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: 3.97). 06/2004; 21(6):685-96. DOI: 10.1089/0897715041269713
Source: PubMed

ABSTRACT 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.

  • [Show abstract] [Hide abstract]
    ABSTRACT: Traumatic brain injury (TBI) is a common event in childhood. It is a recognised cause of hypopituitarism both in adult and paediatric patients. Routine endocrine evaluation has been proposed for adult TBI-survivors; nevertheless, incongruous data have been reported in children. The goal of this study was to describe the prevalence of pituitary dysfunction after TBI in a cohort of children. This is a cross-sectional study comprising retrospective medical record review and prospective testing. Children with brain injury discharged from the Paediatric Intensive Care Unit from year 2004 to 2009 were recruited. Height and weight were recorded, systemic examination was performed and baseline pituitary function tests were undertaken. Provocative tests were performed only if abnormal basal levels were detected. Thirty-six patients were collected; the mean age at assessment was 7.2 years and the mean interval since injury 3.3 years. All patients had skull fracture or intracranial haemorrhage; 36.6 % of them had moderate to severe TBI. No abnormalities were found on examination. Low serum IGF 1 levels were detected in four patients and two patients had low serum cortisol levels with inappropriately normal plasma ACTH concentrations. No evidence of pituitary dysfunction was observed in these patients after clinical follow-up, repeated baseline hormone levels or dynamic function tests. No endocrine sequelae have been detected in this population. The routine endocrine evaluation in children with mild to moderate TBI might not be justified, according to our findings.
    Journal of endocrinological investigation 02/2014; 37(2):143-8. · 1.65 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Traumatic Brain Injury (TBI) initiates a cascade of neuromodulatory damage that blurs the distinctions between physical and psychological medicine. Monitoring endocrine function through labs is not part of the medical care algorithm for treatment of TBI, but the clinical symptoms are easily misidentified as they include: depression, fatigue, poor concentration, irritability and a decline in overall cognitive functioning. The reciprocal flow of change between neuroendocrine health and psychosocial health is well established within the field of neuroscience, social psychology, endocrinology and behavioral neurology, but has not translated into patient care. This paper outlines common neuroendocrine disruptions secondary to TBI and their clinical implications for treating mental health professionals. Wider adoption of the consensus guidelines on the detection and monitoring of endocrine abnormalities post-TBI may diminish the severity of functional impairment and improve quality of life.
    Neurorehabilitation 05/2014; · 1.74 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Hypopituitarism is common after moderate and severe traumatic brain injury (TBI). Herein we address the association between mild TBI and pituitary and metabolic function in retired football players. NFL retirees aged 30-65 years with poor quality of life (QoL) were prospectively enrolled. Pituitary and metabolic syndrome testing was performed. Using a glucagon stimulation test, growth hormone deficiency (GHD) was defined with a standard cut-point of 3ng/ml and with a more stringent BMI-adjusted cut-point. Subjects with and without hormonal deficiency (HD) were compared in terms of QoL, International Index of Erectile Function (IIEF) scores, metabolic parameters and football career data. Of 74 subjects, 6 were excluded due to non-football related TBIs. Of the remaining 68 subjects (mean age 47.3±10.2 years, median NFL years 5, median NFL concussions 3, mean BMI 33.8±6.0), 28 (41.2%) were GHD using a peak GH cutoff of <3ng/ml. However, with a BMI-adjusted definition of GHD, 13 of 68 (19.1%) were GHD. Using this BMI-adjusted definition, overall HD was found in 16(23.5%) subjects: 10(14.7%) with isolated GHD, 3(4.4%) with isolated hypogonadism and 3(4.4%) with both GHD and hypogonadism. Subjects with HD had lower mean scores on the IIEF survey (p=0.016) and trended toward lower scores on SF-36 MCS (p=0.113). Metabolic syndrome was present in 50% of subjects: 5 of 6 (83%) with hypogonadism and 29 of 62 (46.8%) without hypogonadism (p=0.087). Age, BMI, median years in NFL, games played, number of concussions and acknowledged use of performance-enhancing steroids were similar between HD and non-HD groups. In summary, in this cohort of retired NFL players with poor QoL, 23.5% had HD (19% GHD (using BMI-adjusted definition), 9% hypogonadism; 50% had metabolic syndrome. Although the cause of HD is unclear, these results suggest GHD and hypogonadism may contribute to poor QoL, erectile dysfunction and metabolic syndrome in this population.
    Journal of neurotrauma 02/2014; · 4.25 Impact Factor


Available from
May 21, 2014