title: Hypopituitarism following severe traumatic brain injury.
abstract: Although hypopituitarism is a known complication of traumatic head injury, it may be under-recognized due to its subtle clinical manifestations. To address this issue, we determine the prevalence of neuroendocrine abnormalities in patients rehabilitating from severe traumatic brain injury (Glasgow Coma Scale < or = 8). 76 patients (mean age 39 +/- 14 yr; range 18-65; 53 males and 23 females; BMI 25.8 +/- 4.2 kg/m2; mean +/- SD) with a severe traumatic brain injury, an average of 22 +/- 10 months before this study (median, 20 months), underwent a series of standard endocrine tests, including TSH, free T4, T4, T3, prolactin, testosterone (males), estradiol (females), cortisol, ACTH, GH, and IGF-I. All subjects also underwent GH response to GHRH + arginine. Growth hormone deficiency (GHD) was defined as a GH response < 9 microg/L to GHRH + arginine and was confirmed by ITT (< 3 microg/L). Pituitary deficiency was shown in 24% of the patients (18/76). 8% (n = 6) had GHD (GH-peak range [GHRH + arginine]: 2.8-6.3 microg/L; GH-peak range [ITT]: 1.5-2.2 microg/L; IGF-I range: 62-174 microg/L). 17% (n = 13) had hypogonadism (total testosterone < 9.5 nmol/L and low gonadotropins in 12 males; low estradiol, and low gonadotropins in 1 female). Total testosterone levels did not correlate with BMI or age. 2 males with hypogonadism also showed a mild hyperprolactinemia (33 and 41 ng/ml). 3% (n = 2) patients had partial ACTH-deficiency (cortisol-peak [ITT] 392 and 417 nmol/L) and 3% (n = 2) had TSH-deficiency. In summary, we have found hypopituitarism in one-fourth of patients with predominantly secondary hypogonadism and GHD. These findings strongly suggest that patients who suffer head trauma must routinely include neuroendocrine evaluations.
authors.affiliation: Institute of Cardio-Diabetes, Technology-Center Bochum, Bochum, Germany. burkhard.herrmann@uni-essen.de
authors.forename: B L
authors.initials: BL
authors.lastname: Herrmann
authors.forename: J
authors.initials: J
authors.lastname: Rehder
authors.forename: S
authors.initials: S
authors.lastname: Kahlke
authors.forename: H
authors.initials: H
authors.lastname: Wiedemayer
authors.forename: A
authors.initials: A
authors.lastname: Doerfler
authors.forename: W
authors.initials: W
authors.lastname: Ischebeck
authors.forename: R
authors.initials: R
authors.lastname: Laumer
authors.forename: M
authors.initials: M
authors.lastname: Forsting
authors.forename: D
authors.initials: D
authors.lastname: Stolke
authors.forename: K
authors.initials: K
authors.lastname: Mann
mesh_terms: D000293:Adolescent; D000324:Adrenocorticotropic Hormone / Q000172:deficiency; D000328:Adult; D000368:Aged; D001930:Brain Injuries / Q000150:complications*; D005260:Female; D013006:Growth Hormone / Q000172:deficiency; D006801:Humans; D007006:Hypogonadism / Q000209:etiology; D007018:Hypopituitarism / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D011446:Prospective Studies; D013972:Thyrotropin / Q000172:deficiency
chemical_list: D000324:Adrenocorticotropic Hormone; D013972:Thyrotropin; D013006:Growth Hormone