DOI: 10.1159/hrp/adaag020.289 ISSN: 1663-2818

P-231: Recurrent neonatal hyperglycemia in trisomy 21: a feeding-dependent pattern expanding the clinical spectrum of glucose dysregulation

J Maldonado, A Pecchio, M Cunha, T Santiago, M J Schneider, M Bonfim

Abstract

Introduction

Neonatal hyperglycemia in trisomy 21 is poorly characterized, with scarce reports in the literature. Recurrent insulin-requiring episodes unrelated to parenteral nutrition represent a distinct and underrecognized entity in this population.

Objectives

To report a rare case of recurrent neonatal hyperglycemia in a preterm infant with trisomy 21, emphasizing the diagnostic challenge and the role of enteral nutritional modulation as the primary determinant of glycemic behavior.

Methods

Case report of a male infant, 32+5 weeks, 1630g, with trisomy 21, presenting recurrent hyperglycemia (>200 mg/dL) within the first 24 hours of life. Workup included anti-insulin and anti-GAD antibodies, C-peptide, fructosamine, total proteins, and urinary carbohydrate chromatography. Glycemic patterns were analyzed in relation to glucose infusion rate (GIR), enteral feeding velocity, caloric density, and insulin requirements. Parenteral nutrition was not used.

Results

Peak glucose was 288 mg/dL. All metabolic and immunological markers were normal, excluding autoimmune diabetes, inborn errors of metabolism, and neonatal diabetes. Hyperglycemia improved consistently with reduction of GIR and enteral feeding rate, and recurred with increased caloric density or feeding velocity. Insulin infusion was started at 0.01 UI/kg/h, adjusted to 0.014 UI/kg/h, used only during hyperglycemic episodes. No hypoglycemia occurred. Over two months of follow-up, glycemic episodes maintained a consistent and exclusive association with enteral nutritional intake.

Conclusions

This case expands the clinical spectrum of neonatal hyperglycemia in trisomy 21, revealing a feeding-dependent pattern without identifiable metabolic etiology. Sustained over two months, this behavior suggests impaired postprandial glucose regulation intrinsic to trisomy 21. Early recognition is essential to guide safe nutritional advancement alongside glycemic control in this population.

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