The influence of tumor location on the onset of endocrine deficits in pediatric brain tumor survivors.
Giorgio Attinà, Alberto Romano, Palma Maurizi, Tommaso Verdolotti, Stefano Mastrangelo, Antonio Ruggiero
Abstract
Open AccessBackground: Pediatric central nervous system (CNS) tumors are the second most common malignancy in children and are associated with significant long-term morbidity despite advancements in therapy. Endocrine dysfunction is one of the most frequent and impactful late sequelae, requiring timely detection and management. This study aimed to investigate the timing and risk factors associated with endocrine dysfunction in pediatric brain tumor survivors and to propose optimized follow-up protocols. Methods: A cohort of 33 pediatric patients with brain tumors, excluding craniopharyngiomas, pituitary adenomas, and germ cell tumors, treated at the Pediatric Oncology Unit of Fondazione Policlinico Universitario "Agostino Gemelli" IRCCS in Rome (2005-2015), was retrospectively analyzed. Endocrine dysfunction was assessed through clinical and laboratory evaluations, with a median follow-up of 114.1 months. Results: Endocrine dysfunction was identified in a high percentage of patients, with hypothyroidism and panhypopituitarism being the most common. Age at diagnosis and treatment influenced the appearance and the timing of dysfunction. Hypothalamic and suprasellar tumors were associated with early onset, while tumors in posterior cranial fossa exhibited delayed onset. Conclusions: Tumor location and patient age are critical determinants of the timing of endocrine dysfunction in pediatric brain tumor survivors. We propose a stratified follow-up based on tumor location, with immediate evaluation for hypothalamic and supratentorial tumors and periodic assessments for other regions. These tailored recommendations aim to ensure timely detection and management of endocrine complications, improving outcomes and quality of life. Future research with larger cohorts is needed to validate and refine these findings.