ECE2013 Oral Communications Adrenal (6 abstracts)
Neuronal dysfunction in the hippocampi of cured Cushing's syndrome patients, detected by 1H-MR-spectroscopy
Eugenia Resmini 1 , Alicia Santos 1 , Beatriz Gómez-Anson 2 , Olga López-Mourelo 3 , Patricia Pires 3 , Yolanda Vives-Gilabert 3 , Iris Crespo 1 , Maria Portella 4 , Manel de Juan-Delago 2 & Susan Webb 1
1Endocrinology/Medicine Departments, Hospital Sant Pau, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBER-ER, Unidad 747), IIB-Sant Pau, ISCIII and Universitat Autònoma de Barcelona, Barcelona, Spain; 2Neuroradiology Unit, Hospital Sant Pau, and IIB-Sant Pau, UAB, Barcelona, Spain; 3Port d’Informació Científica (PIC) and Institut de Fisica d’Altes Energies (IFAE), Campus UAB Edifici D, Bellaterra, Barcelona, Spain; 4Department of Psychiatry, Hospital Sant Pau, UAB, Barcelona, Spain.
Introduction: Proton magnetic resonance spectroscopy (1H-MRS) is a sensitive, non-invasive imaging technique capable of measuring brain metabolites in vivo. Chronic exposure to endogenous hypercortisolism in Cushing’s syndrome (CS) is associated with negative effects on memory and hippocampal volumes, even after biochemical cure.
Objective: To investigate metabolites in the hippocampi of CS patients and controls, using 1H-MRS.
Patients and methods: Eighteen right-handed cured CS patients (age 44.8±12.5 years, 12.6±3.8 years of education), 18 right-handed healthy controls, matched for age (40.0±11.9) and years of education (14.4±3.8) underwent 3-Tesla magnetic resonance imaging (3T MRI) and 1H-MRS including the head of each hippocampus. Concentrations of Glu (Glutamate), Glx (Glutamate+Glutamine), NAA (NAcetyl-aspartate), total-NAA (NAcetyl-aspartate+N-Acetyl-aspartyl-Glutamate), Cho (Glycerophosphocholine and Phosphocholine compounds), Cr (Creatine) and MI (mionositol) were measured (mmol/l). Hippocampal volumes were additionally calculated using an automated procedure (Freesurfer).
Results: CS patients had lower NAA than controls in the left and right hippocampus (5.2±1.0 vs 6.1±0.7, P<0.05; 4.9±0.8 vs 6.1±0.6, P<0.001 respectively), and lower total-NAA in the right (5.7±0.9 vs 6.3±0.9, P<0.05), suggesting neuronal dysfunction/loss. CS patients had higher Glx than controls in both hippocampi (10.4±1.9 vs 8.6±1.4, P<0.01; 9.9±1.6 vs 8.9±1.3, P<0.05 respectively), suggesting glial proliferation, as a repair mechanism after neuronal dysfunction. No differences were found in the other brain metabolites, and there were no differences in left (3815.78±502.96 mm3) and right (3980.75±369.44 mm3) total hippocampal volumes between CS patients and controls (3945.08±408.90 and 4108.39±365.11 mm3, respectively).
Conclusion: Persistently abnormal metabolites are evidenced in the hippocampi of CS patients despite endocrine cure. These functional alterations could be early markers of glucocorticoids neurotoxicity and would precede hippocampal volume reduction.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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