Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2026) 118 PO34 | DOI: 10.1530/endoabs.118.PO34

1The Institute of Pediatric Endocrinology, Diabetes and Metabolism, Dana Dwek Children’s Hospital, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; 2Pediatric Endocrinology Institute, Shamir (Assaf Harofeh) Medical Center, Beer Yaakov, Israel; 3Meuchedet Health Services, Rishon LeZion, Israel; 4Institute of Endocrinology, Metabolism and Hypertension, Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel; 5Pediatric Endocrinology Unit, Meir Medical Center, Kfar-Saba, Israel; 6Pediatric Endocrinology and Diabetes Unit, Edith Wolfson Medical Center, Holon, Israel; 7Department of Endocrinology, Hadassah Medical Center, Jerusalem, Israel; 8Pediatric Endocrine and Diabetes Unit, Safra Children’s Hospital, Sheba Medical Center, Tel Hashomer, Israel; 9Endocrinology Unit, Shaare Zedek Medical Center, Jerusalem, Israel; 10Pediatric Endocrinology Unit, Ben Gurion University Medical Center, Beer Sheva, Israel; 11Pediatric Endocrinology Unit, Ruth Rappaport Children’s Hospital, Rambam Health Care Campus, Haifa, Israel; 12Endocrine Unit, Soroka Medical Center, Beer-Sheva, Israel; 13Endocrinology, Clalit Health Service South District; 14Division of Endocrinology, Diabetes and Metabolism, Sheba Medical Center, Tel-Hashomer, Israel; 15Pediatric Endocrinology and Diabetes Unit, HaEmek Medical Center, Afula, Israel; 16Children’s Endocrinology Consulting Center, Clalit Health Services, Afula, Israel; 17Institute of Endocrinology, Rabin Medical Center - Beilinson Hospital, Petach Tikva, Israel; 18Barzilai medical center; 19Clalit Migdal Hamea, Tel Aviv; 20Endocrine and diabetes institute, Shamir (Assaf Harofeh) Medical Center, Beer Yaakov, Israel; 21Pediatric Endocrinology Unit, Soroka University Medical Center, Beer Sheva, Israel22Division of Pediatric Endocrinology, Shaare Zedek Medical Center, Jerusalem, Israel; 23Pediatric Endocrinology Unit, Lady Davis Carmel Medical Center and Clalit Health Services, Haifa, Israel; 24Tel-Aviv Sourasky Medical Center, Tel-Aviv, Israel. Correspondence to: [email protected] or [email protected]


Background: Congenital adrenal hyperplasia (CAH) and adrenal insufficiency (AI) from other causes are associated with increased cardiometabolic morbidity, reduced quality of life, and higher mortality. These outcomes are partly attributed to limitations of conventional glucocorticoid (GC) replacement therapy, which fails to replicate the natural circadian rhythm of cortisol secretion. In CAH, supraphysiological GC doses are often required to suppress androgen excess, further contributing to adverse effects. Modified-release hydrocortisone (MR-HC), designed to mimic physiological cortisol secretion, has recently been shown to allow GC dose reduction in CAH and to improve fatigue and quality of life in AI. However, real-world data outside controlled research settings remain limited.

Aim: To assess changes in glucocorticoid dosing, androgen levels, and anthropometric parameters in patients with CAH and other forms of AI after transition to MR-HC therapy.

Methods: A retrospective multicenter chart review was conducted between October 2023 and January 2026. Data were extracted from electronic medical records and are presented as medians with interquartile ranges.

Results: The cohort included 97 patients (54 females): 26 with salt-wasting CAH, 14 with simple virilizing CAH, 44 with non-classic CAH, 6 with 11β-hydroxylase deficiency, and 7 with AI from other causes. Median age at diagnosis was 3.0 years [0.1–8.3], and median age at transition to MR-HC was 17.0 years [13.0–30.0]. Hydrocortisone-equivalent dose adjusted for body surface area decreased significantly after transition, from 13.4 [9.1–15.7] to 11.3 [8.8–14.1] mg/m² (P = 0.005). Friedman test analysis across multiple time points showed a progressive dose reduction following transition (P<0.001), with no difference between classic and non-classic CAH. Median androstenedione and testosterone levels (nmol/l) decreased from 10.4 [4.9–14.9] to 6.5 [1.6–10.9] and from 1.2 [0.80–1.58] to 0.8 [0.40–1.3], respectively (P<0.001 and P = 0.015). Patients with non-CAH AI reported improved energy and well-being. Fourteen patients discontinued MR-HC, mainly due to cost. No adrenal crises requiring hospitalization were reported before or after transition.

Conclusions: In this real-world multicenter cohort, transition to MR-HC was associated with reduced glucocorticoid dosing alongside improved androgen control. These findings support MR-HC as an effective, physiologically aligned therapeutic option for patients with CAH and AI.

Article tools

My recent searches

No recent searches

Authors