Interferon-β Is Less Effective Than Other Drugs in Controlling the Rate of Retinal Ganglion Cell Loss in MS
To investigate the association between disease-modifying therapies (DMTs) and the rate of progressive retinal ganglion cell (RGC) and nerve fiber loss in MS. One hundred five relapsing-remitting patients with MS were followed annually for a median of 4.0 years using optical coherence tomography. Twe...
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| Veröffentlicht in: | Neurology : neuroimmunology & neuroinflammation Jg. 8; H. 3; S. e971 |
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| Sprache: | Englisch |
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American Academy of Neurology
01.05.2021
Lippincott Williams & Wilkins |
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| Abstract | To investigate the association between disease-modifying therapies (DMTs) and the rate of progressive retinal ganglion cell (RGC) and nerve fiber loss in MS.
One hundred five relapsing-remitting patients with MS were followed annually for a median of 4.0 years using optical coherence tomography. Twenty-five healthy subjects were also included as normal controls. The rates of global peripapillary retinal nerve fiber layer (pRNFL), temporal RNFL (tRNFL), and ganglion cell inner plexiform layer (GCIPL) thinning were analyzed according to DMT type using a linear mixed-effects model. Optic radiation lesion volume was measured on brain MRI and included as a covariate to minimize the effects of retrograde transsynaptic degeneration.
The annual rates of RNFL and GCIPL thinning were higher in patients treated with "platform" therapies (interferon-β and glatiramer acetate) compared with DMTs of higher clinical efficacy (including fingolimod, dimethyl fumarate, natalizumab, alemtuzumab, rituximab, and ocrelizumab) (difference = -0.22 μm/y,
= 0.02 for pRNFL; difference = -0.34 μm/y,
= 0.009 for tRNFL; and difference = -0.16 μm/y,
= 0.005 for GCIPL). Based on an analysis of individual treatments (interferon-β, glatiramer acetate, fingolimod, and natalizumab), interferon-β was associated with inferior RGC preservation, relative to the other drugs. No effect difference was found between glatiramer acetate, fingolimod, and natalizumab.
Progressive loss of RGCs in patients with MS is more pronounced in patients treated with interferon-β than other DMTs. This finding may have implications for DMT selection in MS.
This study provides Class IV evidence that for patients with MS, treatment with interferon-β compared with other DMTs leads to a more pronounced rate of retinal ganglion cell loss. |
|---|---|
| AbstractList | To investigate the association between disease-modifying therapies (DMTs) and the rate of progressive retinal ganglion cell (RGC) and nerve fiber loss in MS.OBJECTIVETo investigate the association between disease-modifying therapies (DMTs) and the rate of progressive retinal ganglion cell (RGC) and nerve fiber loss in MS.One hundred five relapsing-remitting patients with MS were followed annually for a median of 4.0 years using optical coherence tomography. Twenty-five healthy subjects were also included as normal controls. The rates of global peripapillary retinal nerve fiber layer (pRNFL), temporal RNFL (tRNFL), and ganglion cell inner plexiform layer (GCIPL) thinning were analyzed according to DMT type using a linear mixed-effects model. Optic radiation lesion volume was measured on brain MRI and included as a covariate to minimize the effects of retrograde transsynaptic degeneration.METHODSOne hundred five relapsing-remitting patients with MS were followed annually for a median of 4.0 years using optical coherence tomography. Twenty-five healthy subjects were also included as normal controls. The rates of global peripapillary retinal nerve fiber layer (pRNFL), temporal RNFL (tRNFL), and ganglion cell inner plexiform layer (GCIPL) thinning were analyzed according to DMT type using a linear mixed-effects model. Optic radiation lesion volume was measured on brain MRI and included as a covariate to minimize the effects of retrograde transsynaptic degeneration.The annual rates of RNFL and GCIPL thinning were higher in patients treated with "platform" therapies (interferon-β and glatiramer acetate) compared with DMTs of higher clinical efficacy (including fingolimod, dimethyl fumarate, natalizumab, alemtuzumab, rituximab, and ocrelizumab) (difference = -0.22 μm/y, p = 0.02 for pRNFL; difference = -0.34 μm/y, p = 0.009 for tRNFL; and difference = -0.16 μm/y, p = 0.005 for GCIPL). Based on an analysis of individual treatments (interferon-β, glatiramer acetate, fingolimod, and natalizumab), interferon-β was associated with inferior RGC preservation, relative to the other drugs. No effect difference was found between glatiramer acetate, fingolimod, and natalizumab.RESULTSThe annual rates of RNFL and GCIPL thinning were higher in patients treated with "platform" therapies (interferon-β and glatiramer acetate) compared with DMTs of higher clinical efficacy (including fingolimod, dimethyl fumarate, natalizumab, alemtuzumab, rituximab, and ocrelizumab) (difference = -0.22 μm/y, p = 0.02 for pRNFL; difference = -0.34 μm/y, p = 0.009 for tRNFL; and difference = -0.16 μm/y, p = 0.005 for GCIPL). Based on an analysis of individual treatments (interferon-β, glatiramer acetate, fingolimod, and natalizumab), interferon-β was associated with inferior RGC preservation, relative to the other drugs. No effect difference was found between glatiramer acetate, fingolimod, and natalizumab.Progressive loss of RGCs in patients with MS is more pronounced in patients treated with interferon-β than other DMTs. This finding may have implications for DMT selection in MS.CONCLUSIONSProgressive loss of RGCs in patients with MS is more pronounced in patients treated with interferon-β than other DMTs. This finding may have implications for DMT selection in MS.This study provides Class IV evidence that for patients with MS, treatment with interferon-β compared with other DMTs leads to a more pronounced rate of retinal ganglion cell loss.CLASSIFICATION OF EVIDENCEThis study provides Class IV evidence that for patients with MS, treatment with interferon-β compared with other DMTs leads to a more pronounced rate of retinal ganglion cell loss. To investigate the association between disease-modifying therapies (DMTs) and the rate of progressive retinal ganglion cell (RGC) and nerve fiber loss in MS. One hundred five relapsing-remitting patients with MS were followed annually for a median of 4.0 years using optical coherence tomography. Twenty-five healthy subjects were also included as normal controls. The rates of global peripapillary retinal nerve fiber layer (pRNFL), temporal RNFL (tRNFL), and ganglion cell inner plexiform layer (GCIPL) thinning were analyzed according to DMT type using a linear mixed-effects model. Optic radiation lesion volume was measured on brain MRI and included as a covariate to minimize the effects of retrograde transsynaptic degeneration. The annual rates of RNFL and GCIPL thinning were higher in patients treated with "platform" therapies (interferon-β and glatiramer acetate) compared with DMTs of higher clinical efficacy (including fingolimod, dimethyl fumarate, natalizumab, alemtuzumab, rituximab, and ocrelizumab) (difference = -0.22 μm/y, = 0.02 for pRNFL; difference = -0.34 μm/y, = 0.009 for tRNFL; and difference = -0.16 μm/y, = 0.005 for GCIPL). Based on an analysis of individual treatments (interferon-β, glatiramer acetate, fingolimod, and natalizumab), interferon-β was associated with inferior RGC preservation, relative to the other drugs. No effect difference was found between glatiramer acetate, fingolimod, and natalizumab. Progressive loss of RGCs in patients with MS is more pronounced in patients treated with interferon-β than other DMTs. This finding may have implications for DMT selection in MS. This study provides Class IV evidence that for patients with MS, treatment with interferon-β compared with other DMTs leads to a more pronounced rate of retinal ganglion cell loss. |
| Author | Barnett, Michael H. Graham, Stuart L. You, Yuyi Parratt, John D.E. Yiannikas, Con Matthews, Jim G. Klistorner, Alexander |
| AuthorAffiliation | From the Department of Clinical Medicine (Y.Y., S.L.G., A.K.), Macquarie University, NSW, Australia; Save Sight Institute (Y.Y., A.K.), The University of Sydney, NSW, Australia; Brain and Mind Centre (M.H.B.), The University of Sydney, NSW, Australia; Sydney Neuroimaging Analysis Centre (M.H.B.), NSW, Australia; Department of Neurology (C.Y., J.D.E.P.), Royal North Shore Hospital, NSW, Australia; and Sydney Informatics and Data Science Hub (J.G.M.), The University of Sydney, NSW, Australia |
| AuthorAffiliation_xml | – name: From the Department of Clinical Medicine (Y.Y., S.L.G., A.K.), Macquarie University, NSW, Australia; Save Sight Institute (Y.Y., A.K.), The University of Sydney, NSW, Australia; Brain and Mind Centre (M.H.B.), The University of Sydney, NSW, Australia; Sydney Neuroimaging Analysis Centre (M.H.B.), NSW, Australia; Department of Neurology (C.Y., J.D.E.P.), Royal North Shore Hospital, NSW, Australia; and Sydney Informatics and Data Science Hub (J.G.M.), The University of Sydney, NSW, Australia |
| Author_xml | – sequence: 1 givenname: Yuyi surname: You fullname: You, Yuyi organization: From the Department of Clinical Medicine (Y.Y., S.L.G., A.K.), Macquarie University, NSW, Australia; Save Sight Institute (Y.Y., A.K.), The University of Sydney, NSW, Australia; Brain and Mind Centre (M.H.B.), The University of Sydney, NSW, Australia; Sydney Neuroimaging Analysis Centre (M.H.B.), NSW, Australia; Department of Neurology (C.Y., J.D.E.P.), Royal North Shore Hospital, NSW, Australia; and Sydney Informatics and Data Science Hub (J.G.M.), The University of Sydney, NSW, Australia – sequence: 2 givenname: Michael surname: Barnett middlename: H. fullname: Barnett, Michael H. – sequence: 3 givenname: Con surname: Yiannikas fullname: Yiannikas, Con – sequence: 4 givenname: John surname: Parratt middlename: D.E. fullname: Parratt, John D.E. – sequence: 5 givenname: Jim surname: Matthews middlename: G. fullname: Matthews, Jim G. – sequence: 6 givenname: Stuart surname: Graham middlename: L. fullname: Graham, Stuart L. – sequence: 7 givenname: Alexander surname: Klistorner fullname: Klistorner, Alexander |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33597189$$D View this record in MEDLINE/PubMed |
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| Cites_doi | 10.1177/1352458514538110 10.1016/j.ophtha.2018.06.022 10.1212/WNL.0000000000002774 10.1007/s40263-018-0521-9 10.1111/ene.13404 10.1212/NXI.0000000000000700 10.1002/ana.25738 10.1212/WNL.0000000000007938 10.1093/brain/aww219 10.1016/S1474-4422(10)70168-X 10.1212/01.wnl.0000295995.46586.ae 10.1001/jama.2018.20588 10.1167/iovs.13-13262 10.1016/S1474-4422(17)30278-8 10.1212/WNL.0000000000003582 |
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| Copyright | American Academy of Neurology Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology. Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Academy of Neurology. 2021 American Academy of Neurology |
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| Title | Interferon-β Is Less Effective Than Other Drugs in Controlling the Rate of Retinal Ganglion Cell Loss in MS |
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