The British Society for Rheumatology Guideline for the Management of Gout

Abstract

Gout is the most common cause of inflammatory arthritis worldwide. In UK general practice, the overall prevalence has increased from 1.4% in 1999 to 2.49% in 2012 [1], despite the availability of effective and potentially curative urate-lowering drugs for >50 years and evidence-based British and European management guidelines for nearly a decade [2, 3]. NICE has accredited the process used by the BSR to produce its guidance for the management of gout. Accreditation is valid for 5 years from 10 June 2013. More information on accreditation can be viewed at www.nice.org.uk/accreditation. For full details on our accreditation visit: www.nice.org.uk/accreditation. Clinical manifestations of gout resulting from monosodium urate crystal deposition include tophi, chronic arthritis, urolithiasis and renal disease as well as recurrent acute arthritis, bursitis and cellulitis. Gouty arthritis and tophi are associated with chronic disability, impairment of health-related quality of life [4–7], increased use of healthcare resources and reduced productivity [8]. Gout is also frequently associated with co-morbidities such as obesity, dyslipidaemia, diabetes mellitus, chronic renal insufficiency, hypertension, cardiovascular disease, hypothyroidism, anaemia, psoriasis, chronic pulmonary diseases, depression and OA [1] as well as with an increase in all-cause mortality (adjusted hazard ratio 1.13, 95% CI: 1.08, 1.18) and urogenital malignancy [1, 9]. Sustained hyperuricaemia is the single most important risk factor for the development of gout. Hyperuricaemia occurs secondarily to reduced fractional clearance of uric acid in > 90% of patients with gout [10]. Age, male gender, menopausal status in females, impairment of renal function, hypertension and the co-morbidities that comprise the metabolic syndrome are all risk factors for incident gout associated with decreased excretion of uric acid, as are the use of diuretic and many anti-hypertensive drugs, ciclosporin, low-dose aspirin, alcohol consumption and lead exposure. Tophi and chronic arthritis [11], alcohol consumption [12] and recent use of diuretic drugs [13] are important risk factors for recurring flares. Genome-wide association studies have identified a number of genes coding for urate anion transporters expressed in the proximal renal tubular epithelium, but these account for <5% of the variation in serum urate [14]. Serum urate levels are influenced by dietary intake and synthesis as well as by renal excretion. Diets high in red meat or seafood, and increased consumption of beer, spirits and fructose- or sugar-sweetened soft drinks are established risk factors for developing gout [15–17]. Single gene disorders associated with urate overproduction, hyperuricaemia and accelerated purine synthesis de novo (such as glycogen storage diseases and Lesch–Nyhan syndrome) are very rare causes of primary gout. Diseases (such as lympho- and myeloproliferative disorders and severe exfoliative psoriasis) and drugs (such as cytotoxics, vitamin B12 and ethanol) associated with increased cellular turnover and destruction can lead to secondary hyperuricaemia and gout [18]. The identification of monosodium urate crystals in joint and tissue samples remains the gold standard for the diagnosis of gout. Although identification of urate deposits by dual-energy CT [19] and US [20] are being used increasingly as an aid to the diagnosis of gout in research and hospital practice, joint aspiration or imaging to confirm crystal presence is rarely undertaken in primary care settings where the majority of patients with gout are managed. For diagnosis in clinical practice, clinical scores, without imaging or synovial fluid analysis, have been proposed [21] that include consideration of the patient’s history and co-morbidities. The British Society for Rheumatology/British Health Professionals in Rheumatology (BSR/BHPR) guideline for the management of gout was published in 2007 [2]. There are four broad reasons why a revised and updated guideline is now required. First, new pharmaceutical treatment have and the for the and of drugs has the prevalence and of gout have increased [1] despite the availability of effective and potentially curative research studies and have that of patients with gout in general urate-lowering and that many patients with gout being with in primary [1, and secondary care of serum uric acid levels to the in the or as has that the of information to patients with gout is and studies have to a of and to effective care are that that these can be and with of information and a of care on guideline published guidelines include the 2012 for the of Gout and the evidence-based for the diagnosis and management of gout by a of in the and guidelines include the US for and guidelines for of Gout and of Gout and the and and for the diagnosis and management of gout that from the for the management of gout published in guideline to revised and for the management of gout in the The guidel