{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T10:51:52Z","timestamp":1789123912612,"version":"build-2803163510"},"reference-count":53,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2004,4,22]],"date-time":"2004-04-22T00:00:00Z","timestamp":1082592000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clinical Endocrinology"],"published-print":{"date-parts":[[2004,5]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:bold><jats:sc>background\u2002<\/jats:sc><\/jats:bold> Pituitary hormone abnormalities have been reported in up to 50% of survivors of traumatic brain injury (TBI) who were investigated several months or longer following the event. The frequency of pituitary dysfunction in the early post\u2010TBI period is unknown.<\/jats:p><jats:p><jats:bold><jats:sc>aim\u2002<\/jats:sc><\/jats:bold> To evaluate the prevalence of anterior and posterior pituitary dysfunction in the early phase following TBI.<\/jats:p><jats:p><jats:bold><jats:sc>subjects\u2002<\/jats:sc><\/jats:bold> Fifty consecutive patients admitted to the neurosurgical unit with severe or moderate TBI [initial Glasgow Coma Scale (GCS) score 3\u201313], and 31 matched healthy control volunteers were studied.<\/jats:p><jats:p><jats:bold><jats:sc>methods\u2002<\/jats:sc><\/jats:bold> The glucagon stimulation test (GST) was performed at a median of 12\u00a0days (range 7\u201320) following TBI. Baseline thyroid function, PRL, IGF\u20101, gonadotrophins, testosterone or oestradiol, plasma sodium, plasma and urine osmolalities or the standard observed water deprivation test were performed. The control subjects underwent the GST for GH and cortisol responses; other parameters were compared to locally derived reference ranges.<\/jats:p><jats:p><jats:bold><jats:sc>results\u2002<\/jats:sc><\/jats:bold> Control data indicated that peak serum GH of &gt;\u00a05\u00a0ng\/ml and cortisol &gt;\u00a0450\u00a0nmol\/l following glucagon stimulation should be taken as normal. Nine TBI patients (18%) had GH response &lt;\u00a05\u00a0ng\/ml (12\u00a0mU\/l). Eight patients (16%) had peak cortisol responses &lt;\u00a0450\u00a0nmol\/l. Compared to controls, basal cortisol values were significantly lower in patients with subnormal cortisol responses to glucagon and significantly higher in patients with normal cortisol responses (<jats:italic>P<\/jats:italic>\u00a0&lt;\u00a00\u00b705). GH and cortisol deficiencies were unrelated to patient age, BMI, initial GCS or IGF\u20101 values (<jats:italic>P<\/jats:italic>\u00a0&gt;\u00a00\u00b705). Forty patients (80%) had gonadotrophin deficiency, with low sex steroid concentrations, which was unrelated to the presence of hyperprolactinaemia. In males there was a positive correlation between serum testosterone concentration and GCS (<jats:italic>r<\/jats:italic>\u00a0= 0\u00b732, <jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b704). One patient had TSH deficiency. Hyperprolactinaemia was present in 26 patients (52%) and serum PRL levels correlated negatively with the GCS score (<jats:italic>r<\/jats:italic>\u00a0=\u22120\u00b736, <jats:italic>P<\/jats:italic>\u00a0=\u00a00\u00b7011). Thirteen patients (26%) had cranial diabetes insipidus (DI) and seven (14%) had syndrome of inappropriate ADH secretion.<\/jats:p><jats:p><jats:bold><jats:sc>conclusion\u2002<\/jats:sc><\/jats:bold> Our data show that post\u2010traumatic neuroendocrine abnormalities occur early and with high frequency, which may have significant implications for recovery and rehabilitation of TBI patients.<\/jats:p>","DOI":"10.1111\/j.1365-2265.2004.02023.x","type":"journal-article","created":{"date-parts":[[2004,12,21]],"date-time":"2004-12-21T23:11:30Z","timestamp":1103670690000},"page":"584-591","source":"Crossref","is-referenced-by-count":243,"title":["Neuroendocrine dysfunction in the acute phase of traumatic brain injury"],"prefix":"10.1111","volume":"60","author":[{"given":"Amar","family":"Agha","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bairbre","family":"Rogers","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Darren","family":"Mylotte","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Faisal","family":"Taleb","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William","family":"Tormey","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jack","family":"Phillips","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher J.","family":"Thompson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2004,4,22]]},"reference":[{"key":"e_1_2_6_2_1","doi-asserted-by":"publisher","DOI":"10.1097\/00005373-198704000-00007"},{"key":"e_1_2_6_3_1","first-page":"285","volume-title":"Principles and Practice of Endocrinology and Metabolism","author":"Baylis P.H.","year":"2001"},{"key":"e_1_2_6_4_1","doi-asserted-by":"publisher","DOI":"10.1210\/jcem.85.4.6506"},{"key":"e_1_2_6_5_1","doi-asserted-by":"crossref","first-page":"918","DOI":"10.1093\/ajcn\/55.5.918","article-title":"Body composition in growth hormone deficient adults","volume":"55","author":"Binnerts A.","year":"1992","journal-title":"American Journal of Clinical Nutrition"},{"key":"e_1_2_6_6_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1651-2227.1989.tb11242.x"},{"key":"e_1_2_6_7_1","doi-asserted-by":"publisher","DOI":"10.1159\/000116907"},{"key":"e_1_2_6_8_1","first-page":"617","article-title":"Glucagon\u2010initiated human growth hormone release: a comparative study","volume":"107","author":"Cain J.P.","year":"1972","journal-title":"Canadian Medical Association Journal"},{"key":"e_1_2_6_9_1","doi-asserted-by":"publisher","DOI":"10.1080\/026990599121016"},{"key":"e_1_2_6_10_1","doi-asserted-by":"publisher","DOI":"10.1097\/00005373-198809000-00011"},{"key":"e_1_2_6_11_1","doi-asserted-by":"publisher","DOI":"10.1210\/jc.84.6.1919"},{"key":"e_1_2_6_12_1","doi-asserted-by":"publisher","DOI":"10.1056\/NEJMra020529"},{"key":"e_1_2_6_13_1","doi-asserted-by":"crossref","first-page":"695","DOI":"10.1152\/jappl.1991.70.2.695","article-title":"Growth hormone treatment in growth hormone deficient adults. 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