Gout is one of the most prevalent rheumatic diseases, its prevalence is estimated at 1-2%. Gout is an inflammatory arthritic condition occurring when monosodium urate crystals deposit on the articular cartilage of joints, on tendons, and in the surrounding tissues. Urate is the end product of purine metabolism and is physiologically present in body fluids. Crystals of urate precipitate when serum urate level exceeds the saturation point (hyperuricaemia), which may be due to increased production or ineffi cient renal excretion of uric acid.
There is epidemiological evidence that the prevalence of gout has increased in Western countries during the past few deacdes. For instance, in the UK, the prevalence of gout rose from 2.6 per 1000 patients in 1975 to 1.9 cases per 1000 in 1999. The prevalence increases wih age, and men are more frequently affected than women. The changing epidemiology is probably related to changes in the prevalence of risk factors for developing hyperuricaemia, which include exessive alcohol consumption, a protein-rich diet, obesity, diuretic therapy, and impaired renal function.
Recent findings confirm previous suggestions that gout may have some genetic basis. A frequent cause of hyperuricaemia, which may have a genetic component, is primary impared renal clearence of uric acid. Approximately 90% of urate filtered by the kidneys is reabsorbed, and this process is mediated by specific transporters, which are genetically encoded. The most important transporter, urate transporter-1(URAT1), is encoded by the SLC22A12 gene, and mutations of this gene, inducing overactivity of URAT1, have been linked to primary gout. Despite the evidence demonstrating the importance of genetic factors in the development of gout, much is yet to be elucidated, in particular, the interaction between genetic predisposition and enviromental triggers. Gout diagnosis is based on EULAR (European League Against Rheumatism) evidence based recommendations.
To a affirm the diagnosis of gout, it is necessary to exclude other conditions that mimic gout. A diagnosis can be assumed when a patient presents with a typical history of recurrent sudden attacks of monoarticular, painful arthritis, particulary at the MTP joint, but a definitive diagnosis of gout is made by detection of uric acid crystals in a sample of joint fluid or tophi aspirates. Imaging techniques are useful to evaluate the extent of crystal deposition and associated structural joint damage, and to monitor the response to urate lowering therapy. Plain radiographs can show joint changes only in patients with advanced or chronic gout, but ultrasound, CT and MRT are more sensitive and can detect tophi and other features, which may be missed with conventional imaging.
EULAR 2006 and ACR 2012 (American College of Rheumatology) evidence based treatment recommendations for gout divide treatment options in two directions. Acute flare treatment is aimed at relieving intense pain and reducing inflammation, and non-steroidal anti-inflammatory drugs at the highest approved doses are the most frequently used agents. Urate lowerning therapy is necessary in order to maintain serum uric acid level below the saturation point for monosodium urate. The nonpharmacological measures include moderation of the intake of animal proteins, alcohol (beer and spirits), and losing weight, if appropriate. Currently approved urate-lowering drugs for gout include xanthine oxidase inhibitors (allopurinol, febuxostat), uricosuric agents(probenetcid, benzbromarone) and uricolytic agents (pegloticase). Urate lowering therapy should be prescribed for long term.