Circulating Levels of Hormones, Lipids, and Immune Mediators in Post-Traumatic Stress Disorder – A 3-Month Follow-Up Study

Jergović, Mladen; Bendelja, Krešo; Mlakar, Ana Savić; Vojvoda, Valerija; Aberle, Neda; Jovanović, Tanja; Rabatić, Sabina; Sabioncello, Ante; Vidović, Anđelko

doi:10.3389/fpsyt.2015.00049

Cited by 55 publications

(37 citation statements)

References 94 publications

(105 reference statements)

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“…This suggests that TNFcould potentially serve as a state marker of PTSD, given the changes in concentrations observed in response to different interventions. An additional longitudinal study found no difference in TNF-concentrations between baseline assessment and after 3 months of treatment-asusual (Jergovi et al 2015). However, in this study TNF-were not detected in a high percentage of participants, so conclusions cannot be drawn.…”

Section: Tnf-in Human Studies Of Ptsdcontrasting

confidence: 43%

“…Only one study demonstrated a loss of their initial statistical significance when including covariates in the analyses (von Känel et al 2007). It is of note that in two of the remaining studies that found no difference in TNF-concentrations between groups, TNF-was not detectable in a high percentage of participants (Gola et al 2013, Jergovi et al 2015, which may account for their findings. The results of invitro investigations of TNF-in PTSD were generally inconsistent.…”

Section: Tnf-in Human Studies Of Ptsdmentioning

confidence: 69%

“…The human studies were further categorized into articles with cross-sectional data using in vivo methods (n=19; including studies measuring serum or plasma concentrations of TNF-), articles with cross-sectional data on TNF-production in-vitro (n=5), or articles with longitudinal data (n=3), two of which considered the effect of treatment interventions on TNF-concentrations. One of the included studies reported both cross-sectional and longitudinal data (Jergovi et al 2015) and another study provided data on in-vivo and in-vitro measurements of TNF- (Gola et al 2013).…”

Section: Characteristics Of Included Studiesmentioning

confidence: 99%

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A SYSTEMATIC REVIEW OF TUMOR NECROSIS FACTOR-α IN POST-TRAUMATIC STRESS DISORDER: EVIDENCE FROM HUMAN AND ANIMAL STUDIES

Hussein

Dalton

Willmund³

et al. 2017

Psychiat Danub

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Section: Tnf-in Human Studies Of Ptsdcontrasting

confidence: 43%

Section: Tnf-in Human Studies Of Ptsdmentioning

confidence: 69%

Section: Characteristics Of Included Studiesmentioning

confidence: 99%

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A SYSTEMATIC REVIEW OF TUMOR NECROSIS FACTOR-α IN POST-TRAUMATIC STRESS DISORDER: EVIDENCE FROM HUMAN AND ANIMAL STUDIES

Hussein

Dalton

Willmund³

et al. 2017

Psychiat Danub

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“…This same discrepancy in the literature also surrounds alterations in anti-inflammatory cytokines in individuals with PTSD (Table 1, B). In some studies, concentrations of IL-8 (Jergovic et al, 2015;Song et al, 2007b) and IL-4 von Kanel et al, 2007) are lower in individuals with PTSD. IL-4 concentrations have also been correlated negatively with total hyperarousal symptoms (von Kanel et al, 2007).…”

Section: Ptsd and Inflammationmentioning

confidence: 99%

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond

Michopoulos

Powers

Gillespie

et al. 2016

Neuropsychopharmacol

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544

376

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The study of inflammation in fear-and anxiety-based disorders has gained interest as growing literature indicates that proinflammatory markers can directly modulate affective behavior. Indeed, heightened concentrations of inflammatory signals, including cytokines and C-reactive protein, have been described in posttraumatic stress disorder (PTSD), generalized anxiety disorder (GAD), panic disorder (PD), and phobias (agoraphobia, social phobia, etc.). However, not all reports indicate a positive association between inflammation and fear-and anxiety-based symptoms, suggesting that other factors are important in future assessments of inflammation's role in the maintenance of these disorders (ie, sex, co-morbid conditions, types of trauma exposure, and behavioral sources of inflammation). The most parsimonious explanation of increased inflammation in PTSD, GAD, PD, and phobias is via the activation of the stress response and central and peripheral immune cells to release cytokines. Dysregulation of the stress axis in the face of increased sympathetic tone and decreased parasympathetic activity characteristic of anxiety disorders could further augment inflammation and contribute to increased symptoms by having direct effects on brain regions critical for the regulation of fear and anxiety (such as the prefrontal cortex, insula, amygdala, and hippocampus). Taken together, the available data suggest that targeting inflammation may serve as a potential therapeutic target for treating these fear-and anxiety-based disorders in the future. However, the field must continue to characterize the specific role pro-inflammatory signaling in the maintenance of these unique psychiatric conditions.

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“…These theories arise from the studies that indicate that alterations in the hypothalamic pituitary-adrenal axis and increased levels of the glucocorticoid hormone cortisol and pro inflammatory and antiinflammatory cytokines contribute to the neurogenesis of various anxiety disorders. The precise basis of these assumptions is unclear, but prevailing findings show that individuals with PTSD and other anxiety disorders are more likely to have medical conditions associated with prolonged immunosuppression, such as rheumatoid arthritis, irritable bowel syndrome, and cardiovascular disease 8,9 . Genetic predisposition contributes to anxiety disorders.…”

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confidence: 99%

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2018

IJPSR

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Anxiety is a common and normal phenomenon, involving multiple brain regions, including amygdala, locus ceruleus and frontal cortex. Moreover, multiple brain transmitters regulate the presence and severity of anxiety; these include classical transmitters such as gamma amino butyric acid, serotonin, and dopamine, as well as neuropeptides that include corticotrophin releasing hormone, substance P, neuropeptide Y, cholecystokinin and vasopressin. Anxiety is highly adaptive and involves both acute fear, related to an immediate threat and anticipatory anxiety that is associated with possible future threat. Certain individuals are predisposed to develop anxiety disorders. Predisposing variables include both genetic factors (that may dispose toward anxious temperament), emotional traumas and other psychologically mediated factors. Anxiety disorders represent a family of conditions with important distinguishing elements. Panic disorder and phobias involve reactions that are reminiscent of acute fear (albeit often worse). Specific and social phobias involve excessive fearful responses to identifiable things or circumstances in the environment. Generalized anxiety disorder is a condition that, essentially, involves anticipatory fear (i.e., worry). Worries of everyday life are enhanced beyond any normal or adaptive functioning. Although complex, anxiety disorders are treatable conditions that respond to certain medications and specialized forms of psychotherapy.

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Circulating Levels of Hormones, Lipids, and Immune Mediators in Post-Traumatic Stress Disorder – A 3-Month Follow-Up Study

Cited by 55 publications

References 94 publications

A SYSTEMATIC REVIEW OF TUMOR NECROSIS FACTOR-α IN POST-TRAUMATIC STRESS DISORDER: EVIDENCE FROM HUMAN AND ANIMAL STUDIES

A SYSTEMATIC REVIEW OF TUMOR NECROSIS FACTOR-α IN POST-TRAUMATIC STRESS DISORDER: EVIDENCE FROM HUMAN AND ANIMAL STUDIES

Inflammation in Fear- and Anxiety-Based Disorders: PTSD, GAD, and Beyond

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