In PTSD, a disorder with a complex clinical picture, diverse symptoms, and different comorbidities, the evaluation of complex biological signals might be used to improve the characterization of the baseline group characteristics, to predict a suicidal risk, to differentiate particular symptoms or syndromes, and to improve the understanding of the underlying neurobiology of PTSD.

The rationale for the use of blood platelets as a limited peripheral model for the central 5-HT synaptosomes lies in the similar pharmacodynamics of 5-HT with central 5-HT neurons [25,26]. Recent reports suggest that platelet 5-HT concentration [27,28], and platelet MAO activity [17,29,30] might serve as biological or trait markers for particular mental disturbances. The hypothesis of a deficit of the serotonergic system in PTSD is based on data showing disturbed 5-HT function in PTSD [14]. Serotonergic alterations might contribute to the cognitive disturbances and deficits in the memory systems occurring in PTSD [14], and platelet 5-HT has been reported to be altered in aggression [25] and impulsivity [31]. In line with previous reports [15,16,32], our data indicate that platelet 5-HT concentration is not altered in war veterans with PTSD. Since biological markers have been proposed to be more closely related to basic psychopathological characteristics, i.e. trait markers [26,31], than to nosological entities (such as PTSD), our data confirm this presumption. This finding supports the hypothesis that platelet 5-HT is more related to particular trait markers, such as aggression [25], impulsivity [31], or to particular symptoms [27,28], suicidal behaviour [26-28], than to state characteristics [26,27].

Platelet MAO shares similar biochemical and pharmacological characteristics, and identical amino acid sequences, with brain MAO-B [33], and was proposed to represent a genetic marker for the size or functional capacity of the central monoamine systems and serotonergic system [28]. We have found increased platelet MAO activity in Croatian war veterans with PTSD, in contrast to previous data [16,17,34]. The discrepancies between studies might be explained by the differences in the time course of PTSD (i.e. acute PTSD in the studies [16,17] vs. chronic PTSD in the present study), and the lack of alcohol comorbidity in the present group when compared to the previous study [34]. Our data, showing increased platelet MAO values in the large numbers of war veterans with combat related PTSD, agree with the altered platelet MAO in different personality and temperamental traits, such as sensation seeking and impulsivity [29,30], and impulse and affect dysregulation [35]. Smoking decreases platelet MAO activity [29,30,36], but after controlling for the effect of smoking, the activity of the enzyme remained elevated (data not shown) in our Croatian war veterans with PTSD.

The noradrenergic system is hyperactive in PTSD, and increased noradrenergic markers, both in cerebrospinal fluid and in plasma and urine, were observed in PTSD patients [11,14]. Noradrenergic neurons arise from the locus ceruleus and project to diverse structures involved in learning and memory (prefrontal cortex, amygdala and hippocampus), and stress response (hypothalamus). These brain regions modulate stress/fear response and emotional memory [11,14]. DBH is an enzyme that catalyzes the conversion of dopamine to noradrenalin. War veterans with chronic combat related PTSD in our study had similar plasma DBH values as healthy subjects. The lack of changes in plasma DBH in our sample might suggest that plasma DBH is not a suitable biological marker of the altered noradrenergic activity in PTSD, or that DBH is altered only in the psychotic subtype of PTSD, as suggested before [37]. To elucidate this relationship, the studies evaluating the relationship of DBH with psychotic PTSD are underway.

The altered plasma levels of cortisol, T3, thyroxin (T4) and thyroid-stimulating hormone (TSH) reflect the dysregulated HPA and/or HPT axis activity in stress-related disorders [11]. The concept of a hyperactive HPT axis, with consequent elevation of total and free T3 in PTSD patients, agrees with our data [21], and confirms the link between stress and clinical hyperthyroidism [11]. Hypersecretion of corticosteroids for prolonged periods can harm cognitive processes that are disturbed in PTSD [14]. Our data [20] show increased plasma cortisol levels in war veterans with combat related PTSD, adding to the contradictory findings regarding the status of basal and stimulated cortisol levels in PTSD patients. Since noradrenergic and HPA systems act synergistically in response to acute or prolonged stressful stimuli, disturbances in noradrenergic and HPA axis systems would elicit a cascade of events and disrupt the regulatory mechanisms modulating response to trauma, and add to the development of PTSD symptoms.

In line with the data showing altered plasma lipid levels in PTSD [38], we have shown that war veterans with PTSD have increased levels of serum cholesterol, and triglycerides, decreased levels of HDL [18], and unaltered levels of LDL. Since increased serum cholesterol is a risk factor for cardiovascular disease in PTSD patients, these findings call for dietary modification for war veterans with PTSD.

The great proportion of our war veterans with chronic combat related PTSD had a severe form of PTSD, complicated with the presence of psychotic or depressive symptoms. Therefore, further studies are underway to elucidate the association between biological markers and particular symptoms occurring in PTSD, and to facilitate the identification of the specific form or subtype of PTSD, disease staging, and monitoring of treatment.

The research of biological markers, which reflect the activity of the central neurotransmitter and/or neuroendocrine systems, should focus on efforts to integrate the data, and to explain the multiple interactions among these neurobiological systems in PTSD, in order to achieve a goal of modern medicine, a tailored pharmacological and non-pharmacological treatment for an individual patient with PTSD at an appropriate point in the course of the disorder.

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