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This Article Accepted manuscript (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. Articles by Pereira, A PubMed PubMed Citation Articles by Kokshoorn, N. Articles by Pereira, A

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

N Kokshoorn, Endocrinology and Metabolism, Leiden University Medical Center, Leiden, 2333 ZA, Netherlands
M Wassenaar, Endocrinology and Metabolism, Leiden University Medical Centre, Leiden, Netherlands
N Biermasz, Endocrinology and Metabolism, Leiden University Medical Centre, Leiden, Netherlands
F Roelfsema, Endocrinology and Metabolism, Leiden University Medical Center, Leiden, Netherlands
J Smit, Endocrinology and Metabolism, Leiden University Medical Centre, Leiden, Netherlands
J Romijn, Endocrinology and Metabolism, Leiden University Medical Centre, Leiden, Netherlands
A Pereira, Endocrinology and Metabolism, Leiden University Medical Center, Leiden, Netherlands

Nieke 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 (cut-off <9µg/L), 11-39% using the glucagon test (cut-off 1-5µg/L), 2% using the GHRH-test (no cut-off) and 15-18% using the insulin tolerance test (ITT) (cut-off <3µg/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 (cut-off <220 or <440 nmol/L), 7-19% using the ACTH-test and 5% with the ITT as first test (cut-off <500 or <550 nmol/L). Secondary hypothyroidism was present in 0-19% (free T4) or 5-15% (TRH 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.