Daniel Lindqvist1, Firdaus S Dhabhar2, Synthia H Mellon3, Rachel Yehuda4, S Marlene Grenon5, Janine D Flory4, Linda M Bierer4, Duna Abu-Amara6, Michelle Coy7, Iouri Makotkine4, Victor I Reus7, F Saverio Bersani8, Charles R Marmar9, Owen M Wolkowitz10. 1. Department of Psychiatry, University of California San Francisco (UCSF) School of Medicine, San Francisco, CA, United States; Lund University, Faculty of Medicine, Department of Clinical Sciences Lund, Psychiatry, Lund, Sweden. 2. Department of Psychiatry & Behavioral Sciences, Sylvester Comprehensive Cancer Center, University of Miami, FL, United States. 3. Department of OB/GYN and Reproductive Sciences, University of California San Francisco (UCSF) School of Medicine, San Francisco, CA, United States. 4. James J. Peters Veterans Administration Medical Center Bronx, New York, United States; Icahn School of Medicine at Mount Sinai, New York, NY, United States. 5. Department of Surgery, University of California, San Francisco, San Francisco, CA, United States; Department of Surgery, Veterans Affairs Medical Center, San Francisco, CA, United States. 6. Steven and Alexandra Cohen Veterans Center for Posttraumatic Stress and Traumatic Brain Injury, Department of Psychiatry, NYU, New York, United States. 7. Department of Psychiatry, University of California San Francisco (UCSF) School of Medicine, San Francisco, CA, United States. 8. Department of Neurology and Psychiatry, Sapienza University of Rome, Rome, Italy. 9. Steven and Alexandra Cohen Veterans Center for Posttraumatic Stress and Traumatic Brain Injury, Department of Psychiatry, NYU, New York, United States. Electronic address: Charles.Marmar@nyumc.org. 10. Department of Psychiatry, University of California San Francisco (UCSF) School of Medicine, San Francisco, CA, United States. Electronic address: Owen.Wolkowitz@ucsf.edu.
Abstract
INTRODUCTION: Several lines of evidence indicate that increased inflammation is associated with Post-Traumatic Stress Disorder (PTSD). We have previously reported that peripheral inflammatory markers are significantly higher in combat-exposed veterans with than without PTSD. This study was designed to replicate these findings in a new study cohort using the same population and recruitment strategies. METHODS: Sixty-one male war veterans (31 PTSD and 30 control subjects) were included in this replication study. Levels of Interleukin-6, Tumor Necrosis Factor-alpha, Gamma interferon, and high-sensitivity C-reactive protein were quantified in blood samples. A standardized "total pro-inflammatory score" was calculated to limit the number of statistical comparisons. The Clinician Administered PTSD Scale (CAPS) rating scale was used to assess PTSD symptom severity. RESULTS: PTSD subjects had significantly higher total pro-inflammatory scores compared to non-PTSD subjects in unadjusted analysis (Cohen's d=0.75, p=0.005) as well as after adjusting for potentially confounding effects of age, BMI, smoking, and potentially interfering medications and somatic co-morbidities (p=0.023). There were no significant correlations between inflammatory markers and severity of symptoms within the PTSD group. CONCLUSIONS: We replicated, in a new sample, our previous finding of increased inflammatory markers in combat-exposed PTSD subjects compared to combat-exposed non-PTSD controls. These findings strongly add to the growing literature suggesting that immune activation may be an important aspect of PTSD pathophysiology, although not directly correlated with current PTSD symptom levels in the PTSD group.
INTRODUCTION: Several lines of evidence indicate that increased inflammation is associated with Post-Traumatic Stress Disorder (PTSD). We have previously reported that peripheral inflammatory markers are significantly higher in combat-exposed veterans with than without PTSD. This study was designed to replicate these findings in a new study cohort using the same population and recruitment strategies. METHODS: Sixty-one male war veterans (31 PTSD and 30 control subjects) were included in this replication study. Levels of Interleukin-6, Tumor Necrosis Factor-alpha, Gamma interferon, and high-sensitivity C-reactive protein were quantified in blood samples. A standardized "total pro-inflammatory score" was calculated to limit the number of statistical comparisons. The Clinician Administered PTSD Scale (CAPS) rating scale was used to assess PTSD symptom severity. RESULTS:PTSD subjects had significantly higher total pro-inflammatory scores compared to non-PTSD subjects in unadjusted analysis (Cohen's d=0.75, p=0.005) as well as after adjusting for potentially confounding effects of age, BMI, smoking, and potentially interfering medications and somatic co-morbidities (p=0.023). There were no significant correlations between inflammatory markers and severity of symptoms within the PTSD group. CONCLUSIONS: We replicated, in a new sample, our previous finding of increased inflammatory markers in combat-exposed PTSD subjects compared to combat-exposed non-PTSD controls. These findings strongly add to the growing literature suggesting that immune activation may be an important aspect of PTSD pathophysiology, although not directly correlated with current PTSD symptom levels in the PTSD group.
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