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Transient gadolinium leakage in natalizumab-treated multiple sclerosis
  1. Sven Haller1,
  2. Frederik Barkhof2,
  3. Mike P Wattjes2,
  4. Patrice H Lalive3,4
  1. 1 Department of Imaging and Medical Informatics, University Hospitals of Geneva and Faculty of Medicine of the University of Geneva, Geneva, Switzerland
  2. 2 Department of Radiology & Nuclear Medicine and PET Research, VU University Medical Centre, Amsterdam, The Netherlands
  3. 3 Department of Clinical Neurosciences, Division of Neurology, Unit of Neuroimmunology and Multiple Sclerosis, Geneva University Hospital and Faculty of Medicine of the University of Geneva, Geneva, Switzerland
  4. 4 Department of Genetic and Laboratory Medicine, Division of Laboratory Medicine, Geneva University Hospital, Geneva, Switzerland
  1. Correspondence to Dr Sven Haller, Service neuro-diagnostique et neuro-interventionnel DISIM, University Hospitals of Geneva, Rue Gabrielle Perret-Gentil 4, 1211 Geneva 14, Switzerland; sven.haller{at}

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Natalizumab (NTZ; Biogen Idec, Cambridge, Massachusetts, USA) is a recombinant humanised immunoglobulin G4 monoclonal antibody approved for the treatment of relapsing-remitting multiple sclerosis (RRMS).1 It selectively inhibits the adhesion α4-β1 receptor on the surface of lymphocytes, monocytes, basophils and eosinophils preventing the interaction of immune cells with the integrin vascular cell adhesion molecule-1 (VCAM-1) on endothelial cells and with structures of the extracellular matrix and hindering cells from leaving the vascular compartment of the brain.2 This mainly hinders circulating cells from leaving the vascular compartment but may also have other consequences on signalling and apoptosis.3

We report the case of a patient with NTZ-treated RRMS who developed a new type of atypical lesion on MRI, consisting of a transient and ill-defined gadolinium enhancement without a typically associated T2 or fluid-attenuated inversion recovery (FLAIR) lesion.


A patient was diagnosed with RRMS in 2004 with, on average, one relapse per 18 months. Treatment was switched from interferon-β1a (IFNβ-1a) 44 µg three times weekly to NTZ. Follow-up imaging was performed 1 year after treatment modification and demonstrated the appearance of two atypical contrast-enhancing lesions. The first lesion appeared in the right temporal white matter adjacent to the ventricular system with a …

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