The relationship between neonatal hypoglycaemia and cord blood C‐peptide levels in neonates of birthing individuals with type 1 diabetes

Abstract

AbstractIntroductionNeonates of individuals with type 1 diabetes (T1D) are at increased risk of neonatal hypoglycaemia. It is hypothesised that this is a result of birthing‐individual hyperglycaemia and subsequent foetal hyperinsulinemia.AimsTo test for association between clinically significant neonatal hypoglycaemia (requiring intravenous glucose treatment) and cord‐blood c‐peptide (CBCP) concentrations in birthing‐individuals with T1D.Materials and MethodsThis is a prospective cohort study of individuals with T1D followed at a single tertiary centre. Clinical variables and glucose control during pregnancy were recorded. Cord‐blood was collected and CBCP concentrations determined. The correlation between clinically significant neonatal hypoglycaemia and CBCP concentrations was determined.ResultsFifty‐four pregnant individuals and their newborns were included in the study. Individuals to neonates who experienced hypoglycaemia had longer diabetes duration (19 vs. 13 years, respectively, p = 0.023), higher HbA1c at conception (7.3 [6.3–8.8] vs. 6.5 [6.0–7.0], respectively, p = 0.042) and higher rates of caesarian section (73.3% vs. 28.2%, respectively, p = 0.005) than individuals to those who did not. CBCP levels were significantly higher in neonates with clinically significant neonatal hypoglycaemia as compared to those who did not experience hypoglycaemia (3.3 mcg/L vs. 1.9 mcg/L, respectively, p = 0.002). After adjustment for possible confounders, every 1 unit higher in CBCP level was associated with a 1.46 (1.02–2.09, p = 0.035)—fold greater risk for neonatal hypoglycaemia. No significant differences were observed in either birthing individual complications or glucose control indices during pregnancy between the two groups.ConclusionsIn neonates of individuals with T1D, higher CBCP levels are an independent risk factor for clinically significant neonatal hypoglycaemia.