Inflammation as a predictor of disease course in posttraumatic stress disorder and depression: A prospective analysis from the Mind Your Heart Study.


Journal

Brain, behavior, and immunity
ISSN: 1090-2139
Titre abrégé: Brain Behav Immun
Pays: Netherlands
ID NLM: 8800478

Informations de publication

Date de publication:
01 2019
Historique:
received: 30 04 2018
revised: 01 10 2018
accepted: 29 10 2018
pubmed: 6 11 2018
medline: 24 1 2020
entrez: 4 11 2018
Statut: ppublish

Résumé

Prior research has focused largely on the pro-inflammatory states of PTSD and depression, with few studies evaluating the direction of inflammation's association with these disorders. To clarify whether inflammation plays a role in the development of PTSD or depression, we assessed the predictive value of inflammatory biomarkers on the courses of these conditions in a cohort of Veterans. This research was part of the Mind Your Heart Study, a prospective cohort study designed to examine PTSD-related health outcomes. Between 2008 and 2010, 746 San Francisco area Veterans Administration patients were enrolled. At baseline, inflammatory biomarkers were measured from fasting morning venous blood draws, and cortisol and catecholamine levels were measured from 24-hour urine samples. PTSD was diagnosed using the PTSD Checklist at baseline and annual follow-up. Depression was evaluated using the 9-item Patient Health Questionnaire at baseline and follow-up. Ordinal logistic regression models were used to assess the predictive value of baseline biomarker levels on clinically relevant courses of PTSD and depression categorized and ordered as none, resolved, developed, and chronic. After adjustment for age and sex, elevated levels of white blood cell count (OR = 1.27(1.10-1.47), p = 0.001), C-reactive protein (OR = 1.20(1.04-1.39), p = 0.02), fibrinogen (OR = 1.19(1.03-1.38), p = 0.02), and ESR (OR = 1.17(1.00-1.36, p = 0.05), and decreased levels of urine cortisol (OR = 0.84(0.71-0.99), p = 0.04) were significant predictors of poorer courses of PTSD. Elevated levels of WBC count (OR = 1.31(1.14-1.50), p < 0.001), CRP (OR = 1.24(1.07-1.43), p = 0.003), fibrinogen (OR = 1.26(1.09-1.46), p = 0.002), and catecholamines (OR = 1.17(1.01-1.36), p = 0.04) were significant predictors of poorer courses of depression. After additionally controlling for physical activity, elevated WBC count (p = 0.002) and decreased levels of urine cortisol (p = 0.05) remained significant predictors of PTSD course, and elevated WBC count (p = 0.001), CRP (p = 0.03), and fibrinogen (p = 0.02) remained significant predictors of depression course. After adjusting for all significant variables, elevated WBC count (p = 0.02) was a significant predictor of a poorer course of PTSD, and elevated WBC count (p = 0.04) and platelet count (p = 0.03) were significant predictors of a poorer course of depression. Increased levels of several inflammatory biomarkers were associated with significantly increased odds of clinically worse courses of PTSD and depression. Inflammation may be a target for prevention and treatment of these mental health disorders.

Sections du résumé

BACKGROUND
Prior research has focused largely on the pro-inflammatory states of PTSD and depression, with few studies evaluating the direction of inflammation's association with these disorders. To clarify whether inflammation plays a role in the development of PTSD or depression, we assessed the predictive value of inflammatory biomarkers on the courses of these conditions in a cohort of Veterans.
METHODS
This research was part of the Mind Your Heart Study, a prospective cohort study designed to examine PTSD-related health outcomes. Between 2008 and 2010, 746 San Francisco area Veterans Administration patients were enrolled. At baseline, inflammatory biomarkers were measured from fasting morning venous blood draws, and cortisol and catecholamine levels were measured from 24-hour urine samples. PTSD was diagnosed using the PTSD Checklist at baseline and annual follow-up. Depression was evaluated using the 9-item Patient Health Questionnaire at baseline and follow-up. Ordinal logistic regression models were used to assess the predictive value of baseline biomarker levels on clinically relevant courses of PTSD and depression categorized and ordered as none, resolved, developed, and chronic.
RESULTS
After adjustment for age and sex, elevated levels of white blood cell count (OR = 1.27(1.10-1.47), p = 0.001), C-reactive protein (OR = 1.20(1.04-1.39), p = 0.02), fibrinogen (OR = 1.19(1.03-1.38), p = 0.02), and ESR (OR = 1.17(1.00-1.36, p = 0.05), and decreased levels of urine cortisol (OR = 0.84(0.71-0.99), p = 0.04) were significant predictors of poorer courses of PTSD. Elevated levels of WBC count (OR = 1.31(1.14-1.50), p < 0.001), CRP (OR = 1.24(1.07-1.43), p = 0.003), fibrinogen (OR = 1.26(1.09-1.46), p = 0.002), and catecholamines (OR = 1.17(1.01-1.36), p = 0.04) were significant predictors of poorer courses of depression. After additionally controlling for physical activity, elevated WBC count (p = 0.002) and decreased levels of urine cortisol (p = 0.05) remained significant predictors of PTSD course, and elevated WBC count (p = 0.001), CRP (p = 0.03), and fibrinogen (p = 0.02) remained significant predictors of depression course. After adjusting for all significant variables, elevated WBC count (p = 0.02) was a significant predictor of a poorer course of PTSD, and elevated WBC count (p = 0.04) and platelet count (p = 0.03) were significant predictors of a poorer course of depression.
CONCLUSIONS
Increased levels of several inflammatory biomarkers were associated with significantly increased odds of clinically worse courses of PTSD and depression. Inflammation may be a target for prevention and treatment of these mental health disorders.

Identifiants

pubmed: 30389462
pii: S0889-1591(18)30764-5
doi: 10.1016/j.bbi.2018.10.012
pii:
doi:

Substances chimiques

Biomarkers 0
Catecholamines 0
Fibrinogen 9001-32-5
C-Reactive Protein 9007-41-4
Hydrocortisone WI4X0X7BPJ

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

220-227

Subventions

Organisme : NIA NIH HHS
ID : T35 AG026736
Pays : United States
Organisme : NHLBI NIH HHS
ID : K23 HL094765
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2018. Published by Elsevier Inc.

Auteurs

Meghana Eswarappa (M)

Icahn School of Medicine at Mount Sinai, New York, NY, USA.

Thomas C Neylan (TC)

Department of Psychiatry, University of California, San Francisco, CA, USA; Veterans Affairs Medical Center, San Francisco, CA, USA.

Mary A Whooley (MA)

Department of Medicine, University of California, San Francisco, CA, USA; Veterans Affairs Medical Center, San Francisco, CA, USA.

Thomas J Metzler (TJ)

Veterans Affairs Medical Center, San Francisco, CA, USA.

Beth E Cohen (BE)

Department of Medicine, University of California, San Francisco, CA, USA; Veterans Affairs Medical Center, San Francisco, CA, USA. Electronic address: beth.cohen@ucsf.edu.

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Classifications MeSH