Low prevalence of hypopituitarism after subarachnoid haemorrhage using confirmatory testing and with BMI-specific GH cut-off levels

被引:21
作者
Gardner, Chris J. [1 ]
Javadpour, Mohsen [2 ,3 ]
Stoneley, Catherine [2 ,3 ]
Purthuran, Mani [2 ,3 ]
Biswas, Shubhabrata [2 ,3 ]
Daousi, Christina [1 ]
MacFarlane, Ian A. [1 ]
Cuthbertson, Daniel J. [1 ]
机构
[1] Aintree Univ Hosp NHS Fdn Trust, Aintree Univ Hosp NHS Fdn Trust, Univ Dept Obes & Endocrinol, Floor Clin Sci Ctr 3, Liverpool L9 7AL, Merseyside, England
[2] Walton Ctr Neurol & Neurosurg NHS Fdn Trust, Dept Neurosurg, Liverpool, Merseyside, England
[3] Walton Ctr Neurol & Neurosurg NHS Fdn Trust, Dept Radiol, Liverpool, Merseyside, England
关键词
HORMONE (GH)-RELEASING HORMONE; GLUCAGON STIMULATION TEST; TRAUMATIC BRAIN-INJURY; BODY-MASS INDEX; GROWTH-HORMONE; PITUITARY-FUNCTION; ENDOCRINE-SOCIETY; DEFICIENCY; DYSFUNCTION; DIAGNOSIS;
D O I
10.1530/EJE-12-0849
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: Hypopituitarism following subarachnoid haemorrhage (SAH) has been reported to be a frequent occurrence. However, there is considerable heterogeneity between studies with differing patient populations and treatment modalities and most importantly employing differing endocrine protocols and (normal) reference ranges of GH. We aimed to examine prospectively a cohort of SAH survivors for development of hypopituitarism post-SAH using rigorous endocrine testing and compare GH response to glucagon stimulation with a cohort of healthy controls of a similar BMI. Design and methods: Sixty-four patients were investigated for evidence of hypopituitarism 3 months post-SAH with 50 patients tested again at 12 months. Glucagon stimulation testing (GST), with confirmation of deficiencies by GHRH/arginine testing for GH deficiency (GHD) and short synacthen testing for ACTH deficiency, was used. Basal testing of other hormonal axes was undertaken. Results: Mean age of patients was 53 +/- 11.7 years and mean BMI was 27.5 +/- 5.7 kg/m(2). After confirmatory testing, the prevalence of hypopituitarism was 12% (GHD 10%, asymptomatic hypocortisolaemia 2%). There was no association between hypopituitarism and post-SAH vasospasm, presence of cerebral infarction, Fisher grade, or clinical grading at presentation. There was a significant correlation between BMI and peak GH to glucagon stimulation in both patients and controls. Conclusions: Identification of 'true' GHD after SAH requires confirmatory testing with an alternative stimulation test and application of BMI-specific cut-offs. Using such stringent criteria, we found a prevalence of hypopituitarism of 12% in our population. European Journal of Endocrinology 168 473-481
引用
收藏
页码:473 / 481
页数:9
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