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  • Glucocorticoid receptor polymorphisms and post-traumatic stress disorder

    Author(s)
    W. Bachmann, Anthony
    L. Sedgley, Teresa
    Jackson, Richard V.
    N. Gibson, John
    McD. Young, Ross
    J. Torpy, David
    Griffith University Author(s)
    Jackson, Richard
    Year published
    2005
    Metadata
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    Abstract
    Post-traumatic stress disorder (PTSD) is reported in some studies to be associated with increased glucocorticoid (GC) sensitivity. Two common glucocorticoid receptor (GR) polymorphisms (N363S and BclI) appear to contribute to the population variance in GC sensitivity. There is some evidence that there may be a genetic predisposition to PTSD. Hence we studied 118 Vietnam war veterans with PTSD for (i) GR polymorphisms, particularly the N363S and the BclI polymorphisms which are thought to be GC sensitising, and (ii) two measures of GC sensitivity, the low-dose 0.25 mg dexamethasone suppression test (LD-DST) and the dermal ...
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    Post-traumatic stress disorder (PTSD) is reported in some studies to be associated with increased glucocorticoid (GC) sensitivity. Two common glucocorticoid receptor (GR) polymorphisms (N363S and BclI) appear to contribute to the population variance in GC sensitivity. There is some evidence that there may be a genetic predisposition to PTSD. Hence we studied 118 Vietnam war veterans with PTSD for (i) GR polymorphisms, particularly the N363S and the BclI polymorphisms which are thought to be GC sensitising, and (ii) two measures of GC sensitivity, the low-dose 0.25 mg dexamethasone suppression test (LD-DST) and the dermal vasoconstrictor assay (DVVA). The DST and GR polymorphisms were also performed in 42 combat exposed Vietnam war veterans without PTSD. Basal plasma cortisol levels were not significantly different in PTSD (399.5ᱹ.2 nmol/L, N=75) and controls (348.6Ჳ.0 nmol/L, N=33) and the LD-DST resulted in similar cortisol suppression in both groups (45.6ᳮ2 vs. 40.8ᴮ1%). The cortisol suppression in PTSD patients does not correlate with Clinician Administered PTSD Scores (CAPS), however there was a significant association between the BclI GG genotype and low basal cortisol levels in PTSD (P=0.048). The response to the DVVA was similar to controls (945ᱲ2, N=106 vs. 730Ჳ6, N=28, P=0.42). PTSD patients with the GG genotype, however, tended to be more responsive to DVVA and in this group the DVVA correlated with higher CAPS scores. The only exon 2 GR polymorphisms detected were the R23K and N363S. Heterozygosity for the N363S variant in PTSD, at 5.1% was not more prevalent than in other population studies of the N363S polymorphism in Caucasians (6.0-14.8%). The GG genotype of the BclI polymorphism found to be associated with increased GC sensitivity in many studies showed a tendency towards increased response with DVVA and correlated with higher CAPS scores. In conclusion, the N363S and BclI GR polymorphisms were not more frequent in PTSD patients than controls and reported population frequencies. Our PTSD group did not display GC hypersensitivity, as measured by the LD-DST and DVVA. In a subset of PTSD patients with the BclI GG genotype, CAPS scores and basal cortisol levels were negatively correlated.
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    Journal Title
    Psychoneuroendocrinology
    Volume
    30
    Issue
    3
    DOI
    https://doi.org/10.1016/j.psyneuen.2004.08.006
    Subject
    Medical and Health Sciences
    Psychology and Cognitive Sciences
    Publication URI
    http://hdl.handle.net/10072/26501
    Collection
    • Journal articles

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