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25-hydroxyvitamin D and the initial presentation of pediatric type 1 diabetes: associations with ketoacidosis
Sofya Ilmer1, Rubab Sohail2, Sharon Hyman1
1Division of Pediatric Endocrinology and Diabetes, Cohen Children's Medical Center at Northwell Health, New Hyde Park, NY, United States.
Insights
Higher vitamin D levels in children with new-onset type 1 diabetes mellitus (T1DM) were linked to less severe diabetic ketoacidosis (DKA) at diagnosis. Vitamin D may offer protection against severe metabolic complications during T1DM onset.
Area of Science:
- Pediatric Endocrinology
- Metabolic Disorders
- Nutritional Science
Background:
- Type 1 Diabetes Mellitus (T1DM) is an autoimmune disease affecting children.
- Diabetic ketoacidosis (DKA) is a severe complication at T1DM onset.
- The role of vitamin D in T1DM presentation is under investigation.
Purpose of the Study:
- To investigate the association between 25-hydroxyvitamin D levels and the initial presentation of T1DM in children.
- To examine the relationship with diabetic ketoacidosis (DKA) presence, severity, and beta-cell function.
Main Methods:
- Retrospective chart review of 99 children with new-onset T1DM.
- Collected data on 25-hydroxyvitamin D, DKA severity markers, HbA1c, and beta-cell function.
- Statistical analyses included correlations and multivariable logistic regression.
Main Results:
- Higher 25-hydroxyvitamin D levels correlated with less severe acidosis (pH, bicarbonate, beta-hydroxybutyrate).
- Increased 25-hydroxyvitamin D was associated with reduced odds of presenting in DKA (OR: 0.94, p=0.03).
- No significant association found between 25-hydroxyvitamin D and HbA1c or beta-cell function.
Conclusions:
- 25-hydroxyvitamin D may have a protective role against severe metabolic decompensation (DKA) at T1DM onset.
- Vitamin D status does not appear to influence beta-cell function at diagnosis.
- Further research is needed to confirm these findings and explore mechanisms.
Introduction:
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.
Methods:
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.
Results:
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.
Discussion:
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.
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