Literature DB >> 10646236

The potential role of hypocortisolism in the pathophysiology of PTSD and psoriasis.

V Thaller1, M Vrkljan, L Hotujac, J Thakore.   

Abstract

Different physical, chemical and psychological stressors can provoke a unique but different endocrine response involving activation of the hypothalamo-pituitary-adrenal (HPA) axis. Inability of adequate compensatory reaction can lead to many disorders. The aim of our study was comparison of cortisol values in diseases provoked by various stressors. Our investigation included 34 posttraumatic stress disorder (PTSD) patients, as an example of disorder caused by extremely strong, acute stressful stimulus, 19 psoriatic patients, as an example of chronic stress stimulus and 17 healthy volunteers. In each patient we determined 24-hour urinary cortisol, serum cortisol at 8 a.m. and 5 p.m., and cortisol in dexamethasone suppression test by the standard radioimmunoassay (RIA) method. PTSD patients showed lower urinary 24-hour cortisol values, (361 +/- 28 nmol/24 h), "stronger" circadian rhythm of serum cortisol (595 +/- 57 nmol/l at 8 a.m. and 242 +/- 23 nmol/l at 5 p.m.) and attenuated suppression of cortisol in dexamethasone suppression test (197 +/- 45 nmol/l) in comparison to healthy volunteers (590 +/- 87 nmol/24 h urine, 590 +/- 32 nmol/l at 8 a.m., 402 +/- 31 nmol/l, and < 86 nmol/l in dexa test). Psoriatic patients showed markedly lower 24-hour cortisol values (150 +/- 98 nmol/24 h), even in comparison to PTSD patients, then serum cortisol values (404 +/- 138 nmol/l at 8 a.m., 187 +/- 80 nmol/l at 5 p.m.) and enhanced suppression of cortisol (23 +/- 5 nmol/l). The model of attenuated feedback inhibition in PTSD patients shows that they are unusually reactive to stress and represents an alternative model of acute stress reaction to extremely strong stressful stimulus. Unusually low cortisol values in psoriatic patients correlate to our hypothesis that in chronic stress-related disease, as psoriasis is, exists, by still undefined mechanism, altered HPA axis function, which is obviously incompetent to realise its immunoregulatory function, so consequentially, clinical signs of psoriasis persist.

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Year:  1999        PMID: 10646236

Source DB:  PubMed          Journal:  Coll Antropol        ISSN: 0350-6134


  14 in total

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Review 2.  PTSD and gene variants: new pathways and new thinking.

Authors:  Kelly Skelton; Kerry J Ressler; Seth D Norrholm; Tanja Jovanovic; Bekh Bradley-Davino
Journal:  Neuropharmacology       Date:  2011-02-26       Impact factor: 5.250

3.  Alterations in stress reactivity after long-term treatment with paroxetine in women with posttraumatic stress disorder.

Authors:  Eric Vermetten; Meena Vythilingam; Christian Schmahl; Carien DE Kloet; Steven M Southwick; Dennis S Charney; J Douglas Bremner
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4.  Exposure to the predator odor TMT induces early and late differential gene expression related to stress and excitatory synaptic function throughout the brain in male rats.

Authors:  Ryan E Tyler; Benjamin Z S Weinberg; Dennis F Lovelock; Laura C Ornelas; Joyce Besheer
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5.  Differential dendritic remodeling in prelimbic cortex of male and female rats during recovery from chronic stress.

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6.  Enhanced cortisol suppression following dexamethasone administration in domestic violence survivors.

Authors:  Michael G Griffin; Patricia A Resick; Rachel Yehuda
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Review 7.  Relations among posttraumatic stress disorder, comorbid major depression, and HPA function: a systematic review and meta-analysis.

Authors:  Matthew C Morris; Bruce E Compas; Judy Garber
Journal:  Clin Psychol Rev       Date:  2012-02-10

8.  Putative biological mechanisms for the association between early life adversity and the subsequent development of PTSD.

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9.  Increase of serum triiodothyronine concentration in soldiers with combat-related chronic post-traumatic stress disorder with or without alcohol dependence.

Authors:  Dalibor Karlović; Srdan Marusić; Marko Martinac
Journal:  Wien Klin Wochenschr       Date:  2004-06-30       Impact factor: 1.704

10.  Post-traumatic Stress Disorder Following Acute Delirium.

Authors:  Corey Bolton; Sarah Thilges; Carissa Lane; Jacob Lowe; Patricia Mumby
Journal:  J Clin Psychol Med Settings       Date:  2021-03
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