Häufige hormonelle Störungen bei Hirnverletzten (Follow-up)

Neuere Studien aus dem Jahr 2009 bestätigen, was wir schon im September 2005 berichtet haben (siehe hier...): Zahlreiche hirnverletzte Menschen weisen Störungen des Hormonsystems (v.a. aber nicht nur des Hypothalamus und der Hirnanhangdrüse) auf. Eine Studie am Universitätsspital Essen (Deutschland) an 246 Patienten mit einer Hirnverletzung zeigt, dass je nach Hormon bis zu 50% der untersuchten Patienten zu tiefe Hormonspiegel aufwiesen. Eine Studie der Abteilung Neurochirurgie der Universität Erlangen (Deutschland) weist nach, dass die Computer-Tomogramm-Befunde (CT), die unmittelbar nach dem Unfall erhoben wurden, keine Voraussage über spätere Hormonstörungen erlaubten.


Im Anhang finden Sie die Abstracts der Studien. Diese können beispielsweise bei www.medline.ch bestellt werden.

Exp Clin Endocrinol Diabetes. 2009 Aug 18. [Epub ahead of print]

Prevalence of Anterior Pituitary Dysfunction in Patients following Traumatic Brain Injury in a German Multi-centre Screening Program.

Berg C, Oeffner A, Schumm-Draeger PM, Badorrek F, Brabant G, Gerbert B, Bornstein S, Zimmermann A, Weber M, Broecker-Preuss M, Mann K, Herrmann BL.

Clinic of Endocrinology, University Hospital of Essen, Germany.

INTRODUCTION: We determined the prevalence of anterior pituitary dysfunction in a multi-centre screening program across five German endocrine centres in patients rehabilitating from TBI (GCS<13). PATIENTS & METHODS: 246 patients (39+/-14 yrs; 133 males, 12+/-8 months after TBI) underwent a series of baseline endocrine tests with central assessment of TSH, free T4, prolactin, LH, FSH, testosterone (m), estradiol (f), cortisol, GH, and IGF-I. If IGF-I was <-2 SDS dynamic testing was performed. GHD was defined according to BMI-dependent cut-off values for GH response to GHRH+arginine of <4.2, <8.0 and <11.5 ng/ml in obese, overweight and lean subjects, respectively, or <3 micro g/l in ITT. Hypocortisolism was suggested when basal cortisol was <200 nmol/l and confirmed by ITT (peak<500 nmol/l). RESULTS: In TBI patients some degree of impaired pituitary function was shown in 21% (n=52/246). Total, multiple and isolated deficits were present in 1%, 2% and 18%, respectively. 19% had an IGF-I of <-1 SDS, 9% of <-2 SDS. In 5% GHD was confirmed. 9% had hypogonadism. 4% had hypocortisolism and 1% of patients had confirmed ACTH-deficiency. 12% had TSH-deficiency. SUMMARY: In summary, in this large series carried out on an unselected group of TBI survivors we have found hypopituitarism in every fifth patient with predominantly secondary hypogonadism and hypothyreosis. Regarding somatotrope insufficiency IGF-I is decreased in 50% of GHD patients. CONCLUSION: These findings strongly suggest that patients who suffer head trauma should routinely undergo endocrine evaluation. © J. A. Barth Verlag in Georg Thieme Verlag KG Stuttgart • New York.

PMID: 19691014 [PubMed - as supplied by publisher]

J Neurotrauma. 2009 Sep;26(9):1435-46.

Neuroendocrine Function following Traumatic Brain Injury and Subsequent Intensive Care Treatment: A Prospective Longitudinal Evaluation.

Kleindienst A, Brabant G, Bock C, Maser-Gluth C, Buchfelder M.

Department of Neurosurgery, University Erlangen-Nuremberg , Erlangen, Germany .

Abstract Neuroendocrine dysfunction following traumatic brain injury (TBI) has been described extensively. However, few studies are longitudinal and most lack subtle radiological, clinical, and repetitive endocrine assessment in the acute phase. Accordingly, we prospectively assessed neuroendocrine function in 71 patients after TBI. Injury was documented by a computed tomography (CT). During the first week, critical clinical data (Glasgow Coma Score, APACHE score), treatment variables such as duration of analgosedation for mechanical ventilation, were related to basal pituitary function. More than 2 years later, a subgroup of patients was re-evaluated using dynamic testing with ACTH and GHRH-arginine tests. The Pearson's correlation analysis and Mann-Whitney rank sum test for group differences were used for statistical analysis. None of the CT findings predicted neuroendocrine dysfunction following TBI. The adaptive response to critical illness with significantly elevated cortisol levels on admission and decreased levels thereafter in patients ventilated for more than 24 h (p < 0.05) was attenuated following severe TBI (p < 0.05). However, the coincidence of low serum cortisol and increased urinary excretion of glucocorticoid metabolites in about 80% of patients challenges the relevance of basal hormone measurements. In ventilated patients, total T3 and free T4 were decreased (p < 0.05), TSH was low on day 3 (p < 0.05), and a gonadotropic insufficiency was present (p < 0.05). The thyrotropic and gonadotropic system recovered completely within the follow-up period. With regard to the somatotropic system, neither brain injury severity nor mechanical ventilation was associated with an insufficiency during the acute phase post-injury. However, initially low GH levels predicted a persistent deficiency (r = 0.731, p < 0.001). We conclude that both severe TBI and prolonged mechanical ventilation result in hormonal disturbances early after injury, suggesting a pathophysiological response to brain injury and subsequent intensive care treatment rather than morphological damage.

PMID: 19459759 [PubMed - in process]

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