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Endocrine changes after pediatric traumatic brain injury

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Abstract

Traumatic brain injury (TBI) is a very common occurrence in childhood, and can lead to devastating long term consequences. Recent research has focused on the potential endocrine consequences of TBI in adults. The research in children is less robust. This paper reviews current literature regarding TBI and possible hypothalamic and pituitary deficiencies in childhood. Acute endocrine changes are commonly found after TBI in pediatric patients, which can include changes in hypothalamic–pituitary–adrenal axis and antidiuretic hormone production and release. In the long term, both temporary and permanent alterations in pituitary function have been found. About 30% of children have hypopituitarism up to 5 years after injury. Growth hormone deficiency and disturbances in puberty are the most common, but children can also experience ACTH deficiency, diabetes insipidus, central hypothyroidism, and elevated prolactin. Every hormonal axis can be affected after TBI in children, although growth hormone deficiency and alterations in puberty are the most common. Because transient and permanent hypopituitarism is common after TBI, survivors should be screened serially for possible endocrine disturbances. These children should undergo routine surveillance at least 1 year after injury to ensure early detection of deficiencies in hormonal production in order to permit normal growth and development.

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Acknowledgments

This review would not have been possible without the diligent efforts of our colleagues Anne-Marie Kaulfers, Samantha Blum, Tammy Weis, Linda Michaud, and Kathi Makoroff.

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  1. Cincinnati Children’s Hospital Medical Center, University of Cincinnati, 3333 Burnet Avenue, MLC 7012, Cincinnati, OH, 45229, USA

    Susan R. Rose & Bethany A. Auble

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  1. Susan R. Rose
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  2. Bethany A. Auble
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Correspondence to Susan R. Rose.

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Rose, S.R., Auble, B.A. Endocrine changes after pediatric traumatic brain injury. Pituitary 15, 267–275 (2012). https://doi.org/10.1007/s11102-011-0360-x

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