Clinical correlation of Purine’s metabolism

Hyperuricemia is observed in excessful formation of uric acid, disbalance of elimination of urates and their intake; decrease of urate binding protein (the concentration of them is more than 0.42mM/L). There are primary, secondary and physiological hyperuricemia. Physiological hyperuricemia is developed in uptake of large amount of tomatoes, meat, tea etc.

Primary hyperuricemia is observed in increase of formation of urates or decrease of their elimination. In this case gout (podagra) is developed. Gout is a heterogenic group of derangements of purine’s metabolism in which hyperuricemia, arthritis, deposition of urates in tissues and urolithiasis may be observed. But not all persons with hyperuricemia gout is developed. 85% of persons with hyperuricemia gout isn’t developed. Urates are easy precipitated at temprerature low than +37C, e.g. +32C is temperature of knee joint; +29C temperature of ankle joint; 1-st tarsal-phalanx joint is coldest joint. This joint is often affected in gout (in 80% of cases of gout).

Secondary hyperuricemia is observed in intake of some medicines or in leukemia, Addison’s anemia.

Uric acid increases the mental functions. 40% of geniuses have hyperuricemia. Uric acid and urates carry out antioxidant function instead of ascorbic acid which isn’t synthesized in the body.

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Jaundices – species, reasons, mechanism, laboratory appearances	\|	Biochemistry of liver

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