Anterior hypopituitarism following traumatic brain injury.
OBJECTIVE
To review evidence that there exists a substantial sub-population of patients with endocrine disorders as a result of traumatic brain injury (TBI) and to underscore the importance of screening patients with TBI considered most at risk for hypopituitarism with the goal of attaining beneficial effects in terms of morbidity and quality of life.


METHODS
Reviewed recent literature regarding the frequency of TBI-induced hypopituitarism.


RESULTS
Studies by Kelly DF, Gaw Gonzalo IT, Cohan P, et al. Hypopituitarism following traumatic brain injury and aneurysmal subarachnoid hemorrhage: A preliminary report. Journal of Neurosurgery 2000;93:743-751, Lieberman SA, Oberoi AL, Gilkison CR, et al. Prevalence of neuroendocrine dysfunction in patients recovering from traumatic brain injury. Journal of Clinical Endocrinology and Metabolism 2001;86:2752-2756 and Aimaretti G, Ambrosio MR, Di Somma C, et al. Traumatic brain injury and subarachnoid haemorrhage are conditions at high risk for hypopituitarism. Screening study at 3 months after the brain injury, In press., found that about one-half to one-third of patients with TBI had anterior pituitary hormone deficiencies, including growth hormone (GH) deficiency in 15-21%, and subtle deficiencies in thyroid, adrenal and gonadal axes. One or more hormonal deficiencies produce diverse physical and psychological symptoms that may mimic symptoms attributed to brain trauma and may impair rehabilitation. A more general concern is the fact that hypopituitarism increases the risk of significant morbidity (e.g. ischaemic heart disease) and mortality (shortened life span).


CONCLUSIONS
To attain maximal improvement in mental and physical functioning as well as in quality of life for victims of TBI, it is crucial that anterior pituitary hormonal function be assessed. Appropriate hormone replacement therapy for those patients with both TBI and TBI-induced pituitary function impairment could, for the first time, allow treatment and correction of underlying causes of TBI sequelae rather than merely symptomatic treatment.
Urban
R J
RJ
Department of Internal Medicine, Division of Endocrinology, University of Texas Medical Branch, Galveston, TX, USA.
Harris
P
P
Masel
B
B
D001930:Brain Injuries / Q000150:complications* / Q000453:epidemiology; D005260:Female; D020249:Hormone Replacement Therapy / Q000379:methods; D019382:Human Growth Hormone / Q000172:deficiency; D006801:Humans; D007018:Hypopituitarism / Q000188:drug therapy / Q000453:epidemiology / Q000209:etiology*; D007031:Hypothalamus / Q000293:injuries; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D008297:Male; D010903:Pituitary Gland, Anterior / Q000098:blood supply / Q000293:injuries*; D010907:Pituitary Hormones / Q000172:deficiency; D015995:Prevalence
D010907:Pituitary Hormones; D019382:Human Growth Hormone; D007334:Insulin-Like Growth Factor I