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This Article Full Text Full Text (PDF) Supplementary Data All Versions of this Article: EJE-09-0601v1 162/1/11    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Kokshoorn, N. E Articles by Pereira, A. M PubMed PubMed Citation Articles by Kokshoorn, N. E Articles by Pereira, A. M

Hypopituitarism following traumatic brain injury: prevalence is affected by the use of different dynamic tests and different normal values

Department of Endocrinology and Metabolic Diseases C4-R, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands

(Correspondence should be addressed to N E Kokshoorn; Email: n.e.kokshoorn{at}lumc.nl)

Abstract

Objective: Traumatic brain injury (TBI) has emerged as an important cause of hypopituitarism. However, considerable variations in the prevalence of hypopituitarism are reported. These can partly be explained by severity of trauma and timing of hormonal evaluation, but may also be dependent on endocrine tests and criteria used for diagnosis of hypopituitarism.

Methods: Systematic review of studies reporting prevalence of hypopituitarism in adults 1 year after TBI focusing on used (dynamic) tests and biochemical criteria.

Results: We included data from 14 studies with a total of 931 patients. There was considerable variation in definition of hypopituitarism. Overall, reported prevalences of severe GH deficiency varied between 2 and 39%. Prevalences were 8–20% using the GHRH–arginine test (cutoff <9 µg/l), 11–39% using the glucagon test (cutoff 1–5 µg/l), 2% using the GHRH test (no cutoff), and 15–18% using the insulin tolerance test (ITT; cutoff <3 µg/l).

Overall, the reported prevalence of secondary adrenal insufficiency had a broad range from 0 to 60%. This prevalence was 0–60% with basal cortisol (cutoff <220 or <440 nmol/l), 7–19% using the ACTH test, and 5% with the ITT as first test (cutoff <500 or <550 nmol/l). Secondary hypothyroidism was present in 0–19% (free thyroxine) or 5–15% (thyroid-releasing hormone stimulation). Secondary hypogonadism was present in 0–29%.

Conclusion: The reported variations in the prevalence rates of hypopituitarism after TBI are in part caused by differences in definitions, endocrine assessments of hypopituitarism, and confounding factors. These methodological issues prohibit simple generalizations of results of original studies on TBI-associated hypopituitarism in the perspective of meta-analyses or reviews.