Eur J Endocrinol
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DOI: 10.1530/eje.1.02071
European Journal of Endocrinology, Vol 154, Issue 2, 259-265
Copyright © 2006 by European Society of Endocrinology
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CLINICAL STUDY

Prevalence of anterior pituitary insufficiency 3 and 12 months after traumatic brain injury

H J Schneider*, M Schneider3,*, B Saller1,2, S Petersenn2, M Uhr, B Husemann3, F von Rosen3 and G K Stalla

Max Planck Institute of Psychiatry, Clinical Neuroendocrinology Group Kraepelinstr. 10, 80804 Munich, Germany, 1 Pfizer GmbH, Pfizerstr. 1, 76032 Karlruhe, Germany, 2 University Hospital Essen, Department of Endocrinology, Hufelandstr. 55 45122 Essen, Germany and 3 Neurologic Clinic Bad Aibling, Kolbermoorer Straße 72, 83043 Bad Aibling, Germany

(Correspondence should be addressed to G K Stalla; Email: stalla{at}mpipsykl.mpg.de)

Objective: Cross-sectional studies report a high prevalence of hypopituitarism after traumatic brain injury (TBI); however, no longitudinal studies on time of manifestation and reversibility exist. This study was conducted to assess hypopituitarism 3 and 12 months after TBI.

Design: This was a prospective, longitudinal, diagnostic study.

Methods: Seventy-eight patients (52 men, 26 women, mean age 36.0 years) with TBI grades I–III and 38 healthy subjects (25 men, 13 women, mean age 36.4 years) as a control group for the GHRH + arginine test were studied. The prevalence ofhypopituitarism was assessed 3 and 12 months after TBI by GHRH + arginine test, short adrenocorticotropic hormone (ACTH) test, and basal hormone measurements in patients.

Results: After 3 months, 56% of all patients had impairments of at least one pituitary axis with axes being affected as follows: gonadotropic 32%, corticotropic 19%, somatotropic 9% and thyrotropic 8%. After 12 months, fewer patients were affected, but in some cases new impairments occurred; 36% still had impairments. The axes were affected as follows after 12 months: gonadotropic 21%, somatotropic 10%, corticotropic 9% and thyrotropic 3%.

Conclusions: Hypopituitarism occurs often in the post-acute phase after TBI and may normalize later, but may also develop after the post-acute phase of TBI.




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