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dc.contributor.authorKeddie, S
dc.contributor.authorCrisp, Sarah
dc.contributor.authorBlackaby, J
dc.contributor.authorCox, A
dc.contributor.authorColes, Alasdair
dc.contributor.authorHart, M
dc.contributor.authorChurch, AJ
dc.contributor.authorVincent, A
dc.contributor.authorZandi, M
dc.contributor.authorLunn, MP
dc.date.accessioned2018-09-20T12:08:17Z
dc.date.available2018-09-20T12:08:17Z
dc.date.issued2018-11
dc.identifier.issn1351-5101
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/280584
dc.description.abstractBACKGROUND AND PURPOSE: The aim was to assess the therapeutic potential of bortezomib in the treatment of refractory N-methyl-d-aspartate receptor (NMDAR) antibody encephalitis and its potential in other immune-mediated, B-cell-driven neurological diseases. METHODS: Two cases of severe NMDAR antibody encephalitis, resistant to first and second line therapy with steroids, intravenous immunoglobulins, plasma exchange, cyclophosphamide and rituximab, were treated with four and five cycles of 1.3 mg/m2 bortezomib at 350 and 330 days following initial presentation. RESULTS: Both patients showed significant clinical improvement with reductions of NMDAR antibody titres following bortezomib treatment. This is the first case in the literature where the NMDAR antibody level was undetectable following treatment with bortezomib. CONCLUSION: Bortezomib's unique ability to target long-lived autoreactive plasma cells appears to be a useful adjunct to standard second line immunosuppressive therapy in treatment-refractory NMDAR antibody encephalitis. The drug's pharmacodynamics, cell targeting and mechanism of action are reviewed, and it is postulated that bortezomib may be useful in a host of B-cell-driven neuroimmunological diseases.
dc.description.sponsorshipnil
dc.format.mediumPrint-Electronic
dc.languageeng
dc.publisherWiley
dc.subjectPlasma Cells
dc.subjectHumans
dc.subjectReceptors, N-Methyl-D-Aspartate
dc.subjectAntineoplastic Agents
dc.subjectTreatment Outcome
dc.subjectAdult
dc.subjectFemale
dc.subjectAnti-N-Methyl-D-Aspartate Receptor Encephalitis
dc.subjectBortezomib
dc.titlePlasma cell depletion with bortezomib in the treatment of refractory N-methyl-d-aspartate (NMDA) receptor antibody encephalitis. Rational developments in neuroimmunological treatment.
dc.typeArticle
prism.endingPage1388
prism.issueIdentifier11
prism.publicationDate2018
prism.publicationNameEur J Neurol
prism.startingPage1384
prism.volume25
dc.identifier.doi10.17863/CAM.27952
dcterms.dateAccepted2018-07-19
rioxxterms.versionofrecord10.1111/ene.13759
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2018-11
dc.contributor.orcidCrisp, Sarah [0000-0002-0007-7775]
dc.contributor.orcidColes, Alasdair [0000-0003-4738-0760]
dc.identifier.eissn1468-1331
rioxxterms.typeJournal Article/Review
cam.issuedOnline2018-08-31
rioxxterms.freetoread.startdate2019-07-23


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