Medical Centre, Venlo, The Netherlands. · Division of Rheumatology, Duke University Medical Center, Durham, North Carolina, USA. · Department of Rheumatology/Medicine, New York University School of Medicine, New York City, New York, USA. · College of Medicine, University of Florida, Gainesville, Florida, USA. · Department of Medicine, Rutgers-Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA. · Department of Internal Medicine, Division of Cardiovascular Medicine, University of Michigan, Ann Arbor, Detroit, Michigan, USA. · Department of Rheumatology, Copenhagen Center for Arthritis Research, Center for Rheumatology and Spinal Disorders, Rigshospitalet Glostrup, Glostrup, Denmark. · Department of Rheumatology, Bichat-Claude Bernard Hospital, University of Sorbonne Paris Cité, Paris, France. · Service de Rhumatologie, Hôpital Lariboisière, Assistance Publique-Hopitaux de Paris, and INSERM UMR-1132 and Université de Paris, Paris, France. · Division of Rheumatology, University of Calgary, Calgary, Alberta, Canada. · Department of Rheumatology, Immunology and Allergy, Canterbury District Health Board, Christchurch, New Zealand. · CEO and CMO, AMPEL BioSolutions, LLC, Charlottesville, Virginia, USA. · School of Clinical Medicine, Faculty of Medicine, The University of Queensland, Brisbane, Queensland, Australia. · Department of Rheumatology, University of Michigan, Ann Arbor, Michigan, USA. · Clinic of Rheumatology, University Hospital 'St. Ivan Rilski', Sofia, Bulgaria. · Department of Medicine, University of Otago, Wellington, Wellington, New Zealand. · Division of Renal Diseases and Hypertension, University of Colorado Denver, Denver, Colorado, USA. · Division of Rheumatology, Duke University School of Medicine, Durham, North Carolina, USA. · Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, Massachusetts, USA. · Arthritis Center, Harvard Medical School, Boston, Massachusetts, USA. · Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA. · Division of Rheumatology, Department of Internal Medicine, Korea University Medical College, Ansan, South Korea. · Weill Cornell Medical College, Hospital for Special Surgery, New York City, New York, USA. · Department of Rheumatology, Hôpital Lariboisière, Assistance Publique-Hopitaux de Paris, and INSERM UMR-1132 and Université de Paris, Paris, France. · Department of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway. · Department of Biochemistry, University of Otago, Dunedin, New Zealand. · Department of Rheumatology, Lille Catholic University, Saint-Philibert Hospital, Lomme, France. · Section of Rheumatology, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA. · Department of Internal Medicine, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands. · Division of Rheumatology, Department of Internal Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand. · Department of Medicine, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand. ·Ann Rheum Dis · Pubmed #31501138.

ABSTRACT: OBJECTIVE: There is a lack of standardisation in the terminology used to describe gout. The aim of this project was to develop a consensus statement describing the recommended nomenclature for disease states of gout. METHODS: A content analysis of gout-related articles from rheumatology and general internal medicine journals published over a 5-year period identified potential disease states and the labels commonly assigned to them. Based on these findings, experts in gout were invited to participate in a Delphi exercise and face-to-face consensus meeting to reach agreement on disease state labels and definitions. RESULTS: The content analysis identified 13 unique disease states and a total of 63 unique labels. The Delphi exercise (n=76 respondents) and face-to-face meeting (n=35 attendees) established consensus agreement for eight disease state labels and definitions. The agreed labels were as follows: 'asymptomatic hyperuricaemia', 'asymptomatic monosodium urate crystal deposition', 'asymptomatic hyperuricaemia with monosodium urate crystal deposition', 'gout', 'tophaceous gout', 'erosive gout', 'first gout flare' and 'recurrent gout flares'. There was consensus agreement that the label 'gout' should be restricted to current or prior clinically evident disease caused by monosodium urate crystal deposition (gout flare, chronic gouty arthritis or subcutaneous tophus). CONCLUSION: Consensus agreement has been established for the labels and definitions of eight gout disease states, including 'gout' itself. The Gout, Hyperuricaemia and Crystal-Associated Disease Network recommends the use of these labels when describing disease states of gout in research and clinical practice.

Next