• DOI:10.1111/j.1749-6632.1997.tb48305.x
• Corpus ID: 33529212

The Dexamethasone Suppression Test and Glucocorticoid Receptors in Borderline Personality Disorder

@article{Grossman1997TheDS,
  title={The Dexamethasone Suppression Test and Glucocorticoid Receptors in Borderline Personality Disorder},
  author={Robert A Grossman and Rachel Yehuda and Larry J. Siever},
  journal={Annals of the New York Academy of Sciences},
  year={1997},
  volume={821}
}

• R. Grossman, R. Yehuda, L. Siever
• Published 1 June 1997
• Psychology, Biology
• Annals of the New York Academy of Sciences

Some researchers have forwarded the provocative idea that borderline personality disorder (BPD) is best conceptualized as a “complex posttraumatic stress disorder.”I4 The prevalence of trauma in patients with BPD is approximately 45-90%.2-5 Trauma in BPD appears to be experienced more often during childhood or laten~y,~.~.’ more frequently involves the patient’s and is notable for its reported severity and duration.’ Phenomenologically, patients with BPD and those with chronic posttraumatic stress disorder (PTSD) display numerous areas of overlapping symptoms including: mood instability; hyperarousal and/or numbing of feelings; avoidance; dissociative symptoms; irritability; aggression; impulsivity; and high rates of substance abuse and suicide. Indeed, approximately 30% of BPD patients also meet diagnostic criteria for PTSD.’ Given the prevalence of trauma in the history of individuals with BPD and the numerous areas of overlapping symptoms between BPD and PTSD, we have chosen to compare hypothalamic-pituitary-adrenal (HPA) axis alterations in these two disorders. The HPA axis in PTSD has been studied through a variety of means. Daily cortisol production was assessed through 24-hour urinary cortisol secretion and repeated sampling of plasma cortisol sampling over the diurnal cycle. As compared to normal controls, PTSD subjects demonstrated both decreased 24-hour urinary cortisol secretionlo.” and decreased average levels of plasma cortis01.’~-’~ In the later study, chronobiological analysis of cortisol data revealed that subjects with PTSD had increased “signal to noise ratio” (amplitude of the coefficient of variation), implying more dynamically active cortisol release and stronger circadian cortisol rhythm (as reflected by the circadian q~otient)l*.’~ in PTSD than in normal controls and subjects with major depression. In order for glucocorticoids to exert genomic effects, they must first couple with glucocorticoid receptors on the cell surface after which translocation to the cell nucleus can occur. Accompanying the aforementioned cortisol alterations is an increased number of lymphocyte glucocorticoid receptors in subjects with PTSD than in normal controls and subjects with major depressive d i~order . ’~ . ’~ Glucocorticoid