ECTRIMS eLearning

GlucoCEST MRI of blood brain barrier disruption in multiple sclerosis – first human experiments and initial results
Author(s): ,
X. Xu
Affiliations:
Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine; F. M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Research Institute
,
P. Bhargava
Affiliations:
Department of Neurology, Johns Hopkins University School of Medicine
,
A. Sehgal
Affiliations:
Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine; F. M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Research Institute
,
B. Dewey
Affiliations:
Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine; Department of Electrical and Computer Engineering, Johns Hopkins University, Baltimore, MD
,
S. By
Affiliations:
Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine; F. M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Research Institute; Philips Healthcare, Gainsville, FL, United States
,
L. Knutsson
Affiliations:
Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine; Department of Medical Radiation Physics, Lund University, Lund, Sweden
,
M. Pomper
Affiliations:
Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine
,
P. Calabresi
Affiliations:
Department of Neurology, Johns Hopkins University School of Medicine
P. van Zijl
Affiliations:
Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine; F. M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Research Institute
ECTRIMS Learn. Xu X. 10/12/18; 228166; P1788
Xiang Xu
Xiang Xu
Contributions
Abstract

Abstract: P1788

Type: Poster Sessions

Abstract Category: N/A

Introduction: It has been demonstrated that natural D-glucose can be used as a contrast agent for MRI using the chemical exchange saturation transfer (glucoCEST) mechanism. In the present work we show the possibility of detecting blood brain barrier (BBB) disruption in multiple sclerosis (MS) using dynamic glucose enhanced (DGE) MRI at 3T.
Methods: Five MS patients gave informed consent and participated in the study. After acquiring standard-of-care structural images, a brief hyperglycemic state was established by intravenous injecting 50 mL 50% D-glucose over a period of 2 min. glucoCEST MRI images were collected continuously before, during and after glucose injection. Approximately 20-30 minutes after glucose injection, Gadoteridol was injected and standard clinical post-contrast T1-weighted images were acquired.
Results and discussion: In a patient with a Gd enhancing lesion, pronounced enhancement was also observed in the area of the lesion with DGE MRI (enhancing lesion: 25.1%; contralateral white matter: 3.2%), a 3-month follow-up scan of the same patient showed no Gd enhancement but residual glucoCEST enhancement (residual enhancing lesion: 5.6%; contralateral white matter: 1.6%). In other patients without Gd enhancement, DGE enhancement was observed in some, but not all lesions. Presence of glucoCEST enhancement in Gd enhancing lesions indicates that glucose has the potential to be an alternative contrast agent to evaluate the disease activity of MS at 3T, removing the need for repeated Gd injections. The fact that we observed glucoCEST enhancement in some MS lesions that were not enhanced by Gd may suggest the presence of minor but persistent BBB disruption/inflammation or increased metabolic activities in the lesions, neither of which can be detected by post-Gd-contrast T1-weighted imaging.
Conclusion: These initial results suggest that glucose transport (passive and active) may be more sensitive than single dose Gd-enhanced MR to detect active MS lesions, and in addition may provide alternative/complementary information.
Disclosure:
Xiang Xu has nothing to disclose. Pavan Bhargava has nothing to disclose
Akansha Sehgal has nothing to disclose.
Blake Dewey has nothing to disclose.
Samantha By is employed by Philips Healthcare.
Linda Knutsson has nothing to disclose.
Martin Pomper has nothing to disclose.
Peter Calabresi has received consulting honoraria from Disarm Therapeutics, and is PI on grants to JHU from MedImmune, Annexon, Biogen, and Sanofi.
Peter C.M. van Zijl is a paid lecturer for Philips Medical Systems and has a patent on the use of glucose as a contrast agent for MRI.

Abstract: P1788

Type: Poster Sessions

Abstract Category: N/A

Introduction: It has been demonstrated that natural D-glucose can be used as a contrast agent for MRI using the chemical exchange saturation transfer (glucoCEST) mechanism. In the present work we show the possibility of detecting blood brain barrier (BBB) disruption in multiple sclerosis (MS) using dynamic glucose enhanced (DGE) MRI at 3T.
Methods: Five MS patients gave informed consent and participated in the study. After acquiring standard-of-care structural images, a brief hyperglycemic state was established by intravenous injecting 50 mL 50% D-glucose over a period of 2 min. glucoCEST MRI images were collected continuously before, during and after glucose injection. Approximately 20-30 minutes after glucose injection, Gadoteridol was injected and standard clinical post-contrast T1-weighted images were acquired.
Results and discussion: In a patient with a Gd enhancing lesion, pronounced enhancement was also observed in the area of the lesion with DGE MRI (enhancing lesion: 25.1%; contralateral white matter: 3.2%), a 3-month follow-up scan of the same patient showed no Gd enhancement but residual glucoCEST enhancement (residual enhancing lesion: 5.6%; contralateral white matter: 1.6%). In other patients without Gd enhancement, DGE enhancement was observed in some, but not all lesions. Presence of glucoCEST enhancement in Gd enhancing lesions indicates that glucose has the potential to be an alternative contrast agent to evaluate the disease activity of MS at 3T, removing the need for repeated Gd injections. The fact that we observed glucoCEST enhancement in some MS lesions that were not enhanced by Gd may suggest the presence of minor but persistent BBB disruption/inflammation or increased metabolic activities in the lesions, neither of which can be detected by post-Gd-contrast T1-weighted imaging.
Conclusion: These initial results suggest that glucose transport (passive and active) may be more sensitive than single dose Gd-enhanced MR to detect active MS lesions, and in addition may provide alternative/complementary information.
Disclosure:
Xiang Xu has nothing to disclose. Pavan Bhargava has nothing to disclose
Akansha Sehgal has nothing to disclose.
Blake Dewey has nothing to disclose.
Samantha By is employed by Philips Healthcare.
Linda Knutsson has nothing to disclose.
Martin Pomper has nothing to disclose.
Peter Calabresi has received consulting honoraria from Disarm Therapeutics, and is PI on grants to JHU from MedImmune, Annexon, Biogen, and Sanofi.
Peter C.M. van Zijl is a paid lecturer for Philips Medical Systems and has a patent on the use of glucose as a contrast agent for MRI.

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