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Tumor location and radiotherapy, respectively, predict the speed of onset and density of long-term neuroendocrinopathy following pediatric glioma, report Dr. Hoong-Wei Gan and coauthors at University College London Institute of Child Health.
In a longitudinal study of 166 children with a median age of 4.9 years at diagnosis, progression-free status and endocrine event–free survival (EEFS) were 47.2% and 20.8%, respectively, despite high overall survival of 81%.
Growth hormone deficiency was the most common disorder (40.3%), followed by central precocious puberty (26%), gonadotropin (20.4%), thyroid-stimulating hormone (13.3%), and adrenocorticotropic hormone (13.3%) deficiencies. Hypothalamic involvement was associated with earlier onset of dysfunction (P < .001), whereas radiotherapy predicted density (P < .001), Dr. Gan and colleagues reported.
The reduction in EEFS is “concerning given the lack of a corresponding improvement in survival,” the authors said.
“Minimizing future endocrine, visual, and cognitive morbidity remains an important therapeutic goal in managing these tumors,” they added. “Optimal treatment strategy for these benign lesions remains elusive; while the absence of longitudinal neuroendocrine morbidity data limits our understanding of their etiology and evolution.”
Read the full report at J Clin Endocrinol Metab. 2015 Jul 28. doi: 10.1210/jc.2015-2028.
Tumor location and radiotherapy, respectively, predict the speed of onset and density of long-term neuroendocrinopathy following pediatric glioma, report Dr. Hoong-Wei Gan and coauthors at University College London Institute of Child Health.
In a longitudinal study of 166 children with a median age of 4.9 years at diagnosis, progression-free status and endocrine event–free survival (EEFS) were 47.2% and 20.8%, respectively, despite high overall survival of 81%.
Growth hormone deficiency was the most common disorder (40.3%), followed by central precocious puberty (26%), gonadotropin (20.4%), thyroid-stimulating hormone (13.3%), and adrenocorticotropic hormone (13.3%) deficiencies. Hypothalamic involvement was associated with earlier onset of dysfunction (P < .001), whereas radiotherapy predicted density (P < .001), Dr. Gan and colleagues reported.
The reduction in EEFS is “concerning given the lack of a corresponding improvement in survival,” the authors said.
“Minimizing future endocrine, visual, and cognitive morbidity remains an important therapeutic goal in managing these tumors,” they added. “Optimal treatment strategy for these benign lesions remains elusive; while the absence of longitudinal neuroendocrine morbidity data limits our understanding of their etiology and evolution.”
Read the full report at J Clin Endocrinol Metab. 2015 Jul 28. doi: 10.1210/jc.2015-2028.
Tumor location and radiotherapy, respectively, predict the speed of onset and density of long-term neuroendocrinopathy following pediatric glioma, report Dr. Hoong-Wei Gan and coauthors at University College London Institute of Child Health.
In a longitudinal study of 166 children with a median age of 4.9 years at diagnosis, progression-free status and endocrine event–free survival (EEFS) were 47.2% and 20.8%, respectively, despite high overall survival of 81%.
Growth hormone deficiency was the most common disorder (40.3%), followed by central precocious puberty (26%), gonadotropin (20.4%), thyroid-stimulating hormone (13.3%), and adrenocorticotropic hormone (13.3%) deficiencies. Hypothalamic involvement was associated with earlier onset of dysfunction (P < .001), whereas radiotherapy predicted density (P < .001), Dr. Gan and colleagues reported.
The reduction in EEFS is “concerning given the lack of a corresponding improvement in survival,” the authors said.
“Minimizing future endocrine, visual, and cognitive morbidity remains an important therapeutic goal in managing these tumors,” they added. “Optimal treatment strategy for these benign lesions remains elusive; while the absence of longitudinal neuroendocrine morbidity data limits our understanding of their etiology and evolution.”
Read the full report at J Clin Endocrinol Metab. 2015 Jul 28. doi: 10.1210/jc.2015-2028.
