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Hypopituitarism is uncommon after aneurysmal subarachnoid haemorrhage
Author(s) -
Klose Marianne,
Brennum Jannick,
Poulsgaard Lars,
Kosteljanetz Michael,
Wagner Aase,
FeldtRasmussen Ulla
Publication year - 2010
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.2010.03791.x
Subject(s) - hypopituitarism , medicine , endocrine system , cohort , prospective cohort study , growth hormone deficiency , insulin tolerance test , adrenocorticotropic hormone , pediatrics , endocrinology , hormone , insulin , insulin resistance , growth hormone , insulin sensitivity
Summary Objective  Aneurysmal subarachnoid haemorrhage (SAH) has recently been reported as a common cause of chronic hypopituitarism, and introduction of routine neuroendocrine screening has been advocated. We aimed at estimating the risk of hypopituitarism after SAH using strict criteria including confirmatory testing in case of suggested insufficiency. Design  Cross‐sectional evaluation with a nested prospective subgroup. Patients and measurements  Endocrine evaluation was performed at a median of 14 months (range 11–26) post‐SAH in 62 patients with SAH and 30 healthy controls. Twenty‐six patients were followed prospectively (median 7 days, and 12 months post‐SAH). Endocrine evaluation included baseline evaluation, which was combined with an insulin tolerance test (ITT) or, if contraindicated, GHRH + arginine tests and a standard ACTH test at evaluation 1–2 years post‐SAH. Pituitary insufficiencies were confirmed by re‐evaluation. Results  Early post‐SAH hormone alterations mimicking central hypogonadism were present in 58% of the patients and associated with a worse clinical state ( P  < 0·05). One to 2 years post‐SAH, initial neuroendocrine evaluation identified seven patients (11%) with abnormal results; three had free T4 and TSH suggestive of central hypothyroidism, three men had testosterone below 10 n m , and one had an insufficient GH and cortisol response to the ITT. None of these abnormalities was confirmed upon confirmatory testing. Conclusion  In the largest reported cohort of patients with SAH to date, with early and late endocrine evaluation, none of the patients had chronic hypopituitarism. Based on these findings, the introduction of routine neuroendocrine screening is not justified, and the data suggest the importance of using strict diagnostic criteria in patients with a low pretest probability of hypopituitarism.

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