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Gout: joints and beyond, epidemiology, clinical features, treatment and co-morbidities.
Maturitas. 2014 Aug; 78(4):245-51.M

Abstract

Gout is a common inflammatory arthritis precipitated by an inflammatory reaction to urate crystals in the joint. Gout is increasingly being recognised as a disease primarily of urate overload with arthritis being a consequence of this pathological accumulation. It is associated with a number of important co-morbidities including chronic kidney disease, obesity, diabetes and cardiovascular disease. The prevalence of gout is increasing around the world. Significant progress has been made in determining the genetic basis for both gout and hyperuricaemia. Environmental risk factors for gout have been identified as certain foods, alcohol and several medications. There is, however, little evidence that changing these environmental risks improves gout on an individual level. Treatment of gout encompasses two strategies: firstly treatment of inflammatory arthritis with non-steroidal anti-inflammatories, corticosteroids, colchicine or interleukin-1 inhibitors. The second and most important strategy is urate lowering, to a target of 0.36 mmol/L (6 mg/dL) or potentially lower in those with tophi (collections of crystalline urate subcutaneously). Along with urate lowering, adequate and prolonged gout flare prophylaxis is required to prevent the precipitation of acute attacks. Newer urate lowering agents are in development and have the potential to significantly expand the potential treatment options. Education of patients regarding the importance of life long urate lowering therapy and prophylaxis of acute attacks is critical to treatment success as adherence with medication is low in chronic diseases in general but especially in gout.

Authors+Show Affiliations

University of Queensland Diamantina Institute, Princess Alexandra Hospital, Brisbane, Australia; Department of Rheumatology, Gold Coast University Hospital, Gold Coast, Australia. Electronic address: philip.c.robinson@gmail.com.Department of Preventive and Social Medicine, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

24880206

Citation

Robinson, Philip C., and Simon Horsburgh. "Gout: Joints and Beyond, Epidemiology, Clinical Features, Treatment and Co-morbidities." Maturitas, vol. 78, no. 4, 2014, pp. 245-51.
Robinson PC, Horsburgh S. Gout: joints and beyond, epidemiology, clinical features, treatment and co-morbidities. Maturitas. 2014;78(4):245-51.
Robinson, P. C., & Horsburgh, S. (2014). Gout: joints and beyond, epidemiology, clinical features, treatment and co-morbidities. Maturitas, 78(4), 245-51. https://doi.org/10.1016/j.maturitas.2014.05.001
Robinson PC, Horsburgh S. Gout: Joints and Beyond, Epidemiology, Clinical Features, Treatment and Co-morbidities. Maturitas. 2014;78(4):245-51. PubMed PMID: 24880206.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Gout: joints and beyond, epidemiology, clinical features, treatment and co-morbidities. AU - Robinson,Philip C, AU - Horsburgh,Simon, Y1 - 2014/05/14/ PY - 2014/04/28/received PY - 2014/05/01/accepted PY - 2014/6/2/entrez PY - 2014/6/2/pubmed PY - 2015/3/31/medline KW - Chronic kidney disease KW - Diabetes mellitus KW - Diet KW - Gout KW - Hypertension KW - Urate SP - 245 EP - 51 JF - Maturitas JO - Maturitas VL - 78 IS - 4 N2 - Gout is a common inflammatory arthritis precipitated by an inflammatory reaction to urate crystals in the joint. Gout is increasingly being recognised as a disease primarily of urate overload with arthritis being a consequence of this pathological accumulation. It is associated with a number of important co-morbidities including chronic kidney disease, obesity, diabetes and cardiovascular disease. The prevalence of gout is increasing around the world. Significant progress has been made in determining the genetic basis for both gout and hyperuricaemia. Environmental risk factors for gout have been identified as certain foods, alcohol and several medications. There is, however, little evidence that changing these environmental risks improves gout on an individual level. Treatment of gout encompasses two strategies: firstly treatment of inflammatory arthritis with non-steroidal anti-inflammatories, corticosteroids, colchicine or interleukin-1 inhibitors. The second and most important strategy is urate lowering, to a target of 0.36 mmol/L (6 mg/dL) or potentially lower in those with tophi (collections of crystalline urate subcutaneously). Along with urate lowering, adequate and prolonged gout flare prophylaxis is required to prevent the precipitation of acute attacks. Newer urate lowering agents are in development and have the potential to significantly expand the potential treatment options. Education of patients regarding the importance of life long urate lowering therapy and prophylaxis of acute attacks is critical to treatment success as adherence with medication is low in chronic diseases in general but especially in gout. SN - 1873-4111 UR - https://www.unboundmedicine.com/medline/citation/24880206/Gout:_joints_and_beyond_epidemiology_clinical_features_treatment_and_co_morbidities_ DB - PRIME DP - Unbound Medicine ER -