engleski

Hypothalamic-pituitary-adrenal axis profile and natural killer cell cytotoxicity in posttraumatic stress disorder - a longitudinal study

Evidence suggests that posttraumatic stress disorder (PTSD) is related to increased medical morbidity, particularly from the autoimmune and cardiovascular diseases (1). The patophysiological mechanisms underlying increased susceptibility to disease are not yet clear. However, it has been implicated that the hypothalamic-pituitary-adrenal (HPA) axis is one of the key mediators in this process (2). Studies of the HPA axis activity (3) and immune cells function (4) in PTSD yielded controversial results. It is believed that PTSD is linked with low plasma cortisol levels and higher glucocorticoid receptor (GCR) expression, suggesting enhanced feedback sensitivity to cortisol (3). In contrast to these findings, Gotovac et al. (5) showed that Croatian combat veterans with PTSD had lower expression of the GCR in peripheral blood lymphocytes with higher serum cortisol concentration than healthy subjects. The reason for such a discrepancy could lie in a considerably shorter duration of allostatic load caused by adaptive response to stress in Croatian combat veterans compared to Vietnam veterans or Holocaust survivors. We assumed that the distinct profile of HPA axis develops over time and tested this hypothesis by measuring lymphocyte GCR expression and serum cortisol concentration in Croatian combat veterans with PTSD and healthy individuals on two occasions with averagely six years between assessments. Possible association of the HPA axis components with the immune function were tested by simultaneous measurement of the natural killer cell cytotoxicity (NKCC).

PTSD; HPA axis; natural killer cell cytotoxicity

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