Comparison of uricase-bound and uricase-loaded erythrocytes as bioreactors for uric acid degradation.

Uric acid is a normal end product of purine catabolism that when it increases in blood over normal values (hyperuricemia) can contribute to a group of diseases characteristic of gout.1 Hyperuricemia can arise by several mechanisms including increased uric acid production or reduced excretion by the kidney. Several approaches have been employed to reduce serum urate levels such as dietary means, promotion of uric acid excretion, administration of uricase and inhibitors of the enzymes responsible for its synthesis.