Hyperuricemia in Acute Illness: a Poor Prognostic Sign JAMES 0. WOOLLISCROFT. M.D. HARRY COLFER, M.D. IRVING H. FOX, M.D. Ann Arbor, Michigan From the Human Purine Research Center, De- partment of Internal Medicine and Biological Chemistry, University of Michigan, Ann Arbor, Michigan. This work was supported by USPttS gant AM19874 and 5MOl RR42. Fte@nt requests should be adckessed to Dr. James 0. WooIlisaoft. Department of Internal Medicine, 5101 Bouth Ambulatory Care Bldg., Box 54. Ann Arbor, Michigan 48109. Manuscript accepted August 3 1, 1981. To clarify the role of the serum urate level and Its change as a po- tential marker for severe tlssue hypoxia, we have measured serum urate levels and urine uric acid excretion In 16 patients with acute cardiovascular disease. The six patlents who dled had a basellne mean serum urate level of 11.1 mg/dl (range, 6.6 to 15.5 mg/dl) and reached a peak mean value of 20.7 mg/dl (range, 13.6 to 33.0 mg/dl). Five of these patients had flndlngs to suggest Increased productlon of uric acid, In addition to decreased excretion of uric acid from Impaired renal function. The 10 survivors had a baseline mean serum urate level of 6.6 mg/dl (range, 1.3 to 14.0 mg/dl) and a maxlmal mean peak value of 7.1 mg/dl (range, 3.9 to 14.0 mg/dl). There was no con&tent evidence for Increased productlon or de- creased excretion of urk a&l. Patients who died had a lower systolic blood pressure, arterial pH and plasma bicarbonate level and a higher heart rate and serum creatlnlne level compared with the patients who survlved. The observations suggest that marked hy- peruricemla at the height of an Illness may predict a fatal outcome. T&sue hypoxia may ccmt&ute to #ds sequence of events by leading to the depletlon of adenoslne trlphosphate (ATP) and activation of purlne nucleotlde degradation to uric acid. Alterations of the serum urate concentration may provide a clue to pathophysiologic mechanisms in systemic disease. Increased urate production, decreased urate excretion or both may result in hyper- uricemia. Since uric acid is the final product of purine nucleotide degradation, an increased concentration of uric acid could result from the accelerated breakdown of tissue nucleotides (Figure 1). Therefore, disorders associated with tissue hypoxia may be accompanied by hyperuricemia from the activation of tissue nucleotide degradation [l-4]. To clarify the role of the serum urate concentration and its changes as a potential marker for severe episodes of tissue hypoxia, we have measured serum urate concentrations and urine uric acid excretion in acutely ill patients. Our study shows that marked increases in serum urate concentration do occur during acute illness and that patients with these changes have a poor prognosis. METHODS Sixteen patients were selected from all patients admitted to the coronary care unit or scheduled for surgery during a three-month period. Patients studied were in Killip class IV, had severe failure due to cardiomyopathy or were scheduled for high risk cardiovascular surgery (Table I). Thirteen patients were male; three were female. All patients were treated in the intensive care units of the University of Michigan Medical Center during the study period. 58 January 1982 The Am&can Journal of Medlclne Volume 72