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J Neurotrauma. 2017 Jan 15;34(2):385-390. doi: 10.1089/neu.2015.4350. Epub 2016 Jun 16.

Hypoaminoacidemia Characterizes Chronic Traumatic Brain Injury.

Author information

1
1 Department of Internal Medicine, University of Texas Medical Branch , Galveston, Texas.
2
3 Transitional Learning Center at Galveston , Galveston, Texas.
3
2 Department of Preventive Medicine and Community Health, University of Texas Medical Branch , Galveston, Texas.
4
4 University of Arkansas for Medical Sciences , Little Rock, Arkansas.
5
5 Centre for Neuro Skills , Bakersfield, California.
6
6 Brain Injury Association of America , Grapevine, Texas.

Abstract

Individuals with a history of traumatic brain injury (TBI) are at increased risk for a number of disorders, including Alzheimer's disease, Parkinson's disease, and chronic traumatic encephalopathy. However, mediators of the long-term morbidity are uncertain. We conducted a multi-site, prospective trial in chronic TBI patients (∼18 years post-TBI) living in long-term 24-h care environments and local controls without a history of head injury. Inability to give informed consent was exclusionary for participation. A total of 41 individuals (17 moderate-severe TBI, 24 controls) were studied before and after consumption of a standardized breakfast to determine if concentrations of amino acids, cytokines, C-reactive protein, and insulin are potential mediators of long-term TBI morbidity. Analyte concentrations were measured in serum drawn before (fasting) and 1 h after meal consumption. Mean ages were 44 ± 15 and 49 ± 11 years for controls and chronic TBI patients, respectively. Chronic TBI patients had significantly lower circulating concentrations of numerous individual amino acids, as well as essential amino acids (p = 0.03) and large neutral amino acids (p = 0.003) considered as groups, and displayed fundamentally altered cytokine-amino acid relationships. Many years after injury, TBI patients exhibit abnormal metabolic responses and altered relationships between circulating amino acids, cytokines, and hormones. This pattern is consistent with TBI, inducing a chronic disease state in patients. Understanding the mechanisms causing the chronic disease state could lead to new treatments for its prevention.

KEYWORDS:

head trauma; metabolism

PMID:
27178787
DOI:
10.1089/neu.2015.4350
[Indexed for MEDLINE]

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