gms | German Medical Science

56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)
3èmes journées françaises de Neurochirurgie (SFNC)

Deutsche Gesellschaft für Neurochirurgie e. V.
Société Française de Neurochirurgie

07. bis 11.05.2005, Strasbourg

Diagnosing ACTH- and growth hormone deficiency in patients after aneurysmal subarachnoid hemorrhage: does basal hormone screening make sense?

Die Diagnose eines ACTH- und Wachstumshormonmangels nach aneurysmatischer Subarachnoidalblutung: sind Cortisol und IGF-1 geeignete Prädiktoren?

Meeting Abstract

  • corresponding author I. Kreitschmann-Andermahr - Dept. of Neurosurgery, University Hospital Aachen
  • E. Poll - Dept. of Neurosurgery, University Hospital Aachen
  • A. Reineke - Dept. of Neurosurgery, University Hospital Aachen
  • E. Siewert - Internal Medicine III, University Hospital Aachen
  • E. Yagmur - Institute for Clinical Chemistry and Pathobiochemistry, University Hospital Aachen
  • J. Gilsbach - Dept. of Neurosurgery, University Hospital Aachen

Deutsche Gesellschaft für Neurochirurgie. Société Française de Neurochirurgie. 56. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC), 3èmes journées françaises de Neurochirurgie (SFNC). Strasbourg, 07.-11.05.2005. Düsseldorf, Köln: German Medical Science; 2005. DocP082

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Veröffentlicht: 4. Mai 2005

© 2005 Kreitschmann-Andermahr et al.
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Neuroendocrine dysfunction is a more frequent sequel of aneurysmal subarachnoid hemorrhage (SAH), than has so far been recognized. Since especially growth hormone (GH) and adrenocorticotroph hormone (ACTH) deficiency are commonly diagnosed by dynamic tests of pituitary function, referral to endocrinological care is increasingly recommended in all patients after aneurysmal SAH. We wanted to elucidate whether IGF-1 and basal morning cortisol levels are of help to predict GH and ACTH deficiency in later endocrine function testing.


In 45 outpatients investigated between 3 months and 5.5 years after aneurysmal SAH for neuroendocrine deficiency, 9 AM cortisol values and IGF-1 values were obtained and an insulin tolerance test (ITT) was additionally performed. Diagnosis of severe GH deficiency (GHD) was made if peak GH levels in the ITT were <3 µg/l and ACTH dysfunction was defined as peak stimulated cortisol levels <500 nmol/l in the ITT. Spearman correlations and receiver operating curves were calculated for 9 AM and peak stimulated cortisol levels as well as for IGF-1 and peak stimulated GH levels.


Based on the ITT criteria, 20 patients were diagnosed with ACTH deficiency and 11 patients exhibited severe GHD. Patients with ACTH deficiency exhibited significantly lower 9 AM mean cortisol values (266 nmol/l) than those without ACTH deficiency (375 nmol/l; Mann-Whitney-U-test p=.003). Mean IGF-1 levels in patients with GHD (139 µg/l ) did not differ significantly from those without GHD (mean 143 µg/l; Mann-Whitney-U-test p=.85). 9 AM cortisol and peak stimulated cortisol correlated significantly (r=.56, p<.001). IGF-1 levels and peak stimulated GH exhibited no significant correlation (r=.14, p=.38). However, a 100% sensitivity for diagnosing ACTH-deficiency resulted in a cut-off value of 444 nmol/l for the 9 AM cortisol and a specificity of 32%.


In our patient group IGF-1 levels were not predictive of GH deficiency as diagnosed by means of the ITT. Although there was a significant correlation between low morning cortisol and verified ACTH deficiency, a cut-off value well within the normal range would have to be chosen in order to single out all patients for testing and would result in a high number of unnecessarily performed tests. We conclude that IGF-1 levels do not help to identify patients with GH deficiency following aneurysmal SAH, whereas basal morning cortisol is of limited value to predict ACTH deficiency in SAH patients.