# Severe Hypertriglyceridemia-Induced Pancreatitis Presenting With Diabetic Ketoacidosis in a Pediatric Patient

## TL;DR

A 12-year-old girl with severe high triglycerides and new-onset diabetes developed pancreatitis and diabetic ketoacidosis, highlighting the importance of recognizing this rare condition in children.

## Contribution

This case highlights the rare but critical overlap of severe hypertriglyceridemia-induced pancreatitis and diabetic ketoacidosis in a pediatric patient with newly diagnosed type 1 diabetes.

## Key findings

- A 12-year-old female presented with severe hypertriglyceridemia-induced pancreatitis and diabetic ketoacidosis at the onset of type 1 diabetes.
- Aggressive treatment with insulin and fluid resuscitation led to recovery of pancreatitis, renal function, and normalization of triglyceride levels.
- Long-term management with insulin and lipid-lowering therapy successfully controlled diabetes and lipid levels for two years post-diagnosis.

## Abstract

Hypertriglyceridemia (HTG) is a recognized cause of acute pancreatitis (AP) in adults, but it remains an uncommon etiology in pediatric patients, particularly when occurring concurrently with new-onset diabetes mellitus (DM) and diabetic ketoacidosis (DKA). We present the case of a previously healthy 12-year-old female who developed severe hypertriglyceridemia-induced acute pancreatitis with simultaneous DKA at initial presentation of type 1 diabetes. The patient arrived at the emergency department with acute epigastric pain, emesis, diarrhea, and severe dehydration. Physical examination revealed xanthelasma and xanthomas, while laboratory testing showed markedly lipemic serum with triglycerides of 15,630 mg/dL, cholesterol of 561 mg/dL, and HbA1c of 10.4%. She was admitted to the pediatric intensive care unit for management of DKA, multiorgan dysfunction, and pancreatitis. Treatment included aggressive intravenous fluid resuscitation, electrolyte correction, and continuous insulin infusion followed by transition to subcutaneous insulin. Over nine days, her triglyceride levels normalized, pancreatitis resolved, and renal function recovered. She was discharged on a diabetic diet, insulin regimen, and lipid-lowering therapy with olezarsen for familial hypertriglyceridemia. Two years post-diagnosis, her diabetes and lipid levels remain well controlled.

This case underscores the diagnostic challenge of acute pancreatitis in pediatric DKA, where overlapping abdominal symptoms may obscure the underlying etiology. The lipemic appearance of blood samples can serve as an important bedside clue to severe hypertriglyceridemia. Recognition of this association is critical, as prompt insulin therapy can simultaneously address both DKA and triglyceride reduction. Clinicians should maintain a high index of suspicion for HTG-induced pancreatitis in children presenting with DKA, particularly when serum appears lipemic, and should investigate for underlying familial dyslipidemia. Early identification and comprehensive management, encompassing fluid and electrolyte balance, metabolic stabilization, and long-term lipid control, are key to preventing recurrence and reducing morbidity in this rare but serious presentation.