Hyperuricemia and gout

A small minority (30 percent) of liver allograft recipients develop elevated uric acid levels. Only 10 percent of this special group will develop clinical evidence of gout such as joint pain. The cause of this problem appears to be a dose-dependent effect of cyclosporine. Cyclosporine appears to reduce uric acid excretion in the distal tubules of the kidney producing this syndrome. Slow reduction in the dosage of cyclosporine may improve hyperuricemia. In resistant cases or in patients who actually develop symptoms of gout, allopurinol administration is usually recommended. Caution should be used in administering azathioprine and allopurinol. These drugs work synergistically to produce severe bone marrow depression, and therefore severe episodes of overimmunosuppression and subsequent severe overwhelming sepsis may occur without careful monitoring of the white blood cell count.