2007
DOI: 10.1016/j.jpsychires.2006.06.009
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Evidence for low-grade systemic proinflammatory activity in patients with posttraumatic stress disorder

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Cited by 369 publications
(288 citation statements)
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“…Finally, we should note that 9 months after the earthquake, the incidence of PTSD was still high among female high school students in earthquake areas without severe property damage. It has been reported that PTSD is associated with a low-grade systemic proinflammatory state, which could contribute to atherosclerosis (von Känel et al 2007). Moreover, PTSD in adolescents has been suggested to be associated with the objective disease states, such as circulatory disease (Seng et al 2005).…”
Section: Discussionmentioning
confidence: 99%
“…Finally, we should note that 9 months after the earthquake, the incidence of PTSD was still high among female high school students in earthquake areas without severe property damage. It has been reported that PTSD is associated with a low-grade systemic proinflammatory state, which could contribute to atherosclerosis (von Känel et al 2007). Moreover, PTSD in adolescents has been suggested to be associated with the objective disease states, such as circulatory disease (Seng et al 2005).…”
Section: Discussionmentioning
confidence: 99%
“…Two studies found elevated levels of anxiety and PTSD to be independently associated with abnormal levels of acute-phase proteins and several proinflammatory cytokines (e.g., IL-6 and TNF-α in cardiac patients) [60]. In addition, Type D personality was associated with higher levels of proinflammatory cytokines and lower levels of anti-inflammatory cytokines in patients with heart failure [61].…”
Section: Inflammationmentioning
confidence: 99%
“…Extensive research has shown that chronic neuroinflammation continues for months to years after injury, [9][10][11][12] and evidence for chronic inflammation has been observed in a number of studies examining patients with PTSD, panic disorder, obsessive-compulsive disorder (OCD), and generalized anxiety disorder. [13][14][15][16][17][18] Glial activation may be involved in the development and maintenance of PTSD, [9][10][11][12] and mounting evidence supports the role of inflammatory processes in both TBI and anxiety disorders. After injury, immune cells rapidly produce endogenous danger signals or ''alarmins,'' which function as potent effectors of innate defense and promote immune system activation by recruiting antigen-presenting cells (APCs) that relay and amplify the inflammatory response.…”
mentioning
confidence: 99%
“…inflammatory response in the brain that exceeds early neuroprotection and results in neurodegenerative changes capable of continuing the inflammatory cycle. 9,27,90 Chronic inflammation has been observed in a number of studies examining patients with trauma-related anxiety disorders, reporting increases in downstream mediators, such as peripheral elevations of TNF-a, interferon-gamma (IFN-c), IL-1b, and IL-6, in patients with PTSD, [13][14][15][16] elevations of TNF-a and IL-6 in patients with OCD, 17 and elevations in proinflammatory cytokines and chemokines (monocyte chemoattractant protein 1, macrophage inflammatory protein 1 alpha, IL-1a, IL-1b, IL-6, IL-8, Eotaxin, granulocyte macrophage colony-stimulating factor, and IFN-c) in individuals with panic disorder and PTSD. 18 Despite compelling evidence implicating excessive inflammatory actions and a generalized inflammatory state in the development of anxiety disorders after TBI, central measures of proinflammatory cytokine elevations specifically related to human PTSD and other anxiety disorders have not yet been performed.…”
mentioning
confidence: 99%