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Review
. 2016 Aug:29:104-10.
doi: 10.1016/j.coph.2016.07.011. Epub 2016 Jul 29.

Co-morbidity of PTSD and immune system dysfunction: opportunities for treatment

Affiliations
Review

Co-morbidity of PTSD and immune system dysfunction: opportunities for treatment

Gretchen N Neigh et al. Curr Opin Pharmacol. 2016 Aug.

Abstract

Posttraumatic stress disorder (PTSD) is defined as a psychiatric disorder; however, PTSD co-occurs with multiple somatic manifestations. People living with PTSD commonly manifest dysregulations in the systems that regulate the stress response, including the hypothalamic-pituitary-adrenal (HPA) axis, and development of a pro-inflammatory state. Additionally, somatic autoimmune and inflammatory diseases and disorders have a high rate of co-morbidity with PTSD. Recognition and understanding of the compounding effect that these disease states can have on each other, evidenced from poorer treatment outcomes and accelerated disease progression in patients suffering from co-morbid PTSD and/or other autoimmune and inflammatory diseases, has the potential to lead to additional treatment opportunities.

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Conflict of interest statement

The authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1. A Psychoneuroimmunological Model of PTSD
Exposure to severe psychological trauma in the presence of pre-existing risk factors leads to PTSD. Immune system changes in PTSD include altered glucocorticoid (GC) sensitivity in target immune cells, shifts in immune cell distribution, immunosenescence, elevated pro-inflammatory cytokines and a decrease in regulatory T cells. A complex interplay of the biological alterations in the stress response known to exist in PTSD, along with immune alterations, are hypothesized to increase the risk for co-morbid somatic autoimmune and inflammatory disorders. Immune interventions may improve both primary PTSD symptoms and co-morbid somatic disorders related to the immune system.

References

    1. Kessler RC, Sonnega A, Bromet E, Hughes M, Nelson CB. Posttraumatic stress disorder in the National Comorbidity Survey. [Internet] Arch Gen Psychiatry. 1995;52:1048–60. - PubMed
    1. Breslau N, Kessler RC, Chilcoat HD, Schultz LR, Davis GC, Andreski P. Trauma and posttraumatic stress disorder in the community: the 1996 Detroit Area Survey of Trauma. [Internet] Arch Gen Psychiatry. 1998;55:626–32. - PubMed
    1. White J, Pearce J, Morrison S, Dunstan F, Bisson JI, Fone DL. Risk of post-traumatic stress disorder following traumatic events in a community sample. [Internet] Epidemiol Psychiatr Sci. 2015;24:249–57. - PMC - PubMed
    1. Heim C, Nemeroff CB. Neurobiology of posttraumatic stress disorder. [Internet] CNS Spectr. 2009;14:13–24. - PubMed
    1. Pace TWW, Heim CM. A short review on the psychoneuroimmunology of posttraumatic stress disorder: from risk factors to medical comorbidities. [Internet] Brain Behav Immun. 2011;25:6–13. - PubMed

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