Review and Hypothesis about Gout

Volume 1 - Issue 1

Carlos Alberto Paterno Marchioli*

Received: February 21, 2018;   Published: February 27, 2018

DOI: 10.32474/ACR.2018.01.000103

Full Text PDF

To view the Full Article   Peer-reviewed Article PDF

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. [18,19].

Introduction| Uric Acid| Plasma Proteins| Personal Experience| Conclusion| References|