![]() The mean cholesterol level of long-term survivors of 177 mg/dL was significantly higher than the norm ( P =. Cholesterol levels were elevated (<200 mg/dL) in 20% of the patients after asparaginase, which may be due to continued treatment with corticosteroids. Changes in cholesterol, in contrast, were not temporally related to asparaginase treatment. These data show a striking temporal association between asparaginase therapy and hypertriglyceridemia. Triglyceride levels for survivors did not differ from the normal range or postasparaginase levels in the newly diagnosed patients. After asparaginase therapy, triglyceride levels (mean, 73 mg/dL ) were significantly lower than levels obtained during asparaginase therapy. LDL reciprocally decreased with increased VLDL during asparaginase therapy. Apolipoprotein B 100 levels increased during asparaginase therapy, although the mechanism of this remains unclear. ![]() Lipoprotein lipase activity was consistently above normative values for all levels of triglyceride and could not be explained by obesity or hyperglycemia. Nuclear magnetic resonance analysis of lipid subclasses showed a significant increase in the smaller, denser forms of very low density lipoprotein (VLDL) and negligible chylomicron fraction in a subset of patients with marked triglyceride elevation. In contrast, 4 of the 13 patients without triglyceride elevation developed pancreatitis 3 of the 4 patients had fasting studies at the height of their abdominal pain. None of the 7 patients with triglyceride levels greater than 1,000 mg/dL developed pancreatitis. The incidence of hypertriglyceridemia did not vary by type of asparaginase or risk status of ALL (defined by white blood cell count and age). Sixty-seven percent of the newly diagnosed patients had fasting triglyceride levels greater than 200 mg/dL during asparaginase therapy 15 patients (42%) had levels greater than 400 mg/dL, 7 with levels greater than 1,000 mg/dL. ![]() 003) than the level of 108 mg/dL (SD 46) before the initiation of asparaginase therapy. The mean peak triglyceride level during asparaginase of 465 mg/dL (standard deviation 492) was significantly higher ( P =. We also evaluated a second population of 30 long-term survivors of childhood ALL a fasting lipid and lipoprotein profile was obtained once at study entry. To further elucidate the incidence and potential mechanism of asparaginase-associated lipid abnormalities in children with acute lymphoblastic leukemia (ALL), we serially obtained fasting lipid and lipoprotein studies on 38 of the 43 consecutively diagnosed children with ALL before, during, and after asparaginase therapy. ![]()
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