Occurrence of Pituitary Dysfunction following Traumatic Brain Injury

Department of Biomedical Sciences and Advanced Therapies-Section of Endocrinology, University of Ferrara, Ferrara, Italy.
Journal of Neurotrauma (Impact Factor: 3.71). 06/2004; 21(6):685-96. DOI: 10.1089/0897715041269713
Source: PubMed


Traumatic brain injury (TBI) may be associated with impairment of pituitary hormone secretion, which may contribute to long-term physical, cognitive, and psychological disability. We studied the occurrence and risk factors of pituitary dysfunction, including growth hormone deficiency (GHD) in 50 patients (mean age 37.6 +/- 2.4 years; 40 males, age 20-60 years; 10 females, age 23-87 years) with TBI over 5 years. Cranial or facial fractures were documented in 12 patients, and neurosurgery was performed in 14. According to the Glasgow Coma Scale (GCS), 16 patients had suffered from mild, 7 moderate, and 27 severe TBI. Glasgow Outcome Scale (GOS) indicated severe disability in 5, moderate disability in 11, and good recovery in 34 cases. Basal pituitary hormone evaluation, performed once at times variable from 12 to 64 months after TBI, showed hypogonadotrophic hypogonadism in 7 (14%), central hypothyroidism in 5 (10%), low prolactin (PRL) levels in 4 (8%), and high PRL levels in 4 (8%) cases. All subjects had normal corticotrophic and posterior pituitary function. Seven patients showed low insulin-like growth factor-I (IGF-I) levels for age and sex. Results of GHRH plus arginine testing indicated partial GHD in 10 (20%) and severe GHD in 4 (8%) cases. Patients with GHD were older (p <0.05) than patients with normal GH secretion. Magnetic resonance imaging demonstrated pituitary abnormalities in 2 patients; altogether pituitary dysfunction was observed in 27 (54%) patients. Six patients (12%) showed a combination of multiple abnormalities. Occurrence of pituitary dysfunction was 37.5%, 57.1%, and 59.3% in the patients with mild, moderate, and severe TBI, respectively. GCS scores were significantly (p <0.02) lower in patients with pituitary dysfunction compared to those with normal pituitary function (8.3 +/- 0.5 vs. 10.2 +/- 0.6). No relationship was detected between pituitary dysfunction and years since TBI, type of injury, and outcome from TBI. In conclusion, subjects with a history of TBI frequently develop pituitary dysfunction, especially GHD. Therefore, evaluation of pituitary hormone secretion, including GH, should be included in the long-term follow-up of all TBI patients so that adequate hormone replacement therapy may be administered.

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Available from: Maria Chiara Zatelli, May 21, 2014
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    • "The prevalence of post-traumatic AGHD can range from 9 to 28%; but this range may be severely underestimated, since many of studies have relied on insensitive biomarkers such as insulin growth factor-1 (IGF-1) to screen for GHD. This variation highlights the challenges for the accurate diagnosis of GHD in this sub-population (Bondanelli et al., 2004; Dimopoulou et al., 2004; Lieberman et al., 2008). "
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    ABSTRACT: Deficiency of growth hormone (GH) in adults results in a syndrome characterized by decreased muscle mass and exercise capacity, increased visceral fat, impaired quality of life, unfavorable alterations in lipid profile and markers of cardiovascular risk, decrease in bone mass and integrity, and increased mortality. When dosed appropriately, GH replacement therapy (GHRT) is well tolerated, with a low incidence of side effects, and improves most of the alterations observed in GH deficiency (GHD); beneficial effects on mortality, cardiovascular events, and fracture rates, however, remain to be conclusively demonstrated. The potential of GH to act as a mitogen has resulted in concern over the possibility of increased de novo tumors or recurrence of pre-existing malignancies in individuals treated with GH. Though studies of adults who received GHRT in childhood have produced conflicting reports in this regard, long-term surveillance of adult GHRT has not demonstrated increased cancer risk or mortality.
    Frontiers in Endocrinology 06/2013; 4:64. DOI:10.3389/fendo.2013.00064
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    • "Neuropathological alterations in neurons are sustained not only in moderate and severe TBI, but also in mild TBI, as indicated by metabolic depression indicative of neuronal injury [38], and other metabolic abnormalities [39–41]. Immune response and inflammation are considered primary to the progression of closed head injury, yet underlying mechanisms are not well understood. "
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    ABSTRACT: It is widely accepted that the brain responds to mechanical trauma and development of most neurodegenerative diseases with an inflammatory sequelae that was once thought exclusive to systemic immunity. Mostly cationic peptides, such as the β-defensins, originally assigned an antimicrobial function are now recognized as mediators of both innate and adaptive immunity. Herein supporting evidence is presented for the hypothesis that neuropathological changes associated with chronic disease conditions of the CNS involve abnormal expression and regulatory function of specific antimicrobial peptides. It is also proposed that these alterations exacerbate proinflammatory conditions within the brain that ultimately potentiate the neurodegenerative process.
    The Scientific World Journal 04/2012; 2012(3):905785. DOI:10.1100/2012/905785 · 1.73 Impact Factor
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    • "T < 10 nmol/l + low/normal LH/FSH preF: menstrual disturb. + E < 20pg/ml No 11 Bondanelli et al., 2004 "
    Brain Injury - Functional Aspects, Rehabilitation and Prevention, 03/2012; , ISBN: 978-953-51-0121-5
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