Abstract
Asp and pred (40 mg/M2/day) were found to act synergistically in producing hyperglycemia during leukemia remission induction. To explain the mechanism, glucose and insulin (μU/ml) levels during oral glucose tolerance test (OGTT) and erythrocyte insulin binding studies were performed serially during the course of therapy in an obese 8-year-old girl with Down's syndrome.
Five days of pred therapy alone resulted in hyperinsulinemia (594 μU/ml) and decreased insulin binding without OGTT deterioration. Following Asp, fasting and postprandial glucose increased to 241 and 514 mg/dl, respectively whereas insulin response was inadequate (peak < 130 μU/ml). These data suggest that the mechanism of Asp and pred induced-hyperglycemia is a combined effect of reduced insulin binding and impaired insulin production or secretion (or both).
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Burghen, G., Pui, CH., Yasuda, K. et al. 1104 DECREASED INSULIN BINDING AND PRODUCTION: PROBABLE MECHANISM FOR HYPERGLYCEMIA DUE TO THERAPY WITH PREDNISONE (PRED) AND L-ASPARAGINASE (ASP). Pediatr Res 15 (Suppl 4), 626 (1981). https://doi.org/10.1203/00006450-198104001-01130
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DOI: https://doi.org/10.1203/00006450-198104001-01130