engleski

Changes in immune and endocrine systems in posttraumatic stress disorder

Introduction and aim. Posttraumatic stress disorder (PTSD) is associated with increased medical morbidity, particularly from the autoimmune and cardiovascular diseases. Changes in the endocrine and immune system are key mediators in this process. The aim of our study was to investigate whether hormones (cortisol and prolactin), proinflammatory cytokines (interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF- )), components of HPA-axis (lymphocyte expression of glucocorticoid receptor (GR)), immune function (natural killer cell cytotoxicity) and peripheral blood percentages of various lymphocyte subpopulations (T cells, helper T cells, cytotoxic T cells, B cells and natural killer cells) change in patients with posttraumatic stress disorder over time. Subjects and methods. We assessed 39 patients with PTSD and 37 sex and age matched healthy volunteers in two time points separated by 5.6 years (median ; interquartile range: 5.4-6.3). Hormones were measured by radioimmunoassay and cytokines were determined by immunoenzyme assays. Immune function was assessed with the in vitro natural killer cell cytotoxicity (NKCC) toward 51Cr-labeled K562 target cells. Lymphocyte counts, immunophenotye and intracellular glucocorticoid receptor expression were determined by three-color flow cytometry. Results. In the first time point cortisol, prolactin, NKCC, lymphocyte count, total T cells and helper T cells were increased, while glucocorticoid receptor expression was decreased in all lymphocyte subpopulations in PTSD patients compared to controls. In the second time point only prolactin levels and lymphocyte counts remained elevated and no significant differences in other variables have been observed. Conclusion. Changes in the endocrine and immune systems are not static in persons with PTSD but rather depend on duration of alostatic load posed by the disorder and its impact on interactions involved in response to stress.

PTSP; imunologija; endokrinologija; kortizol

nije evidentirano