Review and Hypothesis about Gout by Carlos Alberto Paterno Marchioli* in Advancements in Cardiovascular Research (ACR) in Lupine Publishers
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].
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