The prevalence of growth hormone deficiency in survivors of subarachnoid haemorrhage: results from a large single centre study

Another problem description but no solution.
https://link.springer.com/article/10.1007/s11102-017-0825-7

• Authors
• Authors and affiliations

• Sumithra GiritharanEmail author
• Joanna Cox
• Calvin J. Heal
• David Hughes
• Kanna Gnanalingham
• Tara Kearney

• Sumithra Giritharan
  • 1
  • 7
  Email author
• Joanna Cox
  • 2
• Calvin J. Heal
  • 3
• David Hughes
  • 4
• Kanna Gnanalingham
  • 5
  • 6
• Tara Kearney
  • 1
  • 2

1. 1.Department of EndocrinologySalford Royal NHS Foundation TrustGreater ManchesterUK
2. 2.Vascular Research NetworkSalford Royal NHS Foundation TrustGreater ManchesterUK
3. 3.Centre for Biostatistics, Faculty of Biology, Medicine and HealthManchester Academic Health Science Centre, University of ManchesterManchesterUK
4. 4.Department of NeuroradiologySalford Royal NHS Foundation TrustGreater ManchesterUK
5. 5.Department of NeurosurgerySalford Royal NHS Foundation TrustGreater ManchesterUK
6. 6.Manchester Academic Health Sciences Centre (MAHSC), University of ManchesterManchesterUK
7. 7.Department of Endocrinology and DiabetesSalford Royal NHS Foundation TrustGreater ManchesterUK

Open Access

Article

First Online:

18 August 2017

• 33 Downloads

Abstract

Objective

The variation in reported prevalence of growth hormone deficiency (GHD) post subarachnoid haemorrhage (SAH) is mainly due to methodological heterogeneity. We report on the prevalence of GHD in a large cohort of patients following SAH, when dynamic and confirmatory pituitary hormone testing methods are systematically employed.

Design

In this cross-sectional study, pituitary function was assessed in 100 patients following SAH. Baseline pituitary hormonal profile measurement and glucagon stimulation testing (GST) was carried out in all patients. Isolated GHD was confirmed with an Arginine stimulation test and ACTH deficiency was confirmed with a short synacthen test.

Results

The prevalence of hypopituitarism in our cohort was 19% and the prevalence of GHD was 14%. There was no association between GHD and the clinical or radiological severity of SAH at presentation, treatment modality, age, or occurrence of vasospasm. There were statistically significant differences in terms of Glasgow Outcome Scale (GOS; p = 0.03) between patients diagnosed with GHD and those without. Significant inverse correlations between GH peak on GST with body mass index (BMI) and waist hip ratio (WHR) was also noted (p < 0.0001 and p < 0.0001 respectively).

Conclusion

Using the current testing protocol, the prevalence of GHD detected in our cohort was 14%. It is unclear if the BMI and WHR difference observed is truly due to GHD or confounded by the endocrine tests used in this protocol. There is possibly an association between the development of GHD and worse GOS score. Routine endocrine screening of all SAH survivors with dynamic tests is time consuming and may subject many patients to unnecessary side-effects. Furthermore the degree of clinical benefit derived from growth hormone replacement in this patient group, remains unclear. Increased understanding of the most appropriate testing methodology in this patient group and more importantly which SAH survivors would derive most benefit from GHD screening is required.