CRF serum levels differentiate PTSD from healthy controls and TBI in military veterans.
Journal
Psychiatric research and clinical practice
ISSN: 2575-5609
Titre abrégé: Psychiatr Res Clin Pract
Pays: United States
ID NLM: 101776485
Informations de publication
Date de publication:
2021
2021
Historique:
entrez:
25
2
2022
pubmed:
26
2
2022
medline:
26
2
2022
Statut:
ppublish
Résumé
Posttraumatic stress disorder (PTSD) is a serious and frequently debilitating psychiatric condition that can occur in people who have experienced traumatic stessors, such as war, violence, sexual assault and other life-threatening events. Treatment of PTSD and traumatic brain injury (TBI) in veterans is challenged by diagnostic complexity, partially due to PTSD and TBI symptom overlap and to the fact that subjective self-report assessments may be influenced by a patient's willingness to share their traumatic experiences and resulting symptoms. Corticotropin-releasing factor (CRF) is one of the main mediators of hypothalamic pituitary adrenal (HPA)-axis responses in stress and anxiety. We analyzed serum CRF levels in 230 participants including heathy controls (64), and individuals with PTSD (53), TBI (70) or PTSD+TBI (43) by enzyme immunoassay (EIA). Significantly lower CRF levels were found in both the PTSD and PTSD+TBI groups compared to healthy control (PTSD vs Controls: P=0.0014, PTSD + TBI vs Controls: P=0.0011) and chronic TBI participants (PTSD vs TBI: P<0.0001PTSD + TBI vs TBI: P<0.0001) , suggesting a PTSD-related mechanism independent from TBI and associated with CRF reduction. CRF levels negatively correlated with PTSD severity on the CAPS-5 scale in the whole study group. Hyperactivation of the HPA axis has been classically identified in acute stress. However, the recognized enhanced feedback inhibition of the HPA axis in chronic stress supports our findings of lower CRF in PTSD patients. This study suggests that reduced serum CRF in PTSD should be further investigated. Future validation studies will establish if CRF is a possible blood biomarker for PTSD and/or for differentiating PTSD and chronic TBI symptomatology.
Sections du résumé
BACKGROUND AND OBJECTIVE
OBJECTIVE
Posttraumatic stress disorder (PTSD) is a serious and frequently debilitating psychiatric condition that can occur in people who have experienced traumatic stessors, such as war, violence, sexual assault and other life-threatening events. Treatment of PTSD and traumatic brain injury (TBI) in veterans is challenged by diagnostic complexity, partially due to PTSD and TBI symptom overlap and to the fact that subjective self-report assessments may be influenced by a patient's willingness to share their traumatic experiences and resulting symptoms. Corticotropin-releasing factor (CRF) is one of the main mediators of hypothalamic pituitary adrenal (HPA)-axis responses in stress and anxiety.
METHODS AND RESULTS
RESULTS
We analyzed serum CRF levels in 230 participants including heathy controls (64), and individuals with PTSD (53), TBI (70) or PTSD+TBI (43) by enzyme immunoassay (EIA). Significantly lower CRF levels were found in both the PTSD and PTSD+TBI groups compared to healthy control (PTSD vs Controls: P=0.0014, PTSD + TBI vs Controls: P=0.0011) and chronic TBI participants (PTSD vs TBI: P<0.0001PTSD + TBI vs TBI: P<0.0001) , suggesting a PTSD-related mechanism independent from TBI and associated with CRF reduction. CRF levels negatively correlated with PTSD severity on the CAPS-5 scale in the whole study group.
CONCLUSIONS
CONCLUSIONS
Hyperactivation of the HPA axis has been classically identified in acute stress. However, the recognized enhanced feedback inhibition of the HPA axis in chronic stress supports our findings of lower CRF in PTSD patients. This study suggests that reduced serum CRF in PTSD should be further investigated. Future validation studies will establish if CRF is a possible blood biomarker for PTSD and/or for differentiating PTSD and chronic TBI symptomatology.
Identifiants
pubmed: 35211666
doi: 10.1176/appi.prcp.20210017
pmc: PMC8764614
mid: NIHMS1775632
doi:
Types de publication
Journal Article
Langues
eng
Pagination
153-162Subventions
Organisme : NIAAA NIH HHS
ID : P01 AA027057
Pays : United States
Organisme : NIA NIH HHS
ID : R01 AG062572
Pays : United States
Organisme : NINDS NIH HHS
ID : R01 NS104127
Pays : United States
Organisme : NCATS NIH HHS
ID : UL1 TR001445
Pays : United States
Déclaration de conflit d'intérêts
Conflicts of Interest The authors declare no conflicts of interest related to this work. AE received stock options at Mindstrong Health and Akili Interactive for unrelated consulting. CRM received unrelated support from the NIAAA, Department of Defense, Cohen Veterans Network, Robin Hood Foundation, McCormick Foundation, Home Depot Foundation, and the City of New York.
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