25-hydroxyvitamin D and the initial presentation of pediatric type 1 diabetes: associations with ketoacidosis severity and beta-cell function.
Source: PubMed, NCBI / U.S. National Library of Medicine
This retrospective chart review investigated the relationship between 25-hydroxyvitamin D levels and the initial clinical and biochemical presentation of type 1 diabetes mellitus (T1DM) in children under 18 years of age, specifically: (1) presence or absence of diabetic ketoacidosis and the severity of diabetic ketoacidosis (DKA) - among those with DKA, and (2) beta-cell function. This study included 99 children with new-onset Type 1 Diabetes Mellitus (T1DM). Patients were diagnosed at our pediatric endocrinology practice at Northwell Health between June 2023 and February 2025. A diagnosis of T1DM at the time of presentation was confirmed by the presence of at least one positive diabetes-specific autoantibody, and all included patients were required to have a 25-hydroxyvitamin D level measured within two days of presentation. Data extracted from the electronic health record included demographics, 25-hydroxyvitamin D levels at diagnosis, hemoglobin A1C, measures of DKA severity (pH, bicarbonate, beta-hydroxybutyrate, and DKA severity categorization), and beta-cell function (insulin and C-peptide levels). Statistical analyses included univariate tests, Spearman correlations, and multivariable logistic regression adjusting for race, ethnicity, and insurance status. Among 99 patients (mean age 10.3 ± 4.4 years, 50.5% female), 53.5% presented in DKA. After adjusting for race, ethnicity, and insurance status, higher 25-hydroxyvitamin D levels were significantly associated
Abstract
This retrospective chart review investigated the relationship between 25-hydroxyvitamin D levels and the initial clinical and biochemical presentation of type 1 diabetes mellitus (T1DM) in children under 18 years of age, specifically: (1) presence or absence of diabetic ketoacidosis and the severity of diabetic ketoacidosis (DKA) - among those with DKA, and (2) beta-cell function. This study included 99 children with new-onset Type 1 Diabetes Mellitus (T1DM). Patients were diagnosed at our pediatric endocrinology practice at Northwell Health between June 2023 and February 2025. A diagnosis of T1DM at the time of presentation was confirmed by the presence of at least one positive diabetes-specific autoantibody, and all included patients were required to have a 25-hydroxyvitamin D level measured within two days of presentation. Data extracted from the electronic health record included demographics, 25-hydroxyvitamin D levels at diagnosis, hemoglobin A1C, measures of DKA severity (pH, bicarbonate, beta-hydroxybutyrate, and DKA severity categorization), and beta-cell function (insulin and C-peptide levels). Statistical analyses included univariate tests, Spearman correlations, and multivariable logistic regression adjusting for race, ethnicity, and insurance status. Among 99 patients (mean age 10.3 ± 4.4 years, 50.5% female), 53.5% presented in DKA. After adjusting for race, ethnicity, and insurance status, higher 25-hydroxyvitamin D levels were significantly associated with less severe acidosis, showing moderate positive correlations with pH (rho=0.44, p<0.0001) and bicarbonate (rho=0.42, p<0.0001), and a weak negative correlation with beta-hydroxybutyrate (rho=-0.28, p=0.01), indicating higher 25-hydroxyvitamin D levels were associated with less severe acidosis. There was a significant association between 25-hydroxyvitamin D levels and presentation in DKA; each one-unit increase in 25-hydroxyvitamin D was associated with a 6% decrease in the odds of presenting in DKA (OR: 0.94, 95% CI: 0.89-0.99, p=0.03). 25-hydroxyvitamin D levels were significantly associated with DKA severity (p=0.01), with lower levels observed in patients with more severe DKA. No significant association was found between 25-hydroxyvitamin D levels and HbA1c or markers of beta-cell function. These findings suggest a potential protective role of 25-hydroxyvitamin D against severe metabolic decompensation at T1DM onset, specifically relating to DKA, but not beta-cell function. Further research is needed to confirm these findings and explore the potential mechanisms and clinical implications.