Increased adrenocorticotropin suppression after dexamethasone administration in sexually abused adolescents with posttraumatic stress disorder.

Evidence suggests that individuals with posttraumatic stress disorder (PTSD) have enhanced sensitization of the hypothalamic-pituitary-adrenocortical (HPA) axis. Fourteen adolescent inpatients with DSM-IV PTSD were compared with 14 adolescent hospitalized controls without current axis I diagnoses. All patients were drug-naive. The causative trauma had been sexual abuse in all cases. Dexamethasone, 1 mg orally, was given at 11 PM, 5 days after admission. Baseline blood samples were obtained at 8 AM, and on the following day, adrenocorticotropin (ACTH) and cortisol levels were measured at 8 AM, 4 PM, and 11 PM. Clinical assessment included the Impact of Event Scale, Stanford Acute Stress Reaction Questionnaire, Beck Depression Inventory, and Coping Inventory for Stressful Situations. Post-DST ACTH levels were significantly lower in PTSD than in control adolescents (at 8 AM, P <0.005; at 4 PM, P <0.001; and at 11 PM, P <0.05). In patients, post-DST cortisol levels were reduced but not significantly. No correlations were found between ACTH and cortisol levels and time elapsed since trauma. These results demonstrate that sexually abused adolescents with PTSD show ACTH hypersuppression to DST, suggesting enhanced glucocorticoid receptor sensitivity in the pituitary.