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Gout: HELP
Articles by Hyon K. Choi
Based on 69 articles published since 2009
(Why 69 articles?)
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Between 2009 and 2019, Hyon Choi wrote the following 69 articles about Gout.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3
1 Guideline 2012 American College of Rheumatology guidelines for management of gout. Part 2: therapy and antiinflammatory prophylaxis of acute gouty arthritis. 2012

Khanna, Dinesh / Khanna, Puja P / Fitzgerald, John D / Singh, Manjit K / Bae, Sangmee / Neogi, Tuhina / Pillinger, Michael H / Merill, Joan / Lee, Susan / Prakash, Shraddha / Kaldas, Marian / Gogia, Maneesh / Perez-Ruiz, Fernando / Taylor, Will / Lioté, Frédéric / Choi, Hyon / Singh, Jasvinder A / Dalbeth, Nicola / Kaplan, Sanford / Niyyar, Vandana / Jones, Danielle / Yarows, Steven A / Roessler, Blake / Kerr, Gail / King, Charles / Levy, Gerald / Furst, Daniel E / Edwards, N Lawrence / Mandell, Brian / Schumacher, H Ralph / Robbins, Mark / Wenger, Neil / Terkeltaub, Robert / Anonymous2310738. ·University of Michigan, Ann Arbor, MI, USA. ·Arthritis Care Res (Hoboken) · Pubmed #23024029.

ABSTRACT: -- No abstract --

2 Guideline 2012 American College of Rheumatology guidelines for management of gout. Part 1: systematic nonpharmacologic and pharmacologic therapeutic approaches to hyperuricemia. 2012

Khanna, Dinesh / Fitzgerald, John D / Khanna, Puja P / Bae, Sangmee / Singh, Manjit K / Neogi, Tuhina / Pillinger, Michael H / Merill, Joan / Lee, Susan / Prakash, Shraddha / Kaldas, Marian / Gogia, Maneesh / Perez-Ruiz, Fernando / Taylor, Will / Lioté, Frédéric / Choi, Hyon / Singh, Jasvinder A / Dalbeth, Nicola / Kaplan, Sanford / Niyyar, Vandana / Jones, Danielle / Yarows, Steven A / Roessler, Blake / Kerr, Gail / King, Charles / Levy, Gerald / Furst, Daniel E / Edwards, N Lawrence / Mandell, Brian / Schumacher, H Ralph / Robbins, Mark / Wenger, Neil / Terkeltaub, Robert / Anonymous2300738. ·University of Michigan, Ann Arbor, MI, USA. ·Arthritis Care Res (Hoboken) · Pubmed #23024028.

ABSTRACT: -- No abstract --

3 Editorial Editorial: Do Not Let Gout Apathy Lead to Gouty Arthropathy. 2017

FitzGerald, John D / Neogi, Tuhina / Choi, Hyon K. ·University of California, Los Angeles. · Boston University, Boston, Massachusetts. · Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts. ·Arthritis Rheumatol · Pubmed #28002890.

ABSTRACT: -- No abstract --

4 Editorial Crystal deposition diseases. 2014

Choi, Hyon. ·Boston University School of Medicine, Section of Rheumatology and the Clinical Epidemiology Unit, Boston, Massachusetts, USA. ·Curr Opin Rheumatol · Pubmed #24445481.

ABSTRACT: -- No abstract --

5 Editorial Managing gout needs more than drugs: 'Il faut le savoir-faire, l'Art et la maniere'. 2013

Lioté, Frédéric / Choi, Hyon. · ·Ann Rheum Dis · Pubmed #23667169.

ABSTRACT: -- No abstract --

6 Editorial Gout and quality of life. 2009

Kim, Seo Young / Choi, Hyon K. · ·J Rheumatol · Pubmed #19435969.

ABSTRACT: -- No abstract --

7 Review Review: Unmet Needs and the Path Forward in Joint Disease Associated With Calcium Pyrophosphate Crystal Deposition. 2018

Abhishek, Abhishek / Neogi, Tuhina / Choi, Hyon / Doherty, Michael / Rosenthal, Ann K / Terkeltaub, Robert. ·University of Nottingham, UK City Hospital, Nottingham, UK. · Boston University School of Medicine, Boston, Massachusetts. · Massachusetts General Hospital, Boston, Massachusetts. · Medical College of Wisconsin, Milwaukee. · Veterans Affairs, University of California at San Diego, San Diego, California. ·Arthritis Rheumatol · Pubmed #29609209.

ABSTRACT: Calcium pyrophosphate (CPP) crystal deposition (CPPD) is prevalent and can be associated with synovitis and joint damage. The population of elderly persons predominantly affected by CPPD is growing rapidly. Since shortfalls exist in many aspects of CPPD, we conducted an anonymous survey of CPPD unmet needs, prioritized by experts from the Gout, Hyperuricemia and Crystal-Associated Disease Network. We provide our perspectives on the survey results, and we propose several CPPD basic and clinical translational research pathways. Chondrocyte and cartilage culture systems for generating CPP crystals in vitro and transgenic small animal CPPD models are needed to better define CPPD mechanism paradigms and help guide new therapies. CPPD recognition, clinical research, and care would be improved by international consensus on CPPD nomenclature and disease phenotype classification, better exploitation of advanced imaging, and pragmatic new point-of-care crystal analytic approaches for detecting CPP crystals. Clinical impacts of CPP crystals in osteoarthritis and in asymptomatic joints in elderly persons remain major unanswered questions that are rendered more difficult by current inability to therapeutically limit or dissolve the crystal deposits and assess the consequent clinical outcome. Going forward, CPPD clinical research studies should define clinical settings in which articular CPPD does substantial harm and should include analyses of diverse clinical phenotypes and populations. Clinical trials should identify the best therapeutic targets to limit CPP crystal deposition and associated inflammation and should include assessment of intraarticular agents. Our perspective is that such advances in basic and clinical science in CPPD are now within reach and can lead to better treatments for this disorder.

8 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.

9 Review Serum Uric Acid and the Risk of Incident and Recurrent Gout: A Systematic Review. 2017

Shiozawa, Aki / Szabo, Shelagh M / Bolzani, Anna / Cheung, Antoinette / Choi, Hyon K. ·From Takeda Pharmaceuticals International Inc., Deerfield, Illinois; Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA; Redwood Outcomes, Vancouver, British Columbia, Canada. · A. Shiozawa, Associate Director, MPH, Takeda Pharmaceuticals International Inc.; S.M. Szabo, Principal, MSc, Redwood Outcomes; A. Bolzani, Research Associate, MSc, Redwood Outcomes; A. Cheung, Research Associate, MPH, Redwood Outcomes; H.K. Choi, Professor, Director, MD, DrPH, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School. · From Takeda Pharmaceuticals International Inc., Deerfield, Illinois; Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA; Redwood Outcomes, Vancouver, British Columbia, Canada. sszabo@broadstreetheor.com. · A. Shiozawa, Associate Director, MPH, Takeda Pharmaceuticals International Inc.; S.M. Szabo, Principal, MSc, Redwood Outcomes; A. Bolzani, Research Associate, MSc, Redwood Outcomes; A. Cheung, Research Associate, MPH, Redwood Outcomes; H.K. Choi, Professor, Director, MD, DrPH, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School. sszabo@broadstreetheor.com. ·J Rheumatol · Pubmed #28148699.

ABSTRACT: OBJECTIVE: Lowering serum uric acid (SUA) levels can essentially cure gout; however, this is not widely practiced. To summarize epidemiologic evidence related to this causal link, we conducted a systematic review of the published literature reporting the association between SUA level and incident and recurrent gout (i.e., gout flares). METHODS: We systematically searched Medline, EMBASE, and the Cochrane Database of Systematic Reviews using separate search strategies for incident gout and recurrent gout. We screened 646 abstracts to identify 8 eligible articles reporting gout incidence and 913 abstracts to identify 18 articles reporting recurrent gout. RESULTS: For both gout incidence and recurrence, a graded trend was observed where the risk was increased with higher SUA levels. Gout incidence rates per 1000 person-years from population-based studies ranged from 0.8 (SUA ≤ 6 mg/dl) to 70.2 cases (SUA ≥ 10 mg/dl). Recurrent gout risk in clinical cohorts ranged from 12% (SUA ≤ 6 mg/dl) to 61% (SUA ≥ 9 mg/dl) among those receiving urate-lowering therapy (ULT), and 3.7% (SUA 6-7 mg/dl) to 61% (SUA > 9.3 mg/dl) after successful ULT. Retrospective database studies also showed a graded relationship, although the strength of the association was weaker. Studies reporting mean flares or time-to-flare according to SUA showed similar findings. CONCLUSION: This systematic review confirms that higher SUA levels are associated with increased risk of incident and recurrent gout in a graded manner. Although few prospective cohorts have evaluated incident and recurrent gout according to SUA, the existing evidence underscores the need to treat to SUA targets, as recommended by the American College of Rheumatology and the European League Against Rheumatism.

10 Review Review: Gout: A Roadmap to Approaches for Improving Global Outcomes. 2017

Dalbeth, Nicola / Choi, Hyon K / Terkeltaub, Robert. ·University of Auckland, Auckland, New Zealand. · Massachusetts General Hospital and Harvard Medical School, Boston. · VA San Diego Healthcare System and University of California, San Diego. ·Arthritis Rheumatol · Pubmed #27389665.

ABSTRACT: -- No abstract --

11 Review The economic burden of gout: A systematic review. 2015

Rai, Sharan K / Burns, Lindsay C / De Vera, Mary A / Haji, Aliya / Giustini, Dean / Choi, Hyon K. ·Arthritis Research Canada, Vancouver, British Columbia, Canada; Department of Experimental Medicine, University of British Columbia, Vancouver, British Columbia, Canada. · Arthritis Research Canada, Vancouver, British Columbia, Canada; Department of Psychology, York University, Toronto, Ontario, Canada. · Arthritis Research Canada, Vancouver, British Columbia, Canada; Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, British Columbia, Canada. · School of Population and Public Health, University of British Columbia, Vancouver, British Columbia, Canada. · Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada. · Arthritis Research Canada, Vancouver, British Columbia, Canada; Faculty of Medicine, University of British Columbia, Vancouver, British Columbia, Canada; Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Boston, MA. Electronic address: Choi.Hyon@mgh.harvard.edu. ·Semin Arthritis Rheum · Pubmed #25912932.

ABSTRACT: OBJECTIVE: Gout is a painful and disabling joint disease that constitutes the most common inflammatory arthritis in the US. To clarify the economic impact of gout, we systematically reviewed the literature on the direct and indirect costs associated with this disease. METHODS: We conducted a literature search of MEDLINE, EMBASE, International Pharmaceutical Abstracts, NHS Economic Evaluation, and CINAHL databases to identify studies of gout and economics. We systematically reviewed published studies that met our inclusion criteria and extracted and summarized all relevant economic parameters. Reported costs were inflation-adjusted to 2013 US dollars (USD). RESULTS: A total of 15 studies met all eligibility criteria. Three controlled studies reported all-cause total direct costs based on specific populations (i.e., $4733, $16,925, and $18,362 per capita among employed, elderly, and treatment-refractory gout populations, respectively, and $2562, $10,590, and $7188 among corresponding non-gout patients). Two additional studies, although uncontrolled, allowed for estimation of total all-cause direct costs in unselected gout populations ($11,080 and $13,170). Gout-related costs ranged from $172 to $6179, depending on population characteristics. Six studies reported positive associations of direct costs with SUA level, gout attack frequency, or presence of tophi. Four studies reported on indirect costs, which were estimated to be as high as $4341 USD. CONCLUSION: The available data suggest that gout patients incur substantially greater direct and indirect costs as compared with gout-free individuals among elderly and treatment-refractory gouty patients, whereas the costs are considerably less among younger, employed gouty patients. Further, direct costs increased with worsening disease characteristics.

12 Review The genetic basis of gout. 2014

Merriman, Tony R / Choi, Hyon K / Dalbeth, Nicola. ·Department of Biochemistry, University of Otago, Dunedin 9012, New Zealand. Electronic address: tony.merriman@otago.ac.nz. · Section of Rheumatology and Clinical Epidemiology Unit, Boston University School of Medicine, Boston, MA 02118, USA. · Department of Medicine, University of Auckland, Auckland 1023, New Zealand. ·Rheum Dis Clin North Am · Pubmed #24703347.

ABSTRACT: Gout results from deposition of monosodium urate (MSU) crystals. Elevated serum urate concentrations (hyperuricemia) are not sufficient for the development of disease. Genome-wide association studies (GWAS) have identified 28 loci controlling serum urate levels. The largest genetic effects are seen in genes involved in the renal excretion of uric acid, with others being involved in glycolysis. Whereas much is understood about the genetic control of serum urate levels, little is known about the genetic control of inflammatory responses to MSU crystals. Extending knowledge in this area depends on recruitment of large, clinically ascertained gout sample sets suitable for GWAS.

13 Review Epidemiology of gout. 2014

Roddy, Edward / Choi, Hyon K. ·Research Institute for Primary Care and Health Sciences, Keele University, Keele, Staffordshire ST5 5BG, UK. Electronic address: e.roddy@keele.ac.uk. · Section of Rheumatology and Clinical Epidemiology Unit, Boston University School of Medicine, 650 Albany Street, Suite 200, Boston, MA 02118, USA. ·Rheum Dis Clin North Am · Pubmed #24703341.

ABSTRACT: Gout is the most prevalent inflammatory arthritis in men. The findings of several epidemiologic studies from a diverse range of countries suggest that the prevalence of gout has risen over the past few decades. Although incidence data are scarce, data from the United States suggests that the incidence of gout is also rising. Evidence from prospective epidemiologic studies has confirmed dietary factors (animal purines, alcohol, and fructose), obesity, the metabolic syndrome, hypertension, diuretic use, and chronic kidney disease as clinically relevant risk factors for hyperuricemia and gout. Low-fat dairy products, coffee, and vitamin C seem to have a protective effect.

14 Review Dual-energy computed tomography for gout diagnosis and management. 2013

Dalbeth, Nicola / Choi, Hyon K. ·Department of Medicine, University of Auckland, Auckland, New Zealand. n.dalbeth@auckland.ac.nz ·Curr Rheumatol Rep · Pubmed #23292817.

ABSTRACT: The central feature of gout is deposition of monosodium urate crystals. Dual-energy computed tomography (DECT) is a recently developed advanced imaging method that enables visualisation of urate deposits by analysis of the chemical composition of the scanned materials. This review summarises recent research describing the use of DECT in gout management. This technology may assist in both diagnosis and monitoring of the disease. Studies of patients with established disease indicate diagnostic accuracy for gout is high. Excellent inter-reader agreement has been reported for detection of urate deposits by use of DECT. Automated volume assessment software also enables rapid and reproducible measurement of urate deposits within tophi, suggesting that this modality may be useful for monitoring the disease. Although several case reports indicate DECT can be used to reveal reduction in the size of urate deposits, the sensitivity to change in response to urate-lowering therapy has not yet been systematically reported. DECT images reveal variable urate deposition within tophi of the same physical size. The ability to visualise urate deposits in tissue may provide new insights into the pathology and mechanisms of gout.

15 Review The genetics of hyperuricaemia and gout. 2012

Reginato, Anthony M / Mount, David B / Yang, Irene / Choi, Hyon K. ·Rheumatology Division, Rhode Island Hospital, The Warren Alpert Medical School of Brown University, 593 Eddy Street Street, Providence, RI 02903, USA. ·Nat Rev Rheumatol · Pubmed #22945592.

ABSTRACT: Gout is a common and very painful inflammatory arthritis caused by hyperuricaemia. This review provides an update on the genetics of hyperuricaemia and gout, including findings from genome-wide association studies. Most of the genes that associated with serum uric acid levels or gout are involved in the renal urate-transport system. For example, the urate transporter genes SLC2A9, ABCG2 and SLC22A12 modulate serum uric acid levels and gout risk. The net balance between renal urate absorption and secretion is a major determinant of serum uric acid concentration and loss-of-function mutations in SLC2A9 and SLC22A12 cause hereditary hypouricaemia due to reduced urate absorption and unopposed urate secretion. However, the variance in serum uric acid explained by genetic variants is small and their clinical utility for gout risk prediction seems limited because serum uric acid levels effectively predict gout risk. Urate-associated genes and genetically determined serum uric acid levels were largely unassociated with cardiovascular-metabolic outcomes, challenging the hypothesis of a causal role of serum uric acid in the development of cardiovascular disease. Strong pharmacogenetic associations between HLA-B*5801 alleles and severe allopurinol-hypersensitivity reactions were shown in Asian and European populations. Genetic testing for HLA-B*5801 alleles could be used to predict these potentially fatal adverse effects.

16 Review The epidemiology of uric acid and fructose. 2011

Rho, Young Hee / Zhu, Yanyan / Choi, Hyon K. ·Section of Rheumatology, Boston University School of Medicine, Boston, MA 02118, USA. ·Semin Nephrol · Pubmed #22000647.

ABSTRACT: During the past few decades, the mean serum uric acid levels and the prevalence of hyperuricemia in the general population appear to have increased. Correspondingly, the prevalence and incidence of gout have doubled. Potential reasons behind these trends include the increasing prevalence of obesity and metabolic syndrome, Western lifestyle factors, increased prevalence of medical conditions (eg, renal conditions, hypertension, and cardiovascular disorders), and use of medications that increase uric acid levels (eg, diuretics and low-dose aspirin). The substantial increase in sugar-sweetened soft drinks and associated fructose consumption also has coincided with the secular trend of hyperuricemia and gout. Recently, several large-scale epidemiologic studies have clarified a number of these long-suspected risk factors in relation with hyperuricemia and gout. Furthermore, recent studies have illuminated the substantial comorbidities of hyperuricemia and gout, particularly metabolic-cardiovascular-renal conditions. Although many prospective studies have suggested an independent association between serum uric acid levels and the future risk of cardiovascular-metabolic morbidities and mortality, only a limited number of randomized clinical trials and observational studies recently have shown that the use of allopurinol can be beneficial against these outcomes. Because these data are scarce and the effects of allopurinol might not be limited to decreasing serum uric acid levels, the potential causal role of uric acid on these outcomes remains to be clarified with further studies.

17 Review Methods of tophus assessment in clinical trials of chronic gout: a systematic literature review and pictorial reference guide. 2011

Dalbeth, Nicola / Schauer, Cameron / Macdonald, Patricia / Perez-Ruiz, Fernando / Schumacher, H Ralph / Hamburger, Steve / Choi, Hyon K / McQueen, Fiona M / Doyle, Anthony / Taylor, William J. ·Department of Medicine, Faculty of Medical and Health Sciences, University of Auckland, 85 Park Road, Grafton, Auckland, New Zealand. n.dalbeth@auckland.ac.nz ·Ann Rheum Dis · Pubmed #21216814.

ABSTRACT: OBJECTIVE: To identify methods of tophus measurement for gout studies, summarise the properties of these methods and compile a detailed pictorial reference guide to demonstrate the methods. METHODS: A systematic search strategy for methods of tophus measurement was formulated. For each method, papers were assessed by two reviewers to summarise information according to the specific components of the Outcomes Measures in Rheumatology (OMERACT) filter: feasibility, truth and discrimination. Detailed images were obtained to construct the reference guide. RESULTS: Eight methods of tophus measurement were identified: counting the total number of tophi, physical measurement using tape measure, physical measurement using Vernier callipers, digital photography, ultrasonography (US), MRI, CT and dual energy CT. Feasibility aspects of the methods are well documented. Physical measurement techniques are more feasible than advanced imaging methods, but do not allow for assessment of intra-articular tophi or for data storage and central reading. The truth aspect of the filter has been documented for many methods, particularly Vernier callipers, US, MRI and CT. Reliability of most methods has been reported as very good or excellent. Sensitivity to change has been reported for all methods except MRI and CT. CONCLUSION: A variety of methods of tophus assessment have been described for use in clinical trials of chronic gout. Physical measurement techniques (particularly the Vernier calliper method) and US measurement of tophus size appear to meet most aspects of the OMERACT filter.

18 Review Genetics of gout. 2010

Choi, Hyon K / Zhu, Yanyan / Mount, David B. ·Section of Rheumatology and the Clinical Epidemiology Unit, Boston University School of Medicine, Boston, Massachusetts 02118, USA. hchoius@bu.edu ·Curr Opin Rheumatol · Pubmed #20110790.

ABSTRACT: PURPOSE OF REVIEW: This review provides an update on recent findings with regards to the genetics of hyperuricemia and gout, including recent data from genome-wide association studies (GWAS). RECENT FINDINGS: Five GWAS around the same time reported that genetic variants of SLC2A9/GLUT9 were associated with lower serum uric acid (SUA) levels and the effects were stronger among women (e.g. SUA level difference per copy of a minor allele, -0.46 mg/dl in women vs. -0.22 mg/dl in men). One study involving four cohorts and one meta-analysis of 14 genome-wide scans found that genetic variants of ABCG2 were associated with higher SUA concentrations and these effects were stronger among men (e.g. uric acid level difference per copy of the minor allele, 0.32 mg/dl in men vs. 0.18 mg/dl in women). Limited data indicate that these associations likely translate into those with the risk of gout. Functional determination that GLUT9 and ABCG2 can transport urate at the apical border of proximal tubules implicates them as substantial players in the renal excretion of urate. Furthermore, five novel genetic loci have been reported in the meta-analysis of 14 genome-wide scans. SUMMARY: Combined with their activities as urate transporters and their strong associations with serum uric acid concentrations, GLUT9 and ABCG2 appeared to be important modulators of uric acid levels and likely of the risk of gout. Together with a growing list of environmental risk factors, these genetic data add considerably to our understanding of the pathogenesis of hyperuricemia and gout.

19 Review A prescription for lifestyle change in patients with hyperuricemia and gout. 2010

Choi, Hyon K. ·Section of Rheumatology and the Clinical Epidemiology Unit, Boston, Massachusetts 02118, USA. hchoius@bu.edu ·Curr Opin Rheumatol · Pubmed #20035225.

ABSTRACT: PURPOSE OF REVIEW: This review summarizes the recent data on lifestyle factors that influence serum uric acid levels and the risk of gout and attempts to provide holistic recommendations, considering both their impact on gout as well as on other health implications. RECENT FINDINGS: Large-scale studies have clarified a number of long-suspected relations between lifestyle factors, hyperuricemia, and gout, including purine-rich foods, dairy foods, various beverages, fructose, and vitamin C supplementation. Furthermore, recent studies have identified the substantial burden of comorbidities among patients with hyperuricemia and gout. SUMMARY: Lifestyle and dietary recommendations for gout patients should consider overall health benefits and risk, since gout is often associated with the metabolic syndrome and an increased future risk of cardiovascular disease (CVD) and mortality. Weight reduction with daily exercise and limiting intake of red meat and sugary beverages would help reduce uric acid levels, the risk of gout, insulin resistance, and comorbidities. Heavy drinking should be avoided, whereas moderate drinking, sweet fruits, and seafood intake, particularly oily fish, should be tailored to the individual, considering their anticipated health benefits against CVD. Dairy products, vegetables, nuts, legumes, fruits (less sugary ones), and whole grains are healthy choices for the comorbidities of gout and may also help prevent gout by reducing insulin resistance. Coffee and vitamin C supplementation could be considered as preventive measures as these can lower urate levels, as well as the risk of gout and some of its comorbidities.

20 Clinical Trial Effects of Febuxostat in Early Gout: A Randomized, Double-Blind, Placebo-Controlled Study. 2017

Dalbeth, Nicola / Saag, Kenneth G / Palmer, William E / Choi, Hyon K / Hunt, Barbara / MacDonald, Patricia A / Thienel, Ulrich / Gunawardhana, Lhanoo. ·University of Auckland, Auckland, New Zealand. · University of Alabama at Birmingham. · Massachusetts General Hospital, Harvard Medical School, Boston. · Takeda Development Center Americas, Deerfield, Illinois. · RRD International, Rockville, Maryland. ·Arthritis Rheumatol · Pubmed #28975718.

ABSTRACT: OBJECTIVE: To assess the effect of treatment with febuxostat versus placebo on joint damage in hyperuricemic subjects with early gout (1 or 2 gout flares). METHODS: In this double-blind, placebo-controlled study, 314 subjects with hyperuricemia (serum uric acid [UA] level of ≥7.0 mg/dl) and early gout were randomized 1:1 to receive once-daily febuxostat 40 mg (increased to 80 mg if the serum UA level was ≥6.0 mg/dl on day 14) or placebo. The primary efficacy end point was the mean change from baseline to month 24 in the modified Sharp/van der Heijde erosion score for the single affected joint. Additional efficacy end points included change from baseline to month 24 in the Rheumatoid Arthritis Magnetic Resonance Imaging Scoring (RAMRIS) scores for synovitis, erosion, and edema in the single affected joint, the incidence of gout flares, and serum UA levels. Safety was assessed throughout the study. RESULTS: Treatment with febuxostat did not lead to any notable changes in joint erosion over 2 years. In both treatment groups, the mean change from baseline to month 24 in the modified Sharp/van der Heijde erosion score for the single affected joint was minimal, with no between-group differences. However, treatment with febuxostat significantly improved the RAMRIS synovitis score at month 24 compared with placebo treatment (change from baseline -0.43 versus -0.07; P <0.001), decreased the overall incidence of gout flares (29.3% versus 41.4%; P < 0.05), and improved serum UA control (62.8% versus 5.7%; P < 0.001). No major safety concerns were reported. CONCLUSION: Urate-lowering therapy with febuxostat improved magnetic resonance imaging-determined synovitis and reduced the incidence of gout flares in subjects with early gout.

21 Clinical Trial An open-label, 6-month study of allopurinol safety in gout: The LASSO study. 2015

Becker, Michael A / Fitz-Patrick, David / Choi, Hyon K / Dalbeth, Nicola / Storgard, Chris / Cravets, Matt / Baumgartner, Scott. ·Department of Medicine, University of Chicago Medicine, MC0930, 5841 S Maryland Ave, Chicago, IL 60637. Electronic address: mbecker@medicine.bsd.uchicago.edu. · East-West Medical Research Institute, Honolulu, HI. · Harvard Medical School, Boston, MA; Gout and Crystal Arthropathy Center, Massachusetts General Hospital, Boston, MA. · Department of Medicine, University of Auckland, Auckland, New Zealand. · Clinical Research and Development, Ardea Biosciences Inc., San Diego, CA. · Medical Affairs, Ardea Biosciences, Inc., San Diego, CA, USA. · Biostatistics, Ardea Biosciences, Inc., San Diego, CA, USA. ·Semin Arthritis Rheum · Pubmed #26190562.

ABSTRACT: OBJECTIVES: Allopurinol is the most widely prescribed serum uric acid-lowering therapy (ULT) in gout. To achieve serum uric acid (sUA) concentrations associated with clinical benefit, allopurinol is serially uptitrated with sUA monitoring. Suboptimal dosing is a key contributor to poor clinical outcomes, but few data are available on the safety and efficacy of dose-titrated allopurinol, particularly at doses > 300 mg/d. The objective of this open-label study was to investigate the safety and efficacy of allopurinol under conditions where investigators were encouraged to titrate to optimal, medically appropriate doses. METHODS: Long-term Allopurinol Safety Study Evaluating Outcomes in Gout Patients (LASSO) was a large, 6-month, multicenter study of allopurinol (NCT01391325). Adults meeting American Rheumatism Association Criteria for Classification of Acute Arthritis of Primary Gout and ≥ 2 gout flares in the previous year were eligible. Investigators were encouraged (but not required) to titrate allopurinol doses to achieve target sUA < 6.0mg/dL. The primary objective was evaluation of the safety of dose-titrated allopurinol by clinical and laboratory examinations at monthly visits. Secondary objectives included sUA-lowering efficacy and gout flare frequency. RESULTS: Of 1735 patients enrolled, 1732 received ≥ 1 allopurinol doses. The maximal daily allopurinol dose during study was < 300 mg in 14.4%, 300 mg in 65.4%, and > 300 mg in 20.2% of patients; dosing duration was 115.5, 152.0, and 159.7 days, respectively. Overall, baseline demographic characteristics and comorbidity rates were similar across these three categories, but patients receiving > 300-mg maximal dose had more severe gout. Treatment-emergent adverse events possibly related to allopurinol occurred in 15.2%, 9.5%, and 11.4% of patients in the < 300-, 300-, and > 300-mg categories, respectively. Rash incidence was low (1.5%) and allopurinol hypersensitivity syndrome was not reported. No clinically meaningful changes occurred in laboratory values. sUA < 6.0mg/dL at month 6 was achieved by 35.9% of patients overall: 22.4%, 35.0%, and 48.3% in dosing categories < 300, 300, and > 300 mg, respectively. CONCLUSIONS: This large multicenter study found that the allopurinol dose-titration strategy was well tolerated, without new safety signals emerging over 6 months. However, despite encouragement to treat to target, significant proportions of patients did not achieve target sUA.

22 Article New Perspectives in Rheumatology: Implications of the Cardiovascular Safety of Febuxostat and Allopurinol in Patients With Gout and Cardiovascular Morbidities Trial and the Associated Food and Drug Administration Public Safety Alert. 2018

Choi, Hyon / Neogi, Tuhina / Stamp, Lisa / Dalbeth, Nicola / Terkeltaub, Robert. ·Massachusetts General Hospital, Boston. · Boston University School of Medicine, Boston, Massachusetts. · University of Otago, Christchurch, New Zealand. · University of Auckland, Auckland, New Zealand. · VA San Diego Healthcare System and University of California San Diego, La Jolla, California. ·Arthritis Rheumatol · Pubmed #29869840.

ABSTRACT: Recently, the US Food and Drug Administration (FDA) issued a public safety alert, responding to the results of the now-published Cardiovascular Safety of Febuxostat and Allopurinol in Patients With Gout and Cardiovascular Morbidities (CARES) trial. The CARES trial showed no significant difference between allopurinol and febuxostat in the primary composite end point of cardiovascular (CV) events in subjects with gout and established CV comorbidities at baseline. However, there was a significantly increased risk of CV and all-cause mortality with febuxostat. Urate-lowering therapy (ULT) is central to the long-term management of gout, and xanthine oxidoreductase inhibitor (XOI) therapy is the consensus first-line approach. Allopurinol is generally the first XOI used, but febuxostat is an effective XOI option, and is commonly used when allopurinol is not tolerated. These data are further relevant since CV comorbidities are common in gout. Here, we examine why the CARES trial was done, and discuss other, ongoing comparative studies of febuxostat and allopurinol whose results are awaited. We assess the strengths and limitations of the CARES trial, and appraise the robustness and biologic plausibility of the results. The CARES trial does not prove that febuxostat raises CV mortality risk, but suggests greater risk with febuxostat than allopurinol. The CARES trial results do not support first-line use of febuxostat ULT, and raise questions about febuxostat placement at various pharmacologic ULT decision tree branches. Alternatives to febuxostat that are frequently effective include allopurinol dose escalation and uricosuric therapy alone or combined with allopurinol. The FDA safety alert highlights the need for shared ULT medical decision-making with gout patients, including discussion of the CV safety of febuxostat.

23 Article How patients with gout become engaged in disease management: a constructivist grounded theory study. 2018

Howren, Alyssa / Cox, Susan M / Shojania, Kam / Rai, Sharan K / Choi, Hyon K / De Vera, Mary A. ·Faculty of Pharmaceutical Sciences, University of British Columbia, 2405 Wesbrook Mall, Vancouver, BC, V6T 1Z3, Canada. · Arthritis Research Canada, Richmond, BC, Canada. · Collaboration for Outcomes Research and Evaluation, Vancouver, BC, Canada. · University of British Columbia, School of Population & Public Health, Vancouver, BC, Canada. · Faculty of Medicine, Department of Medicine, Division of Rheumatology, University of British Columbia, Vancouver, BC, Canada. · Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA, USA. · Population Health Sciences Program, Graduate School of Arts and Sciences, Harvard University, Cambridge, MA, USA. · Division of Rheumatology, Allergy and Immunology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. · Faculty of Pharmaceutical Sciences, University of British Columbia, 2405 Wesbrook Mall, Vancouver, BC, V6T 1Z3, Canada. mdevera@mail.ubc.ca. · Arthritis Research Canada, Richmond, BC, Canada. mdevera@mail.ubc.ca. · Collaboration for Outcomes Research and Evaluation, Vancouver, BC, Canada. mdevera@mail.ubc.ca. ·Arthritis Res Ther · Pubmed #29859127.

ABSTRACT: BACKGROUND: Prior qualitative research on gout has focused primarily on barriers to disease management. Our objective was to use patients' perspectives to construct an explanatory framework to understand how patients become engaged in the management of their gout. METHODS: We recruited a sample of individuals with gout who were participating in a proof-of-concept study of an eHealth-supported collaborative care model for gout involving rheumatology, pharmacy, and dietetics. Semistructured interviews were used. We analyzed transcripts using principles of constructivist grounded theory involving initial coding, focused coding and categorizing, and theoretical coding. RESULTS: Twelve participants with gout (ten males, two females; mean age, 66.5 ± 13.3 years) were interviewed. The analysis resulted in the construction of three themes as well as a framework describing the dynamically linked themes on (1) processing the diagnosis and management of gout, (2) supporting management of gout, and (3) interfering with management of gout. In this framework, patients with gout transition between each theme in the process of becoming engaged in the management of their gout and may represent potential opportunities for healthcare intervention. CONCLUSIONS: Findings derived from this study show that becoming engaged in gout management is a dynamic process whereby patients with gout experience factors that interfere with gout management, process their disease and its management, and develop the practical and perceptual skills necessary to manage their gout. By understanding this process, healthcare providers can identify points to adapt care delivery and thereby improve health outcomes.

24 Article Statin use and mortality in gout: A general population-based cohort study. 2018

Keller, Sarah F / Rai, Sharan K / Lu, Na / Oza, Amar / Jorge, April M / Zhang, Yuqing / Choi, Hyon K. ·Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit St, Bulfinch 165, Boston, MA 02114. Electronic address: sfkeller@partners.org. · Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit St, Bulfinch 165, Boston, MA 02114. · Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, 55 Fruit St, Bulfinch 165, Boston, MA 02114; Clinical Epidemiology Unit, Boston University School of Medicine, 650 Albany Street, Suite X-200, Boston, MA 02118. ·Semin Arthritis Rheum · Pubmed #29801703.

ABSTRACT: OBJECTIVES: Gout is associated with a higher risk of cardiovascular disease and premature mortality. We examined the potential survival benefit of statin use among gout patients in the general population. METHODS: We performed an incident user cohort study with time-stratified propensity score matching using a database representative of the UK general population between January 1999 and December 2014. To account for potential confounders, we compared propensity score-matched cohorts of statin initiators and non-initiators within 1-year cohort accrual blocks. We estimated the hazard ratio (HR) for mortality using a Cox proportional hazard model and the mortality rate difference using an additive hazard model. We examined potential subgroup effects stratified by key factors, including circulatory disease history. RESULTS: Among 17,018 statin initiators, 2025 deaths occurred during the follow-up (mean = 5.0 years) with a mortality rate of 24.0/1000 person-years (PY). The number of deaths and all-cause mortality rate among matched comparators during the follow-up (mean = 4.6 years) were 2503 and 31.7/1000 PY respectively. Compared with non-initiators, statin initiators experienced a 16% lower relative risk of all-cause mortality (HR = 0.84, 95% CI: 0.79-0.89) and 7.7 (95% CI: 6.1-9.3) fewer deaths per 1000 PY. This protective association was stronger among those without prior circulatory disease (HRs = 0.65 vs. 0.85; p for interaction = 0.02). CONCLUSION: In this general population-based cohort study, statin initiation was associated with a lower risk of mortality in gout, potentially with greater benefits among those without prior circulatory disease. The proper use of statins may help to substantially improve the premature mortality in gout.

25 Article Mitochondrial genetic variation and gout in Māori and Pacific people living in Aotearoa New Zealand. 2018

Gosling, Anna L / Boocock, James / Dalbeth, Nicola / Harré Hindmarsh, Jennie / Stamp, Lisa K / Stahl, Eli A / Choi, Hyon K / Matisoo-Smith, Elizabeth A / Merriman, Tony R. ·Department of Biochemistry, University of Otago, Dunedin, New Zealand. · Department of Anatomy, University of Otago, Dunedin, New Zealand. · Department of Human Genetics, David Geffen School of Medicine, University of California, Los Angeles, California, USA. · Department of Medicine, University of Auckland, Auckland, New Zealand. · Ngāti Porou Hauora Charitable Trust, Te Puia Springs, Tairāwhiti, New Zealand. · Department of Medicine, University of Otago, Christchurch, New Zealand. · Department of Psychiatry, Mount Sinai School of Medicine, New York, New York, USA. · Section of Rheumatology and Clinical Epidemiology Unit, Boston University School of Medicine, Boston, Massachusetts, USA. ·Ann Rheum Dis · Pubmed #29247128.

ABSTRACT: OBJECTIVE: Mitochondria have an important role in the induction of the NLRP3 inflammasome response central in gout. The objective was to test whether mitochondrial genetic variation and copy number in New Zealand Māori and Pacific (Polynesian) people in Aotearoa New Zealand associate with susceptibility to gout. METHODS: 437 whole mitochondrial genomes from Māori and Pacific people (predominantly men) from Aotearoa New Zealand (327 people with gout, 110 without gout) were sequenced. Mitochondrial DNA copy number variation was determined by assessing relative read depth using data produced from whole genome sequencing (32 cases, 43 controls) and targeted resequencing of urate loci (151 cases, 222 controls). Quantitative PCR was undertaken for replication of copy number findings in an extended sample set of 1159 Māori and Pacific men and women (612 cases, 547 controls). RESULTS: There was relatively little mitochondrial genetic diversity, with around 96% of those sequenced in this study belonging to the B4a1a and derived sublineages. A B haplogroup heteroplasmy in hypervariable region I was found to associate with a higher risk of gout among the mitochondrial sequenced sample set (position 16181: OR=1.57, P CONCLUSION: Association of reduced copy number with gout in hyperuricaemia was replicated over three Polynesian sample sets. Our data are consistent with emerging research showing that mitochondria are important for the colocalisation of the NLRP3 and ASC inflammasome subunits, a process essential for the generation of interleukin-1β in gout.

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