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Endocrine Abstracts (2025) 110 P93 | DOI: 10.1530/endoabs.110.P93

ECEESPE2025 Poster Presentations Adrenal and Cardiovascular Endocrinology (169 abstracts)

Assessment of adrenal function after glucocorticoid therapy for childhood onset first episode nephrotic syndrome

Palak Garg 1 , Anju Seth 1 , Abhijeet Saha 1 , Preeti Singh 1 & Ritu Singh 2


1Kalawati Saran Children Hospital, Lady Hardinge Medical College, Paediatrics, New Delhi, India; 2Lady Hardinge Medical College, Biochemistry, New Delhi, India


JOINT2103

Background: Adrenal insufficiency (AI) is a significant concern in children having prolonged glucocorticoid therapy for childhood onset first-episode nephrotic syndrome. As AI results in impaired cortisol response during stressful conditions, which can lead to life-threatening adrenal crisis if stress dose of corticosteroid is not administered on time. Therefore, this highlights the need for regular monitoring of adrenal function after discontinuing steroid therapy.

Objectives: 1. To assess the proportion of children having adrenal insufficiency within 5 days after discontinuing steroid therapy for first episode nephrotic syndrome and again after 6–8 weeks.

2. To assess features of steroid toxicity at both time points.

Methods: This study included 40 children with first-episode nephrotic syndrome who received standard corticosteroid therapy as per ISPN guidelines. Adrenal function was assessed within 5 days and again at 6–8 weeks after discontinuing steroids by measuring 0800 h basal and 1-hour post ACTH stimulation serum cortisol levels (obtained after 25 IU I/M injection of Acton Prolongatum). Basal serum cortisol < 3 μg/dL were considered low and suggestive of adrenal insufficiency. Confirmed adrenal insufficiency was defined as post-stimulation serum cortisol <18 μg/dL. Steroid toxicity features were also assessed at both time points.

Results: Mean basal and post-stimulated cortisol levels increased significantly from first to second assessment (P<0.001 for both) indicating progressive adrenal recovery with time after discontinuing steroid therapy. Low basal cortisol was present in 42.5% cases at first and 2.5% cases at second assessment. Adrenal insufficiency was present in 52.5% within 5 days of stopping steroids which decreased to 27.5% at 6–8 weeks. Steroid toxicity at first assessment included moon face (97.5%), buffalo hump (25%), hirsutism (42.5%), pre-hypertension (25%) and hypertension (12.5%) which was reduced to 72.5%, 10%, 22.5%, 7.5%, and 5% respectively by the second assessment. Impaired fasting sugar was seen in 17.5% at first and 12.5% at second assessment. No children were overweight, obese, diabetic or showed clinical symptoms of adrenal insufficiency during study period. Hypertension and impaired blood sugar were significantly associated with adrenal insufficiency at the first assessment, but not at the second.

Conclusion: Over half of the children had adrenal insufficiency soon after stopping steroids, with more than a quarter still affected at 6–8 weeks. This highlights the need for regular adrenal function monitoring post-steroid therapy to prevent adrenal crisis and optimize the use of stress-dose steroids. The study also demonstrates the reversible nature of steroid-related side effects after treatment cessation.

Volume 110

Joint Congress of the European Society for Paediatric Endocrinology (ESPE) and the European Society of Endocrinology (ESE) 2025: Connecting Endocrinology Across the Life Course

European Society of Endocrinology 
European Society for Paediatric Endocrinology 

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