Abstract

Uric acid (UA) is converted from xanthine, the degradation product of purine nucleotides, by the enzyme xanthine oxidase (XO). Because hyperuricemia can be induced not only by inflammatory risk factors but is also associated with the generation of new acute and chronic inflammation, therefore, elevation of uric acid in blood (hyperuricemia) is considered as a sensitive marker of underlying inflammation taking place at various site of the body. In addition, anti-inflammatory medications have been shown to reduce the level of serum uric acid. As expected, hyperuricemia are detectable in almost all inflammatory diseases. It should be noted that hyperuricemia is not a risk factor but rather a risk marker signaling the presence of risk for the development of severe clinical complications. It is because that most damages found with hyperuricemia are not caused directly by UA but by superoxide free radical produced at the same time with UA by the enzyme XO. It should also be noted that serum UA has been found to be only a weak predictor of cardiovascular disease in general asymptomatic population but a significant independent predictor among subjects who are at high risk.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.