Detailed assessment of hypothalamic damage in craniopharyngioma patients with obesity.


Journal

International journal of obesity (2005)
ISSN: 1476-5497
Titre abrégé: Int J Obes (Lond)
Pays: England
ID NLM: 101256108

Informations de publication

Date de publication:
03 2019
Historique:
received: 30 11 2017
accepted: 24 06 2018
revised: 07 06 2018
pubmed: 6 9 2018
medline: 14 2 2020
entrez: 6 9 2018
Statut: ppublish

Résumé

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. We performed qualitative and quantitative volumetric analyses of HT damage. The results were explored in relation to feeding related peptides and body fat. A cross-sectional study of childhood onset CPs involving 3 Tesla MRI, was performed at median 22 years after first operation; 41 CPs, median age 35 (range: 17-56), 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. 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) mm A decrease in HT volume was associated with an increase in fat mass and leptin. We present a method with a high inter-rater reliability (0.94) that can be applied by nonradiologists for the assessment of HT damage. The method may be valuable in the risk assessment of diseases involving the HT.

Sections du résumé

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. We performed qualitative and quantitative volumetric analyses of HT damage. 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 first operation; 41 CPs, median age 35 (range: 17-56), 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) mm
CONCLUSIONS
A decrease in HT volume was associated with an increase in fat mass and leptin. We present a method with a high inter-rater reliability (0.94) that can be applied by nonradiologists for the assessment of HT damage. The method may be valuable in the risk assessment of diseases involving the HT.

Identifiants

pubmed: 30181653
doi: 10.1038/s41366-018-0185-z
pii: 10.1038/s41366-018-0185-z
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

533-544

Auteurs

S Fjalldal (S)

Department of Endocrinology, Skåne University Hospital, Lund, Sweden.

C Follin (C)

Department of Endocrinology, Skåne University Hospital, Lund, Sweden.

S Gabery (S)

Translational Neuroendocrine Research Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.

P C Sundgren (PC)

Department of Medical Imaging and Physiology, Skåne University Hospital, Lund, Sweden.
Department of Diagnostic Radiology, Clinical Sciences, Lund University, Lund, Sweden.

I M Björkman-Burtscher (IM)

Department of Medical Imaging and Physiology, Skåne University Hospital, Lund, Sweden.
Department of Diagnostic Radiology, Clinical Sciences, Lund University, Lund, Sweden.
Lund University BioImaging Center, Lund University, Lund, Sweden.

J Lätt (J)

Department of Medical Imaging and Physiology, Skåne University Hospital, Lund, Sweden.

P Mannfolk (P)

Department of Medical Imaging and Physiology, Skåne University Hospital, Lund, Sweden.

C H Nordström (CH)

Department of Neurosurgery, Skåne University Hospital, Lund, Sweden.

L Rylander (L)

Division of Occupational and Environmental Medicine, Lund University, Lund, Sweden.

B Ekman (B)

Department of Endocrinology and Medical and Health Sciences, Linköping University, Linköping, Sweden.

R Cheong (R)

Translational Neuroendocrine Research Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.

A Pålsson (A)

Department of Endocrinology, Skåne University Hospital, Lund, Sweden.

Å Petersén (Å)

Translational Neuroendocrine Research Unit, Department of Experimental Medical Science, Lund University, Lund, Sweden.

E M Erfurth (EM)

Department of Endocrinology, Skåne University Hospital, Lund, Sweden. Eva_Marie.Erfurth@med.lu.se.

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