Hypopituitarism after acute brain injury |
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Affiliation: | 1. Gubra, Hørsholm, Denmark;2. Department of Human Nutrition, University of Copenhagen, Frederiksberg, Denmark;3. Department of Biomedical Sciences, School of Veterinary Medicine, Cornell University, Ithaca, NY, USA;4. Department of Molecular Biosciences, University of California, Davis, CA, USA;5. Department of Surgery, Chungnam National University Hospital, Daejeon, Korea |
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Abstract: | Acute brain injury has many causes, but the most common is trauma. There are 1.5–2.0 million traumatic brain injuries (TBI) in the United States yearly, with an associated cost exceeding $10 billion. TBI is the most common cause of death and disability in young adults less than 35 years of age. The consequences of TBI can be severe, including disability in motor function, speech, cognition, and psychosocial and emotional skills. Recently, clinical studies have documented the occurrence of pituitary dysfunction after TBI and another cause of acute brain injury, subarachnoid hemorrhage (SAH). These studies have consistently demonstrated a 30–40% occurrence of pituitary dysfunction involving at least one anterior pituitary hormone following a moderate to severe TBI or SAH. Growth hormone (GH) deficiency is the most common pituitary hormone disorder, occurring in approximately 20% of patients when multiple tests of GH deficiency are used. Within 7–21 days of acute brain injury, adrenal insufficiency is the primary concern. Pituitary function can fluctuate over the first year after TBI, but it is well established by 1 year. Studies are ongoing to assess the effects of hormone replacement on motor function and cognition in TBI patients. Any subject with a moderate to severe acute brain injury should be screened for pituitary dysfunction. |
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