title: Patients with gout can be cured in primary care.
abstract: Gout affects 2.5% of the total UK population and is four times more common in men than women. The peak prevalence and incidence in the UK is in those aged 80-84 years. Gout is associated with comorbidities such as nephrolithiasis, chronic renal impairment, metabolic syndrome, depression and heart disease. It is also associated with increased mortality. Untreated gout can result in disabling irreversible peripheral joint damage and chronic usage-related pain. However, gout is curable. The pathogenic agents that cause gout i.e.urate crystals can be eliminated through a combination of effective patient education and evidence-based, targeted urate-lowering therapy. Gout is caused by the precipitation of monosodium urate crystals in and around a joint. The crystals preferentially form in peripheral, cooler joints and especially in those with osteoarthritis. It is thought that some of these preformed crystals within articular cartilage spill over into the joint space and trigger an acute attack of inflammation. Uric acid is predominantly renally excreted and the common heritable component of gout results from relative inefficiency of urate excretion. Chronic kidney disease, metabolic syndrome and drugs that reduce renal function (e.g. thiazide diuretics, beta-blockers and ACE inhibitors) will all lead to reduced elimination. Patients with chronic gout can present with monoarthritis but more commonly present with asymmetrical polyarthritis or tophi. Joints affected by osteoarthritis are preferentially targeted, the most common sites of involvement are feet, knees, hands and elbows. Diagnosis can be confirmed in primary care by taking a good history and clinical examination. An acute peripheral monoarthritis which reaches its peak within 24 hours and causes 'the worst pain ever experienced' is characteristic of an acute attack. A patient may have co-existing risk factors for gout such as osteoarthritis, obesity, hypertension, renal impairment, diuretic and antihypertensive drug use or increased beer or spirit consumption. A raised serum uric acid can confirm the diagnosis, however, this can be normal in the acute phase. Radiographs are rarely helpful but joint ultrasound may demonstrate deposits in cartilage, the synovium and peri-articular sites.
authors.affiliation: Department of Academic Rheumatology, University of Nottingham, UK.
authors.forename: Frances
authors.initials: F
authors.lastname: Rees
authors.forename: Michael
authors.initials: M
authors.lastname: Doherty
mesh_terms: D000369:Aged, 80 and over; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use*; D001175:Arthrography / Q000379:methods; D003078:Colchicine / Q000627:therapeutic use*; D019468:Disease Management; D016903:Drug Monitoring; D004359:Drug Therapy, Combination; D005260:Female; D006073:Gout / Q000150:complications / Q000175:diagnosis / Q000188:drug therapy / Q000453:epidemiology / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D016916:Joint Deformities, Acquired / Q000209:etiology / Q000517:prevention & control; D008297:Male; D011320:Primary Health Care / Q000379:methods; D012307:Risk Factors; D055502:Secondary Prevention; D006113:United Kingdom / Q000453:epidemiology; D014527:Uric Acid / Q000097:blood*; D014528:Uricosuric Agents / Q000627:therapeutic use*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D014528:Uricosuric Agents; D014527:Uric Acid; D003078:Colchicine