Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists · 2025
Glucocorticoid-Induced Positive Feedback in Cushing Disease: Insights From a Spanish Multicenter Cohort.
СтатьяМногоцентровое исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Biagetti Betina, Cardona-Arias Andres, Soto-Moreno Alfonso, Ollero García María Dolores, Moure Rodríguez María Dolores, Gonzalez-Fernandez Laura, Castro Ana, Guerrero-Pérez Fernando, Iglesias Pedro, Camara Rosa, Paja Miguel, Lázaro Victoria Alcázar, Simo-Servat Andreu, Lozano-Aida Claudia, Echarri Ana Irigaray, Valero Lucía Manzano, Villar-Taibo Rocío, Bernabéu Ignacio, Fajardo-Montañana Carmen, Aulinas Anna, García-Centeno Rogelio, Hanzu Felicia, Araujo-Castro Marta, Neuroendocrinology Task Force of Spanish Society of Endocrinology
Аннотация
OBJECTIVE: Cushing disease (CD) is characterized by impaired glucocorticoid negative feedback. In rare cases, patients exhibit glucocorticoid-induced positive feedback (GIPF), which may represent a distinct corticotroph adenoma phenotype. We aimed to investigate the prevalence, clinical and biochemical features, and surgical outcomes of GIPF in a large multicenter cohort.
METHODS: A retrospective cohort study from the SPAIN-CUSHING registry. We included 139 patients with CD who had a complete overnight 1-mg dexamethasone suppression test. GIPF was defined as higher serum cortisol after dexamethasone compared with baseline. Clinical, biochemical, and radiological characteristics, as well as surgical outcomes, were compared between groups. Recurrence was evaluated in patients undergoing transsphenoidal surgery, with recurrence-free survival assessed by Kaplan-Meier analysis.
RESULTS: Thirteen patients (9.3%) showed GIPF. These patients had lower body mass index (26.4 vs 29.8 kg/m2, P = .032), higher urinary free cortisol expressed as the upper limit of normal ratio (4.7 vs 2.8 upper limit of normal, P = .047), and a markedly greater adrenocorticotropin response to desmopressin (525.0 vs 63.1 pg/mL, P = .022). Tumor size, proportion of macroadenomas, and cavernous sinus invasion did not differ. Despite this, after surgery remission was significantly lower in GIPF (28.6% vs 70.2%, P = .036), and Kaplan-Meier analysis showed reduced recurrence-free survival in GIPF patients (log-rank P = .04). Clinical phenotypes and comorbidities were otherwise similar.
CONCLUSION: GIPF occurs in up to 9% of patients with CD and is associated with poorer surgical outcomes and lower remission rates. This phenotype likely represents a distinct subtype of corticotroph adenoma, highlighting the need for closer follow-up and molecular characterization.
METHODS: A retrospective cohort study from the SPAIN-CUSHING registry. We included 139 patients with CD who had a complete overnight 1-mg dexamethasone suppression test. GIPF was defined as higher serum cortisol after dexamethasone compared with baseline. Clinical, biochemical, and radiological characteristics, as well as surgical outcomes, were compared between groups. Recurrence was evaluated in patients undergoing transsphenoidal surgery, with recurrence-free survival assessed by Kaplan-Meier analysis.
RESULTS: Thirteen patients (9.3%) showed GIPF. These patients had lower body mass index (26.4 vs 29.8 kg/m2, P = .032), higher urinary free cortisol expressed as the upper limit of normal ratio (4.7 vs 2.8 upper limit of normal, P = .047), and a markedly greater adrenocorticotropin response to desmopressin (525.0 vs 63.1 pg/mL, P = .022). Tumor size, proportion of macroadenomas, and cavernous sinus invasion did not differ. Despite this, after surgery remission was significantly lower in GIPF (28.6% vs 70.2%, P = .036), and Kaplan-Meier analysis showed reduced recurrence-free survival in GIPF patients (log-rank P = .04). Clinical phenotypes and comorbidities were otherwise similar.
CONCLUSION: GIPF occurs in up to 9% of patients with CD and is associated with poorer surgical outcomes and lower remission rates. This phenotype likely represents a distinct subtype of corticotroph adenoma, highlighting the need for closer follow-up and molecular characterization.