Gout is a common progressive crystal arthropathy caused by deposition of monosodium urate crystals in tissues, which results in a painful and difficult-to-treat chronic gouty arthritis. The prevalence of gout and hyperuricaemia is increasing and treatment is suboptimal for many patients due to inappropriate dosing of urate-lowering drugs, intolerance to therapy, or poor patient compliance. Our increased understanding of the pathophysiology, genetics and biology of gout and hyperuricaemia have led to identification of risk factors for this disease, as well as to improved ways of controlling urate levels and to the development of new therapeutic approaches, such as agents that target the NALP3 inflammasome and IL-1. This Collection of articles covers recent developments in this field, with the aim of informing rheumatologists with regards to the prevention and management of this common inflammatory crystal arthritis.
Image of urate crystals courtesy of Dr. Anne-Kathrin Tausche from the Department of Rheumatology, University Clinic Carl Gustav Carus, Technical University of Dresden, Germany.
REVIEWS
Optimizing current treatment of gout
Frances Rees, Michelle Hui & Michael Doherty
doi:10.1038/nrrheum.2014.32
Nature Reviews Rheumatology advance online publication, Published online 11 March 2014
Despite the availability of effective treatments, the clinical management of gout is frequently suboptimal, leading to continued acute attacks and the risk of irreversible joint damage in many patients. In this article, the authors review the available treatments and barriers to successful management, and discuss how gout could be 'cured' by improving the current standard of care, with individualized management plans incorporating patient education, application of recommended best practice and shared decision-making.
Targeting inflammasomes in rheumatic diseases
Alexander So, Annette Ives, Leo A. B. Joosten & Nathalie Busso
doi:10.1038/nrrheum.2013.61
Nature Reviews Rheumatology 9, 391-399 (2013)
As molecular complexes that promote inflammation, inflammasomes have been implicated in several autoimmune and autoinflammatory disorders, including cryopyrin-associated periodic syndromes and microcrystal-induced pathologies. Here, the authors discuss the roles of inflammasomes in these conditions, as well as their potential involvement in other rheumatic diseases, and consider therapeutic approaches to inhibit inflammasome activity.
Uric acid as a danger signal in gout and its comorbidities
Kenneth L. Rock, Hiroshi Kataoka & Jiann-Jyh Lai
doi:10.1038/nrrheum.2012.143
Nature Reviews Rheumatology 9, 13-23 (2013)
Uric acid not only triggers inflammation in gout in its crystallized form, monosodium urate, but is also associated with comorbidities of the disease. New insights into the role of uric acid as a danger signal for both adaptive and innate immune responses could help to explain the pathogenesis of gout and point to potential new avenues of therapy for this and other sterile inflammatory diseases.
The genetics of hyperuricaemia and gout
Anthony M. Reginato, David B. Mount, Irene Yang & Hyon K. Choi
doi:10.1038/nrrheum.2012.144
Nature Reviews Rheumatology 8, 610-621 (2012)
In this update on the genetics of hyperuricaemia and gout, the authors describe the associations between common genetic variants, serum uric acid levels and gout as well as the role of these genetic variants in gout pathogenesis. Pharmacogenetic associations between HLA-B*5801 and severe allopurinol-hypersensitivity reactions and the potential causal role of urate in cardiovascular disease are also discussed.
Mechanisms of joint damage in gout: evidence from cellular and imaging studies
Fiona M. McQueen, Ashika Chhana & Nicola Dalbeth
doi:10.1038/nrrheum.2011.207
Nature Reviews Rheumatology 8, 173-181 (2012)
Advances in the fields of cell biology and imaging have allowed researchers to dig deeper into the underlying mechanisms of joint damage in patients with tophaceous gout. This Review describes some of the recent advances in our understanding of bone erosion and cartilage damage in this disease.
NEWS & VIEWS
Crystal arthritis: Environment and genetics in gout: a maze for clinicians?
Fernando Perez-Ruiz & Ana María Herrero-Beites
doi:10.1038/nrrheum.2013.173
Nature Reviews Rheumatology 10, 8-9 (2014)
Gout: Multinational gout guidelines: how do we move beyond 'déjà vu'?
Robert Terkeltaub
doi:10.1038/nrrheum.2013.142
Nature Reviews Rheumatology 9, 567-569 (2013)
Crystal arthritis: Is HLAB genotyping the future of gout pharmacogenomics?
Jasvinder A. Singh
doi:10.1038/nrrheum.2013.20
Nature Reviews Rheumatology 9, 200-202 (2013)
Crystal arthritis: New ACR guidelines for gout management hold some surprises
Thomas Bardin & Pascal Richette
doi:10.1038/nrrheum.2012.216
Nature Reviews Rheumatology 9, 9-11 (2013)
Crystal arthritis: A new 'package of care' strategy for effective gout management
Nicola Dalbeth
doi:10.1038/nrrheum.2012.129
Nature Reviews Rheumatology 8, 507-508 (2012)
YEAR IN REVIEW
Gout in 2013: Imaging, genetics and therapy: gout research continues apace
Fiona M. McQueen
doi:10.1038/nrrheum.2013.164
Nature Reviews Rheumatology 10, 67-69 (2014)
RESEARCH HIGHLIGHTS
Diagnosis: Dual-energy CT and ultrasound compared for gouty arthritis
doi:10.1038/nrrheum.2013.172
Nature Reviews Rheumatology 9, 696 (2013)
Crystal arthritis: Attacks of gout more frequent in hospitalized patients
doi:10.1038/nrrheum.2013.155
Nature Reviews Rheumatology 9, 636 (2013)
Crystal arthritis: Intensive urate-lowering therapy improves structural joint damage in patients with tophaceous gout
Jenny Buckland
doi:10.1038/nrrheum.2013.120
Nature Reviews Rheumatology 9, 506 (2013)
Therapy: Efficacy of rilonacept in preventing gout flare during ULT
doi:10.1038/nrrheum.2013.51
Nature Reviews Rheumatology 9, 259 (2013)
Genetics: Metabolic pathways newly implicated in gout epidemiology
Emma Leah
doi:10.1038/nrrheum.2013.1
Nature Reviews Rheumatology 9, 64 (2013)
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