Hepatic ATP concentrations and glycolytic enzyme activities in Reye syndrome

Abstract

these cells might have acquired leukemic morphology, and account for the change to leukemic bone marrow as noted in Patients 1 and 2, and in the patient reported by Appleyard. 4 Patient 3 might have had rapid turnover of cells such as the normal appearing ones found in the hypertrophied white pulp of his spleen, and he might have died before these cells acquired leukemic morphology. Another factor in the hyperuricemia noted in our patients might have been an increased baseline of de novo synthesis of uric acid, as occurs in primary gout. 7 The positive family history for renal stones in Patient 1, the elevated uric acid excretion in the mother and brother of Patient 3, and the family history of gout in the patient reporte d by Vining and Thompson'-' support this possibility. 8 The role of toxic substances in the pathogenesis of the hyperuricemia in Patients 1 and 3 is also a possibility. These substances might have interfered with the ability of the patients to excrete the uric acid produced by their hematologic disease, thus leading to hyperuricemic renal failure. 9 The toxic substances might also have been contributing agents in the underlying disease, especially in Patient 3, who was exposed to a combination of two potential toxins.'