Abstract
Studies of traumatic brain injury from all causes have found evidence of chronic hypopituitarism, defined by deficient production of one or more pituitary hormones at least 1 year after injury, in 25–50% of cases. Most studies found the occurrence of posttraumatic hypopituitarism (PTHP) to be unrelated to injury severity. Growth hormone deficiency (GHD) and hypogonadism were reported most frequently. Hypopituitarism, and in particular adult GHD, is associated with symptoms that resemble those of PTSD, including fatigue, anxiety, depression, irritability, insomnia, sexual dysfunction, cognitive deficiencies, and decreased quality of life. However, the prevalence of PTHP after blast-related mild TBI (mTBI), an extremely common injury in modern military operations, has not been characterized. We measured concentrations of 12 pituitary and target-organ hormones in two groups of male US Veterans of combat in Iraq or Afghanistan. One group consisted of participants with blast-related mTBI whose last blast exposure was at least 1 year prior to the study. The other consisted of Veterans with similar military deployment histories but without blast exposure. Eleven of 26, or 42% of participants with blast concussions were found to have abnormal hormone levels in one or more pituitary axes, a prevalence similar to that found in other forms of TBI. Five members of the mTBI group were found with markedly low age-adjusted insulin-like growth factor-I (IGF-I) levels indicative of probable GHD, and three had testosterone and gonadotropin concentrations consistent with hypogonadism. If symptoms characteristic of both PTHP and PTSD can be linked to pituitary dysfunction, they may be amenable to treatment with hormone replacement. Routine screening for chronic hypopituitarism after blast concussion shows promise for appropriately directing diagnostic and therapeutic decisions that otherwise may remain unconsidered and for markedly facilitating recovery and rehabilitation.
Highlights
Recent studies investigating chronic pituitary dysfunction resulting from TBI have reported a prevalence of posttraumatic hypopituitarism (PTHP) ranging from 5 to 95% with a median of 35%, the variation being primarily due to differences in screening criteria (Bavisetty et al, 2008; Srinivasan et al, 2009; Berg et al, 2010; Englander et al, 2010; High et al, 2010; Kokshoorn et al, 2010, 2011; Krahulik et al, 2010; Park et al, 2010; Pavlovic et al, 2010; Reimunde et al, 2011; Schneider et al, 2011)
The mild TBI (mTBI) Veteran participants (T group) whose samples were obtained from the repository were a convenience sample of 26 male Veterans recruited from VA Puget Sound Health Care System (VAPSHCS), all of whom had documented hazardous duty experience in Iraq and/or Afghanistan with the U.S Armed Forces and had reported experiencing at least one blast exposure in the war zone that resulted in acute mTBI as defined by ACRM criteria (American Congress of Rehabilitation Medicine, 1993) except that Glasgow Coma Scale scores were not obtained in the combat setting
Medications with potential neuroendocrine effects taken by deployment control (DC) subjects were opiates (1/7), selective serotonin reuptake inhibitors (SSRIs) (1/7), and serotonin and norepinephrine reuptake inhibitors (SNRIs) (1/7). Five subjects in this group were not taking any neuroactive medications. Our findings in this preliminary study support the hypothesis that blast mTBI carries a risk of PTHP similar to that found in several previous studies of hypopituitarism in the general population after TBI from all causes
Summary
Recent studies investigating chronic pituitary dysfunction resulting from TBI have reported a prevalence of posttraumatic hypopituitarism (PTHP) ranging from 5 to 95% with a median of 35%, the variation being primarily due to differences in screening criteria (Bavisetty et al, 2008; Srinivasan et al, 2009; Berg et al, 2010; Englander et al, 2010; High et al, 2010; Kokshoorn et al, 2010, 2011; Krahulik et al, 2010; Park et al, 2010; Pavlovic et al, 2010; Reimunde et al, 2011; Schneider et al, 2011). Pituitary hormone disorders are frequently among the immediate consequences of TBI; some resolve during the following months while a smaller proportion of new dysfunctions emerge (Agha et al, 2005; Aimaretti et al, 2005; Schneider et al, 2006, 2011; Tanriverdi et al, 2006, 2008b; Klose et al, 2007; Krahulik et al, 2010). The risk factors and the mechanisms, other than immediate trauma-induced tissue damage and subsequent edema, for chronic hypothalamo-pituitary dysfunction due to TBI are unclear. There is evidence that the apolipoprotein E (APOE) ε3/ε3 genotype may be associated with a reduced risk of TBI-related hypopituitarism. Pituitary dysfunction in patients with TBI has been found to be significantly less prevalent in individuals with the APOE ε3/ε3 genotype (17.7%)
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