Abstract
The first identification about gout as clinical entity was made by the Egyptians in the year 2640 b.C. (Schwartz 2006). For many centuries it was not unveil the mystery of the origin of the illness. Gout is the unique pathology that belongs to the human race. When uric acid is deposited in the articulate tissue produce an intense inflammation, basic element in the development of gout. Interesting is the evidence of ultra sonographic signs of monosodium urate crystalline articulate deposits in 25% of clinically asymptomatic hyperuricaemic subjects (more than 8mg/ dL) [1], and approximately 9% of the joints without clinical signs of flogosis [2]. Large epidemiological studies have now demonstrated that gout is an independent risk factor for incident coronary heart disease, [3-6] heart failure, [7] stroke [8] peripheral artery disease [9] and death cardiovascular [10,11]. But, several meta-analyses have concluded that hyperuricaemia is an independent risk factor for coronary heart disease [12,13] and also, for the development of hypertension [14,15]. The standard diagnostic goal remains the identification of the typical birefringence of crystals of uric acid under polarized light microscope in the synovial fluid and in the aspirated material from the tophi [16,17]. Hyperuricaemia with or without urate deposit (modern denomination of the formerly called gout) is currently one of the most frequent dysmetabolic diseases.
Highlights
The first identification about gout as clinical entity was made by the Egyptians in the year 2640 b.C. (Schwartz 2006)
Large epidemiological studies have demonstrated that gout is an independent risk factor for incident coronary heart disease, [3,4,5,6] heart failure, [7] stroke [8] peripheral artery disease [9] and death cardiovascular [10,11]
Several meta-analyses have concluded that hyperuricaemia is an independent risk factor for coronary heart disease [12,13] and for the development of hypertension [14,15]
Summary
The first identification about gout as clinical entity was made by the Egyptians in the year 2640 b.C. (Schwartz 2006). When uric acid is deposited in the articulate tissue produce an intense inflammation, basic element in the development of gout. To uric acid has been attributed a possible role of cardiovascular risk prevalently the left ventricular hypertrophy for an increase in inflammatory mediators, such as tumor necrosis factor alpha and activation, and the rennin angiotensin system, increase in interstitial fibrosis of the myocardium and producing endothelial dysfunction [20,21]. Scientific evidence has suggested the possibility of a pathophysiological correlation between the action of xanthine oxidase and the genesis of cardiovascular damage in patients with chronic hyperuricaemia with and without uric acid deposits [24,25]
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