Uric acid represents the end-product of purine metabolism in humans and the great
apes where it has played some evolutive roles over the time [
[1]
]. The production of uric acid is largely regulated by xanthine oxidoreductase (XOR)
that is converting hypoxanthine to uric acid and is partially responsible for the
increase in the serum levels of urate and its possible biological and pathological
effects [
[1]
]. Historically the increase in serum urate has been linked to some dietary habits
(e.g. alcohol, red meat, seafood, etc.) that however explain only a minor proportion
of the variance in serum uric acid levels when compared with inherited genetic variants
[
[2]
]. More importantly, uric acid is also synthesized in the liver, intestines, muscle,
and vascular endothelium and this endogenous production could be more strictly related
to the effects of increased serum urate beyond its crystal precipitation at the level
of joints, soft tissue, kidneys, and other organs [
[3]
]. Accumulating evidence has demonstrated the role of increased serum urate as a possible
etiologic mechanism in the pathogenesis of cardiovascular, metabolic, and renal diseases
[
4
,
5
,
6
]. In particular, the presence of hyperuricemia above the levels of 5.5 mg/dL has been
reported as a risk factors for hypertension, atrial fibrillation (AF), chronic kidney
disease (CKD), heart failure (HF), coronary artery disease (CAD), and cardiovascular
death [
[4]
,
[5]
]. In addition, elevated levels of serum uric acid have been reported to increase
the relative risk of diabetes and metabolic syndrome acting though an interference
with insulin sensitivity that has been reported as significantly reduced in presence
of increased serum urate before the development of hyperglycemia and correlated risk
factors [
[7]
]. This observations and many others in the same direction have supported the idea
that uric acid per se or the mechanism of its production can be involved in the progressive
reduction in tissue insulin sensitivity that may explain the progression toward metabolic
abnormalities, increased blood pressure and atherogenic dyslipidemia that can largely
contribute to the excess in the risk of cardiovascular disease observed in patients
with elevated serum urate levels.To read this article in full you will need to make a payment
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Article info
Publication history
Published online: July 20, 2022
Accepted:
July 6,
2022
Received:
June 29,
2022
Identification
Copyright
© 2022 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.
