Association of Intrusive Posttraumatic Stress Symptoms With Elevated C-Reactive Protein Levels in World Trade Center Responders.

Objective: Greater severity of posttraumatic stress disorder (PTSD) symptoms has been linked to elevated C-reactive protein (CRP), a marker of systemic inflammation. The association between PTSD symptoms and CRP levels has been difficult to interpret due to confounding associations between CRP levels and medical comorbidities associated with PTSD and heterogeneity of trauma exposures and PTSD symptoms. The objective of this study was to characterize the relation between clinician-rated PTSD symptom dimensions, medical conditions, and CRP levels among individuals exposed to the World Trade Center (WTC) attacks. WTC rescue, recovery, and clean-up workers were recruited from the WTC Health Program General Responder Cohort. Methods: Participants were assessed using the Clinician-Administered PTSD Scale, completed a questionnaire about medical conditions, and underwent a morning fasting blood draw. Two multivariable binary logistic regression analyses were conducted to identify correlates of elevated CRP levels (>3 mg/dL) and associations between specific PTSD symptom dimensions and elevated CRP levels. Results: After adjusting for demographics, trauma exposure, and medical comorbidities, obesity (odds ratio [OR]=2.96; 95% CI [1.68, 5.21]), lower high-density lipoprotein cholesterol (OR=0.97; 95% CI [0.95, 0.99]), and greater severity of intrusive PTSD symptoms (OR=1.38; 95% CI [1.08, 1.75]) were associated with elevated CRP levels. Post hoc analyses revealed that, among intrusive symptoms, emotional reactivity to trauma cues was independently associated with elevated CRP levels (OR=1.50; 95% CI [1.15, 1.96]). Conclusions: The results suggest that intrusive PTSD symptoms may contribute to systemic inflammation in WTC responders. This finding suggests that targeting both PTSD symptoms and obesity/dyslipidemia may help mitigate risk for elevated systemic inflammation. Prim Care Companion CNS Disord 2026;28(5):25m04177. Author affiliations are listed at the end of this article.