Key result
Combined medical therapy normalizes severe hypertriglyceridemia to ~88 mg/dL in pediatric DKA.
Why the study?
Severe hypertriglyceridemia (triglycerides >2000 mg/dL) is rare in pediatric patients with diabetic ketoacidosis and markedly increases the risk of acute pancreatitis, presenting unique management challenges.
Does intravenous insulin infusion combined with oral fenofibrate, rosuvastatin, and omega-3 fatty acids normalize severe hypertriglyceridemia and dyslipidemia in a pediatric patient with new-onset type 1 diabetes mellitus and diabetic ketoacidosis?
Case Report (n=1)
No
Does intravenous insulin infusion combined with oral fenofibrate, rosuvastatin, and omega-3 fatty acids normalize severe hypertriglyceridemia and dyslipidemia in a pediatric patient with new-onset type 1 diabetes mellitus and diabetic ketoacidosis?
In pediatric diabetic ketoacidosis complicated by severe hypertriglyceridemia, reducing intravenous insulin after acidosis resolution can trigger a rebound surge in triglycerides, which can be effectively managed by readjusting the insulin infusion rate and adding oral fenofibrate, rosuvastatin, and omega-3 fatty acids.
May support insulin titration plus adjunctive agents for severe hypertriglyceridemia in pediatric DKA; leaves open need for controlled trials.
Diabetic ketoacidosis (DKA) is a life-threatening complication of type 1 diabetes mellitus (T1DM). Although mild hypertriglyceridemia (HTG) is common in DKA, severe HTG (triglycerides >2000 mg/dL) is rare in pediatric patients and markedly increases the risk of acute pancreatitis (AP). This report describes a unique case of new-onset T1DM presenting with DKA and extreme dyslipidemia, highlighting management challenges. An 11-year-old girl presented with fatigue, dehydration, and Kussmaul breathing. Laboratory tests confirmed DKA (pH 7.01, blood glucose 490 mg/dL) and showed a severely lipemic blood sample. Initial management included fluid resuscitation and an intravenous insulin infusion. Although DKA resolved within 48 hours, triglyceride (TG) levels surged from 1271 to 3967 mg/dL on the fourth day after reducing the intravenous insulin infusion rate from 0.1 to 0.05 IU/kg/h, accompanied by mild abdominal pain. AP was ruled out by ultrasound, and enzyme levels were normal. Management required readjusting the insulin infusion rate and initiating oral lipid-lowering agents (fenofibrate, rosuvastatin, and omega-3). TG levels normalized within 20 days, though low-density lipoprotein (LDL) remained elevated, consistent with the beta shift phenomenon. A significant family history of hyperlipidemia suggested a genetic predisposition. Severe HTG is a critical complication of pediatric DKA that requires prompt recognition and treatment. Intravenous insulin remains the primary treatment, but clinicians must monitor for rebound lipid levels after acidosis resolves. Oral lipid-lowering therapies are effective adjuncts, especially when plasmapheresis is unavailable. This case emphasizes the need for individualized management and long-term lipid monitoring in pediatric T1DM.
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Alfaqaih et al. (2026) conducted a case report in New-onset Type 1 Diabetes Mellitus presenting with Diabetic Ketoacidosis and Severe Dyslipidemia (n=1). Intravenous insulin infusion, fluid resuscitation, fenofibrate, rosuvastatin, and omega-3 fatty acids was evaluated on Normalization of serum triglyceride and lipid levels. Adjusted intravenous insulin and oral fenofibrate, rosuvastatin, and omega-3 normalized severe hypertriglyceridemia from 3967 to 87.6 mg/dL within 20 days in a child with diabetic ketoacidosis.
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