Document Detail


Neuroendocrine function following traumatic brain injury and subsequent intensive care treatment: a prospective longitudinal evaluation.
MedLine Citation:
PMID:  19459759     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Neuroendocrine dysfunction following traumatic brain injury (TBI) has been described extensively. However, few studies are longitudinal and most lack subtle radiological, clinical, and repetitive endocrine assessment in the acute phase. Accordingly, we prospectively assessed neuroendocrine function in 71 patients after TBI. Injury was documented by a computed tomography (CT). During the first week, critical clinical data (Glasgow Coma Score, APACHE score), treatment variables such as duration of analgosedation for mechanical ventilation, were related to basal pituitary function. More than 2 years later, a subgroup of patients was re-evaluated using dynamic testing with ACTH and GHRH-arginine tests. The Pearson's correlation analysis and Mann-Whitney rank sum test for group differences were used for statistical analysis. None of the CT findings predicted neuroendocrine dysfunction following TBI. The adaptive response to critical illness with significantly elevated cortisol levels on admission and decreased levels thereafter in patients ventilated for more than 24 h (p < 0.05) was attenuated following severe TBI (p < 0.05). However, the coincidence of low serum cortisol and increased urinary excretion of glucocorticoid metabolites in about 80% of patients challenges the relevance of basal hormone measurements. In ventilated patients, total T3 and free T4 were decreased (p < 0.05), TSH was low on day 3 (p < 0.05), and a gonadotropic insufficiency was present (p < 0.05). The thyrotropic and gonadotropic system recovered completely within the follow-up period. With regard to the somatotropic system, neither brain injury severity nor mechanical ventilation was associated with an insufficiency during the acute phase post-injury. However, initially low GH levels predicted a persistent deficiency (r = 0.731, p < 0.001). We conclude that both severe TBI and prolonged mechanical ventilation result in hormonal disturbances early after injury, suggesting a pathophysiological response to brain injury and subsequent intensive care treatment rather than morphological damage.
Authors:
Andrea Kleindienst; Georg Brabant; Christoph Bock; Christiane Maser-Gluth; Michael Buchfelder
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of neurotrauma     Volume:  26     ISSN:  1557-9042     ISO Abbreviation:  J. Neurotrauma     Publication Date:  2009 Sep 
Date Detail:
Created Date:  2009-09-01     Completed Date:  2009-12-30     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8811626     Medline TA:  J Neurotrauma     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1435-46     Citation Subset:  IM    
Affiliation:
Department of Neurosurgery, University Erlangen-Nuremberg, Erlangen, Germany. andrea.kleindienst@uk-erlangen.de
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adrenal Cortex Hormones / blood
Adult
Aged
Aged, 80 and over
Brain Injuries / physiopathology*,  radiography
Female
Follow-Up Studies
Glasgow Coma Scale
Hormones / blood
Human Growth Hormone / blood
Humans
Intensive Care
Longitudinal Studies
Male
Middle Aged
Neurosecretory Systems / physiopathology*
Prospective Studies
Receptors, Somatotropin / metabolism
Thyroid Hormones / blood
Treatment Outcome
Young Adult
Chemical
Reg. No./Substance:
0/Adrenal Cortex Hormones; 0/Hormones; 0/Receptors, Somatotropin; 0/Thyroid Hormones; 12629-01-5/Human Growth Hormone

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