ReviewGout: Joints and beyond, epidemiology, clinical features, treatment and co-morbidities
Introduction
Gout is a common inflammatory arthritis associated with important co-morbidities including cardiovascular disease, chronic kidney disease, obesity and type 2 diabetes. Gout is caused by an inflammatory reaction to urate crystals in joints. It is the commonest inflammatory arthritis in men and after the menopause is a common cause of inflammatory arthritis in women [1]. However, while historically gout has been viewed purely as a disease first manifesting as arthritis it is increasingly being recognised as a urate overload disease, often associated with extensive co-morbidities and with inflammatory arthritis being a manifestation of later stage disease [2]. A recent proposal to introduce disease stages is shown in Table 1. Gout has a significant impact on the working age population and impacts on work presenteeism, productivity and physical function [3], [4], [5]. Gout is growing in prevalence in developed countries and in addition is poorly recognised and treated [6], [7], [8], [9]. This manuscript aims to review the epidemiology of gout, its treatments and highlight its important co-morbidities.
Section snippets
Clinical features and impact of gout
The first attack (or ‘flare’) of gout commonly, although not universally, occurs in the first metatarsophalangeal joint and is referred to as ‘podagra’. Some individuals may only have one to two attacks of gout, or have extremely intermittent attacks months apart, but the majority will suffer from increasingly frequent attacks. Subsequent attacks commonly involve additional joints such as the knee and as gout progresses it can cause polyarticular attacks and tophus development, although tophi
Epidemiology of gout
Fundamentally gout is a urate overload disease, historically the mechanism of overload was divided into over production or under excretion [2]. Recently, the intestinal excretion of urate by the transporter ABCG2 has been identified as very important [11]. This has led to the proposal of new classification system for hyperuricaemia, see Table 2.
Clinical gouty arthritis is strongly linked to the level of serum urate, with increasing levels of hyperuricaemia leading to a progressively increasing
Treatment overview
Treatment of gout falls into two main categories: symptomatic relief during an acute episode of gout and urate lowering therapy (ULT) for long-term prevention of further flares. Integral to treatment is adequate prophylaxis of acute gout flares during ULT therapy. Historically ULT and the concomitant prevention of flares during ULT has often been managed sub-optimally.
Co-morbidities
Gout often occurs in the presence of other conditions, such as hypertension, renal impairment, diabetes mellitus and cardiovascular disease. Hyperuricaemia may actually be an independent risk factor for some of these conditions [66]. Likewise, some of these conditions and their associated treatments can influence SUA levels. In this sense gout truly is about ‘more than joints’ and can having wide-ranging health implications.
Conclusions
There is a growing body research into the causes, mechanisms and treatment of gout and this has, in part, been stimulated by the new therapeutics in development. There is, however, much further to learn. While there are readily available cheap therapies they are not being prescribed adequately, and even when they are not being taken as prescribed. This is undoubtedly multi-factorial, including, but not limited to, problems with disease education, literacy and numeracy and cross-cultural
Contributors
P.R. and S.H. contributed equally to the manuscript intellectual content, drafting, and approving the final draft of the manuscript.
Competing interest
Disclosure: P.R. has undertaken consulting for AstraZeneca Australia. S.H. has no disclosures.
Funding
S.H. has received no funding for this article. P.R. is funded by the National Health and Medical Research Council of Australia (NHMRC) grant no. GNT1017662.
Provenance and peer review
Commissioned and externally peer reviewed.
Acknowledgements
The authors would like to thank Nicola Dalbeth for her comments on a draft of this manuscript. P.R. is funded by the National Health and Medical Research Council of Australia (NHMRC).
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