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Endocrine Abstracts (2015) 37 GP20.04 | DOI: 10.1530/endoabs.37.GP.20.04

ECE2015 Guided Posters Pituitary – Hypopituitarism (9 abstracts)

Irradiation-induced hypopituitarism in adult brain tumour survivors: single-centre longitudinal data

Nikolaos Kyriakakis 1 , Julie Lynch 1 , Susan C Short 2 , Paul Hatfield 2 , Carmel Loughrey 2 , Georgina Gerrard 2 , Steve M Orme 1 & Robert D Murray 1


1Endocrinology, Leeds Centre for Diabetes and Endocrinology, St James’s University Hospital, Leeds, UK; 2Oncology, Leeds Cancer Centre, St James’s University Hospital, Leeds, UK.


Introduction: Radiation-induced hypopituitarism is a well-recognized complication of cranial radiotherapy (cXRT) for childhood brain tumours when the hypothalamo–pituitary axis is within the irradiation field. Few data are available for survivors of adult brain tumours who have received cranial irradiation.

Methods: We retrospectively reviewed medical records of patients referred to Endocrinology following cXRT for primary non-pituitary brain tumours during adulthood. Longitudinal data regarding pituitary-related treatment outcomes were collected. The ITT and/or GST were used to assess GH and HPA axes integrity. Basal values for the additional anterior pituitary hormones were used to determine gonadotropin, TSH and prolactin status.

Results: 107 patients (mean age 40.0±13.1 years) with mean duration of post-cXRT follow-up of 9.1±5.7 years were studied. 32.7, 19.6, 20.6 and 27.1% of patients had tumours located in the anterior, middle, posterior cranial fossa and central (perisellar) regions respectively. 94.4% received fractionated photon radiotherapy (mean dose 51.7±6.5Gy, mean number of fractions 28.6±3.5), while the remaining patients received proton beam or stereotactic radiotherapy. Evidence of pituitary dysfunction was present in 88.8% of patients. The GH axis was affected in 86.9% of patients (severe GHD 64.5%, partial GHD 22.4%), followed by LH/FSH (34.6%), ACTH (23.4%), and TSH (11.2%) axes. Clinically significant ACTH deficiency necessitating glucocorticoid replacement was present in only 10.3% of cases. Hyperprolactinaemia was noted in 15.0% of patients. Single pituitary axis dysfunction was found in 41.1% of patients, while multiple axes were affected in 47.7% of cases. Longitudinal data analysis showed accumulation of pituitary hormone deficits the longer the duration of follow-up.

Conclusions: Pituitary dysfunction in survivors of adult brain tumours following cXRT is very common. The majority of deficits develop within 5 years post-cXRT, however late onset or progression of severity of a previously developed hormone deficiency was also observed. Long-term follow-up of these patients in specialist endocrine centres is strongly recommended.

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