Prevention of Posttraumatic Stress Disorder (PTSD) With Early Hydrocortisone Treatment: Pilot
Information source: Kent State University
ClinicalTrials.gov processed this data on December 21, 2014
Link to the current ClinicalTrials.gov record.
Condition(s) targeted: Posttraumatic Stress Disorder
Intervention: Hydrocortisone (Drug); placebo (Drug)
Sponsored by: Kent State University
Official(s) and/or principal investigator(s):
Doulas L Delahanty, PhD, Principal Investigator, Affiliation: Kent State University
Douglas L Delahanty, PhD, Phone: (330) 672-2395, Email: firstname.lastname@example.org
People experience a wide range of outcomes following a traumatic event. Although rates
differ depending on type of trauma, 20-60% of trauma victims may develop posttraumatic
stress disorder (PTSD). However, not all trauma victims develop PTSD. Previous research
has found that trauma victims who develop PTSD excrete lower levels of urinary cortisol
immediately after a trauma than victims who do not develop PTSD. Other research has
suggested that increasing levels of cortisol may protect against the development of PTSD in
patients such as yourself- but this has not yet been examined. Cortisol is a naturally
occurring hormone in your body, and the present study is designed to test whether increasing
cortisol levels can protect against or decrease symptoms of PTSD. Participants in this
study will be randomly assigned to one of two treatment groups. Participants will receive
either hydrocortisone (20mg, twice per day) or a placebo (a sugar pill) for 10 days with a
six-day taper. There is an equal chance of being in either treatment group, and neither the
participant nor the experimenters will know which treatment was received (except in case of
Official title: Prevention of PTSD With Early Hydrocortisone Treatment: Pilot
Study design: Allocation: Randomized, Endpoint Classification: Efficacy Study, Intervention Model: Parallel Assignment, Masking: Double Blind (Subject, Investigator), Primary Purpose: Prevention
Primary outcome: Clinician-Administered PTSD Scale (CAPS)
Posttraumatic stress disorder (PTSD) is the fourth most common psychiatric disorder and is
estimated to affect more than ten million American children and adults at some point in
their lives. Although a number of pre-, peri-, and acute phase post-trauma variables (e. g.,
prior trauma history, subjective life threat, injury) have been shown to increase one's risk
of developing PTSD, initial psychological reaction to a traumatic event is an imperfect
predictor of subsequent diagnosis. In addition, early psychological interventions have
generally proven ineffective, and in some cases, detrimental with regards to subsequent
symptomatology. In light of this, researchers have recently begun to examine possible
pharmacological interventions that could be administered in the acute phase of responding to
trauma to prevent or reduce the severity of subsequent post-traumatic stress.
Biopsychological research has frequently (but not always) indicated that patients with PTSD
excrete lower levels of cortisol than similarly-exposed trauma victims who do not develop
PTSD. Further, recent research has shown that lower cortisol levels present soon after a
trauma are associated with increased risk for developing PTSD symptoms. These results
suggest that higher levels of cortisol during and immediately after a traumatic event may
buffer the development of PTSD symptoms. In addition, preliminary findings have suggested
that exogenously elevating patients' levels of cortisol during and immediately following
trauma results in decreased incidence of PTSD. However, these data were collected on
relatively small samples of trauma patients with confounding medical conditions (e. g.,
shock, cardiac surgery, or paralysis). A randomized controlled trial (RCT) is necessary to
determine the efficacy of early cortisol administration at buffering the development of
post-traumatic stress in a heterogeneous trauma sample.
Prior to conducting a large-scale RCT, it is necessary to pilot test the efficacy of early
cortisol treatment at reducing or preventing PTSD symptoms in a representative sample of
heterogeneous trauma victims. The proposed research is designed to examine the efficacy of
hydrocortisone (commercially-available cortisol) in preventing post-traumatic stress in a
small-scale, randomized, double-blind trial. More specifically, incidence of PTSD and
comorbid disorders (i. e., mood, anxiety and substance abuse/dependence disorders), severity
of symptoms, health-related quality of life, and hormonal correlates of distress will be
prospectively examined in trauma victims who are randomly assigned to receive either a
course of hydrocortisone or placebo within 12 hours of the traumatic event. As
psychological and physiological reactions to trauma may develop over a number of months
post-trauma, prospective follow-up will allow us to examine the efficacy of cortisol
administration at reducing both early as well as delayed development of symptoms. The
proposed research will provide pilot data and effect size estimates for a subsequent
large-scale trial, should pilot results be promising.
Specific objectives of the proposed research include:
1. Examination of the effects of early (within 12 hours of trauma) cortisol administration
on subsequent symptoms of PTSD in trauma victims. Specifically, victims admitted to
the Level 1 trauma unit of a local hospital will be randomly assigned to receive
double-blind, low-dose cortisol (20mg, twice daily: bid) or placebo for ten days plus a
6-day taper period. Symptoms of psychopathology will be measured at 1- and 3-months
post-trauma. Secondary analyses will examine the effects of cortisol on disorders
commonly comorbid with PTSD (i. e., anxiety, mood, and substance abuse/dependence
disorders) and on health-related quality of life.
2. Examination of the extent to which early cortisol administration influences the
relationship between preexisting and trauma-related factors and psychophysiological
responses to trauma. In particular, as lifetime incidence of psychopathology, prior
trauma exposure, and injury severity have been associated with increased risk for PTSD,
we will examine whether this relationship is weakened in patients receiving the
cortisol regimen. Due to budgetary constraints of the R34 mechanism and the exploratory
nature of the proposed research, we will not be able to recruit enough participants to
sufficiently examine this objective, and it is thus considered a secondary aim.
However, results will be used to strengthen and guide the design of a subsequent R01
Minimum age: 18 Years.
Maximum age: N/A.
- involved in a traumatic event and admitted to the level 1 trauma center within 12
hours after the trauma
- Glasgow coma scale score of less than 14 (at the time that you speak to patient)
- Amnestic for the events during and immediately following the traumatic event
- Unable to understand consent procedure or current substance abuse
- Traumatic event occurred more than 12 hours before initial medication dose can be
given (i. e., patient life-flight or transferred after significant time has passed).
- Allergy to cortisol.
- Pregnant or breast-feeding
- Traumatic event of potentially ongoing nature that the participant is likely to be
re-exposed to during the study (e. g. domestic violence)
- Presence of injuries (e. g. pelvic or lower extremity fractures) requiring readmission
for surgery 1-2 weeks later once swelling has diminished. Patients requiring such
delayed operative procedures will be excluded.
- Presence of medical condition that contraindicates the administration of cortisol,
including (but not necessarily limited to) peptic ulcers, Cushing's disease,
hypothyroidism, current alcoholism or cirrhosis, hepatitis, diverticulitis,
nonspecific ulcerative colitis, myasthenia gravis, seizure disorders, renal
insufficiency, disorders of immunosuppression, current viral or bacterial infection,
diabetes mellitus, history of myocardial infarction, or recipient of solid organ or
bone marrow transplant.
- On a current corticosteroid regimen (inhaled, oral, or injection). This may include
patients with asthma, multiple sclerosis, arthritis, allergic conditions, optic
neuritis, or tuberculosis
- Corticosteroid use in the previous 6 months
- Current use of medications that may have potentially dangerous interactions with
cortisol including other corticosteroids, any immunosuppressant medications, drugs
affecting hepatic microsomal enzymes, cyclosporine, and anticholinesterase agents.
- Injuries requiring treatment with steroids (e. g., suspected spinal cord injury,
- Patients must be able to take oral medications within 12 hours post-trauma.
Locations and Contacts
Douglas L Delahanty, PhD, Phone: (330) 672-2395, Email: email@example.com
Akron City Hospital, Akron,, Ohio 44309, United States; Recruiting
William Wallon, MD, Phone: 330-971-1721, Email: FallonW@summa-health.org
William Fallon, MD, Sub-Investigator
Delahanty DL, Raimonde AJ, Spoonster E. Initial posttraumatic urinary cortisol levels predict subsequent PTSD symptoms in motor vehicle accident victims. Biol Psychiatry. 2000 Nov 1;48(9):940-7.
Delahanty, D.L., Royer, D.K., Spoonster, E., & Raimonde, A.J. (2003). Peritraumatic dissociation is inversely related to catecholamine levels in initial urine samples of motor vehicle accident victims. Journal of Trauma and Dissociation, 4, 65-80.
Flesher MR, Delahanty DL, Raimonde AJ, Spoonster E. Amnesia, neuroendocrine levels and PTSD in motor vehicle accident victims. Brain Inj. 2001 Oct;15(10):879-89.
Delahanty DL, Raimonde AJ, Spoonster E, Cullado M. Injury severity, prior trauma history, urinary cortisol levels, and acute PTSD in motor vehicle accident victims. J Anxiety Disord. 2003;17(2):149-64.
Delahanty DL, Bogart LM, Figler JL. Posttraumatic stress disorder symptoms, salivary cortisol, medication adherence, and CD4 levels in HIV-positive individuals. AIDS Care. 2004 Feb;16(2):247-60.
Pitman RK, Sanders KM, Zusman RM, Healy AR, Cheema F, Lasko NB, Cahill L, Orr SP. Pilot study of secondary prevention of posttraumatic stress disorder with propranolol. Biol Psychiatry. 2002 Jan 15;51(2):189-92.
Schelling G, Kilger E, Roozendaal B, de Quervain DJ, Briegel J, Dagge A, Rothenhäusler HB, Krauseneck T, Nollert G, Kapfhammer HP. Stress doses of hydrocortisone, traumatic memories, and symptoms of posttraumatic stress disorder in patients after cardiac surgery: a randomized study. Biol Psychiatry. 2004 Mar 15;55(6):627-33.
Schelling G, Briegel J, Roozendaal B, Stoll C, Rothenhäusler HB, Kapfhammer HP. The effect of stress doses of hydrocortisone during septic shock on posttraumatic stress disorder in survivors. Biol Psychiatry. 2001 Dec 15;50(12):978-85.
Starting date: June 2005
Last updated: January 27, 2009