Endocrine Abstracts (2017) 49 EP1070 | DOI: 10.1530/endoabs.49.EP1070

Detailed assessment of hypothalamic damage in craniopharyngioma patients with obesity

Sigridur Fjalldal1, Cecilia Follin1, Sanaz Gabery2, Pia Maly Sundgren3,4, Isabella Björkman-Burtscher3,4, Jimmy Lätt3, Peter Mannfolk3, Carl-Henrik Nordström5, Lars Rylander6, Bertil Ekman7, Anna Pålsson1, Æsa Petersén2 & Eva-Marie Erfurth1


1Department of Endocrinology, Skåne University Hospital, Lund, Sweden; 2Translational Neuroendocrine Research Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden; 3Department of Medical Imaging and Physiology, Skåne University Hospital, Lund, Sweden; 4Department of Diagnostic Radiology, Clinical Sciences, Lund University, Lund, Sweden; 5Department of Neurosurgery, Skåne University Hospital, Lund, Sweden; 6Division of Occupational and Environmental Medicine, Lund University, Lund, Sweden; 7Department of Endocrinology and Medical and Health Sciences, Linköping University, Linköping, Sweden.


Background/objectives: Hypothalamic obesity (HO) occurs in 50% of patients with the pituitary tumor Craniopharyngioma (CP). Attempts have been made to predict the risk of HO based on hypothalamic (HT) damage on magnetic resonance imaging (MRI), but none have included volumetry. Qualitative and quantitative (volumetric) analyses of HT damage was performed. The results were explored in relation to feeding related peptides and body fat.

Subjects/methods: A cross-sectional study of childhood onset CPs involving 3 Tesla MRI, was performed at median 22 years after 1st operation. 41 CPs, median age 35 (range 18-56), of whom 23 had HT damage, were compared to 32 controls. After exclusions, 35 patients and 31 controls remained in the MRI study. Main outcome measures were the relation of metabolic parameters to HT volume and qualitative analyses of HT damage.

Results: Metabolic parameters scored persistently very high in vascular risk particularly among HT damaged patients. Patients had smaller HT volumes compared to controls 769 (35–1168) mm3 vs 879 (775–1086) mm3; P<0.001. HT volume correlated negatively with fat mass and leptin among CP patients (rs=−0.67; P<0.001; rs=−0.53; P=0.001), and explained 39% of the variation in fat mass. For every 100 mm3 increase in HT volume fat mass decreased by 2.7 kg (95% CI: 1.5–3.9; P<0.001). Qualitative assessments revealed HT damage in 3 out of 6 patients with normal volumetry, but HT damage according to operation records.

Conclusions: A decrease in HT volume was associated with an increase in fat mass and leptin. We present a reproducible method with a high inter-rater reliability (0.94) that can be applied by non-radiologist for the assessment of HT damage. The method may be valuable in the risk assessment of diseases involving the HT.