Endocrine Abstracts

Introduction: The most prevalent hereditary disease of adrenal steroid production is congenital adrenal hyperplasia (CAH), which is caused by a 21-hydroxylase deficiency. With or without salt wasting, patients with the typical form of CAH exhibit androgen excess. Leptin participates in endocrine and metabolic processes in addition to controlling energy balance. This study examined BMI values for children and teens with CAH in comparison to population-based benchmarks. Current BMI SD scores were associated with potential contributing variables such glucocorticoid therapy, skeletal development, birth weight and length, and parental BMI (SDS). The effects of blood leptin levels that had been adjusted for BMI, gender, and Tanner stage were examined.

Method: 80 patients with CAH were a part of this study. All patients underwent replacement therapy and had molecular genetic studies reveal they all had classic CAH. In accordance with current recommendations, the effectiveness of therapy was assessed during follow-up visits based on the clinical presentation and laboratory measurement results. The patients were divided into groups based on their existing metabolic control, simple virilizing, and salt wasting. A commercial radioimmunoassay was used to quantify leptin levels and convert them to SDS. Standard parametric and nonparametric approaches were applied for statistical analyses.

Results: Patients with CAH ranged in chronologic age from 0.20 to 17.9 years. In the entire group, the BMI SDS ranged from 2.6 to 4.2 and was significantly higher than 0.14 subjects had a BMI SDS of 3.0, which showed high prevalence of obesity among patients with CAH than the general population. BMI SDS and chronological age showed a positive correlation. Between children using other medications, the BMI SDS did not substantially differ. Doses of hydrocortisone showed a favorable correlation with BMI SDS. Children receiving medicine did not have high relative probability of having a BMI SDS of 3.0 than those receiving hydrocortisone therapy. Children with obese parents had high relative risk of childhood obesity than children without obese parents (relative risk: 4.85). Serum leptin levels were in the range of 0.11 to 31 g/l, and were strongly linked with Tanner stage, chronologic age, and BMI SDS.

Conclusion: Children and teenagers with CAH are more likely to become obese. Elevated BMI SDS was caused by age, advanced bone age maturation, despite obesity not linked to birth weight and length, serum leptin levels, or glucocorticoid dosage.