Neuroendocrine dysfunction in the acute phase of traumatic brain injury

Agha, Amar; Rogers, Bairbre; Mylotte, Darren; Taleb, Faisal; Tormey, William; Phillips, Jack; Thompson, Christopher J.

doi:10.1111/j.1365-2265.2004.02023.x

Cited by 273 publications

(239 citation statements)

References 50 publications

Supporting

Mentioning

215

Contrasting

Unclassified

Order By: Relevance

“…A positive correlation between cortisol concentrations and injury severity has been demonstrated in patients with mild or moderate TBI, but not in those with severe injury (51). On the contrary, adrenal insufficiency has been found in 16% of patients during the early phase post-TBI, suggesting post-traumatic damage at the hypothalamic -pituitary level (49). Primary or secondary adrenal insufficiency has been shown in 15% of patients with moderate to severe TBI, 7-60 days after injury, by using the low-dose ACTH test and corticotropin-releasing hormone (CRH) test (54).…”

Section: Consequences Of Tbimentioning

confidence: 91%

“…However, IGF-I levels did not differ between GHD and non-GHD patients (49). Elevated serum cortisol concentrations are generally present during the initial phase after trauma, and are associated with increased ACTH release, presumably driven by corticotropin-releasing factor (CRF), cytokines and noradrenergic system activation (50 -52).…”

Section: Consequences Of Tbimentioning

confidence: 99%

See 1 more Smart Citation

Hypopituitarism after traumatic brain injury

Bondanelli

Ambrosio²,

Zatelli³

et al. 2005

eur j endocrinol

182

152

View full text Add to dashboard Cite

Traumatic brain injury (TBI) is one of the main causes of death and disability in young adults, with consequences ranging from physical disabilities to long-term cognitive, behavioural, psychological and social defects. Post-traumatic hypopituitarism (PTHP) was recognized more than 80 years ago, but it was thought to be a rare occurrence. Recently, clinical evidence has demonstrated that TBI may frequently cause hypothalamic -pituitary dysfunction, probably contributing to a delayed or hampered recovery from TBI. Changes in pituitary hormone secretion may be observed during the acute phase post-TBI, representing part of the acute adaptive response to the injury. Moreover, diminished pituitary hormone secretion, caused by damage to the pituitary and/or hypothalamus, may occur at any time after TBI. PTHP is observed in about 40% of patients with a history of TBI, presenting as an isolated deficiency in most cases, and more rarely as complete pituitary failure. The most common alterations appear to be gonadotropin and somatotropin deficiency, followed by corticotropin and thyrotropin deficiency. Hyper-or hypoprolactinemia may also be present. Diabetes insipidus may be frequent in the early, acute phase post-TBI, but it is rarely permanent. Severity of TBI seems to be an important risk factor for developing PTHP; however, PTHP can also manifest after mild TBI. Accurate evaluation and long-term follow-up of all TBI patients are necessary in order to detect the occurrence of PTHP, regardless of clinical evidence for pituitary dysfunction. In order to improve outcome and quality of life of TBI patients, an adequate replacement therapy is of paramount importance.European Journal of Endocrinology 152 679-691

show abstract

Section: Consequences Of Tbimentioning

confidence: 91%

Section: Consequences Of Tbimentioning

confidence: 99%

Hypopituitarism after traumatic brain injury

Bondanelli

Ambrosio²,

Zatelli³

et al. 2005

eur j endocrinol

182

152

View full text Add to dashboard Cite

show abstract

“…Increased prolactin was the most commonly observed endocrine alteration. Hyperprolactinaemia is a wellknown phenomenon in the acute phase of a brain injury that may persist in 31% of patients during rehabilitation (30), and it was reported in up to 47% of the TBI patients who had other endocrine failures during long-term follow-up (31). Although hyperprolactinaemia may indicate pituitary stalk and/or hypothalamic injury, prolactin is one of the first hormones to increase in acute phases of severe illness, whereas prolactin is no longer as high in chronic phases (24).…”

Section: European Journal Of Endocrinologymentioning

confidence: 99%

Early endocrine alterations reflect prolonged stress and relate to 1-year functional outcome in patients with severe brain injury

Marina

Klose

Nordenbo

et al. 2015

European Journal of Endocrinology

View full text Add to dashboard Cite

Objective: Severe brain injury may increase the risk of developing acute and chronic hypopituitarism. Pituitary hormone alterations developed in the early recovery phase after brain injury may have implications for long-term functional recovery. The objective of the present study was to assess the pattern and prevalence of pituitary hormone alterations 3 months after a severe brain injury with relation to functional outcome at a 1-year follow-up. Design: Prospective study at a tertiary university referral centre. Methods: A total of 163 patients admitted to neurorehabilitation after severe traumatic brain injury (TBI, nZ111) or non-TBI (nZ52) were included. The main outcome measures were endocrine alterations 3.3 months (median) after the brain injury and their relationship to the functioning and ability of the patients at a 1-year follow-up, as measured by the Functional Independence Measure and the Glasgow Outcome Scale-Extended. Results: Three months after the injury, elevated stress hormones (i.e. 30 min stimulated cortisol, prolactin and/or IGF1) and/or suppressed gonadal or thyroid hormones were recorded in 68 and 32% of the patients respectively. At 1 year after the injury, lower functioning level (Functional Independence Measure) and lower capability of performing normal life activities (Glasgow Outcome Scale-Extended) were related to both the elevated stress hormones (P%0.01) and the reduced gonadal and/or thyroid hormones (P%0.01) measured at 3 months. Conclusion: The present study suggests that brain injury-related endocrine alterations that mimic secondary hypogonadism and hypothyroidism and that occur with elevated stress hormones most probably reflect a prolonged stress response 2-5 months after severe brain injury, rather than pituitary insufficiency per se. These endocrine alterations thus seem to reflect a more severe disease state and relate to 1-year functional outcome.

show abstract

“…However, the patient populations examined in most of these studies were inhomogeneous, with intervals between trauma and hormone assessment of 3 months to 23 years (8), 49^8 months (9), 12 -64 months (10) and 6-36 months (11), and differing methods and cutoffs for endocrine testing. In a recent study, hormonal assessments in a very early phase after TBI (mean 12 days after trauma) indicated a substantial prevalence of pituitary deficiencies (14). However, in this early phase, it is not clear whether these hormonal changes are specifically due to brain trauma or are an unspecific reaction to critical illness (15).…”

Section: Introductionmentioning

confidence: 99%

Prevalence of anterior pituitary insufficiency 3 and 12 months after traumatic brain injury

Schneider

Saller³

et al. 2006

eur j endocrinol

196

191

View full text Add to dashboard Cite

Objective: Cross-sectional studies report a high prevalence of hypopituitarism after traumatic brain injury (TBI); however, no longitudinal studies on time of manifestation and reversibility exist. This study was conducted to assess hypopituitarism 3 and 12 months after TBI. Design: This was a prospective, longitudinal, diagnostic study. Methods: Seventy-eight patients (52 men, 26 women, mean age 36.0 years) with TBI grades I -III and 38 healthy subjects (25 men, 13 women, mean age 36.4 years) as a control group for the GHRH þ arginine test were studied. The prevalence ofhypopituitarism was assessed 3 and 12 months after TBI by GHRH þ arginine test, short adrenocorticotropic hormone (ACTH) test, and basal hormone measurements in patients. Results: After 3 months, 56% of all patients had impairments of at least one pituitary axis with axes being affected as follows: gonadotropic 32%, corticotropic 19%, somatotropic 9% and thyrotropic 8%. After 12 months, fewer patients were affected, but in some cases new impairments occurred; 36% still had impairments. The axes were affected as follows after 12 months: gonadotropic 21%, somatotropic 10%, corticotropic 9% and thyrotropic 3%. Conclusions: Hypopituitarism occurs often in the post-acute phase after TBI and may normalize later, but may also develop after the post-acute phase of TBI.European Journal of Endocrinology 154 259-265

show abstract

Neuroendocrine dysfunction in the acute phase of traumatic brain injury

Abstract: Our data show that post-traumatic neuroendocrine abnormalities occur early and with high frequency, which may have significant implications for recovery and rehabilitation of TBI patients.

Cited by 273 publications

References 50 publications

Hypopituitarism after traumatic brain injury

Hypopituitarism after traumatic brain injury

Early endocrine alterations reflect prolonged stress and relate to 1-year functional outcome in patients with severe brain injury

Prevalence of anterior pituitary insufficiency 3 and 12 months after traumatic brain injury

Contact Info

Product

Resources

About