To the Editor: Glycemic variability is a common finding in NICU. Hyperglycemia is globally encountered with an incidence rate of 20–80% in the NICU’s, with preterms being at the highest risk [1, 2]. Neonatologists often use critical blood glucose value of 180 mg/dl (10 mmol/L) to define significant hyperglycemia necessitating treatment. We report an intriguing case of severe acute hyperglycemia over the range of 1000 mg/dl (55 mmol/L) as early as 2 h of life in a growth restricted 35 wk male preterm neonate weighing 1187 g (<3rd centile). He was product of a non-consanguineous marriage, delivered to a multigravida mother with bad obstetric history and no previous live issue. Iatrogenic causes, early onset sepsis and stress related hyperglycemia was ruled out. In contrast to Dr. Hay’s experience of certainly every severe hyperglycemia being a result of error [2], no iatrogenic cause related to the dextrose infusate was found in this case. Blood work was significant for elevated insulin levels (18 uIU/ml), positive urinary glucose, and elevated Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) index of 42.6, indicating insulin resistance (IR). Hyperglycemia responded to high dose insulin infusion, early introduction of parenteral amino acids and limiting the glucose infusion rate below 4 mg/kg/min. HOMA-IR, mathematically calculated as serum glucose concentration (mg/dl) x serum insulin concentration (mIU/ml)/405, is a robust indirect tool for the surrogate assessment of IR [3]. Repeat serum insulin after 48 h was 5.9 uIU/ml, and HOMA-IR reduced to 0.99. HOMA-IR value of more than 2.5 is suggestive of IR even in neonates, encountered particularly in growth restricted neonates [4]. It has negative correlation with gestational age and birth weight. Pro insulin levels and genetic testing could not be done due to financial constraints. The infant was discharged home after adequate weight gain over 4 wk.