ESPE Abstracts (2018) 89 P-P2-031

The Relationship Between Vitamin D Status and Metabolic Abnormalities in Females with Classical Congenital Adrenal Hyperplasia: A Pilot Study

Mona Hassana, Amany Ibrahima, Marise Abdoua, Sahar Abdel Attyb & Diana Nabilc


aPediatric Department, DEMPU, Faculty of Medicine, Cairo University, Cairo, Egypt; bDepartment of Clinical and Chemical Pathology, Faculty of Medicine, Cairo University, Cairo, Egypt; cPediatric Department, Faculty of Medicine, Cairo University, Cairo, Egypt


Congenital adrenal hyperplasia (CAH) patients have a higher frequency of obesity, visceral adiposity, hyperinsulinism, insulin resistance and hyperandrogenism. There is increasing evidence that low vitamin D status is associated with impaired β-cell function, insulin resistance and impaired glucose tolerance.

Objectives: This pilot aimed to determine the status of serum 25 (OH) D levels in CAH female patients who are followed up in Diabetes Endocrine Metabolism Pediatric Unit clinic over 8 months between 2016 and 2017. We also examined the effect of vitamin D replacement therapy on glucose metabolism, insulin, and androgen levels in female CAH patients.

Methods: Sixteen girls with CAH their ages ranged from 8 to 17 years were included in the study. Six months after the administration of cholecalciferol orally in dose of 4000–6000 IU.

Results: Serum 25 (OH) D level significantly increased from 16.35±5.24 ng/ml to 30.8±10.6 (P-value=0.0001). Although Homeostatic Model Assessment Insulin Resistance (HOMA-IR) was significantly correlated to serum insulin levels and other insulin resistance and sensitivity indices before and after vitamin D therapy, no significant correlation was witnessed between HOMA-IR and Serum 25 (OH) D level, 17 hydroxy-progesterone and steroid dosage before or after therapy.

Conclusion: Girls with CAH have mostly deficient vitamin D levels. Future research using a randomized control trial with a sufficient sample size and longer duration is required to examine the effect of detected insulin resistance which may affect adrenal androgen production, decrease the therapeutic efficacy of glucocorticoids, and contribute to subsequent development of metabolic syndrome and its complications in these patients.

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