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dc.contributor.authorKvistad, Silje
dc.contributor.authorMyhr, Kjell-Morten
dc.contributor.authorHolmøy, Trygve
dc.contributor.authorSaltyte Benth, Jurate
dc.contributor.authorLøken-Amsrud, Kristin Ingeleiv
dc.contributor.authorWergeland, Stig
dc.contributor.authorBeiske, Antonie Giæver
dc.contributor.authorBjerve, Kristian S
dc.contributor.authorHovdal, Harald Olav
dc.contributor.authorLilleås, Finn
dc.contributor.authorMidgard, Rune
dc.contributor.authorPedersen, Tom
dc.contributor.authorBakke, Søren Jacob
dc.contributor.authorTorkildsen, Øivind
dc.date.accessioned2017-06-06T11:48:46Z
dc.date.available2017-06-06T11:48:46Z
dc.date.created2017-01-04T10:38:54Z
dc.date.issued2016
dc.identifier.citationNeurology: Neuroimmunology and neuroinflammation. 2016, 3 (4), .nb_NO
dc.identifier.issn2332-7812
dc.identifier.urihttp://hdl.handle.net/11250/2444434
dc.description.abstractObjective: To study whether tobacco use is associated with MRI and clinical disease activity in patients with multiple sclerosis (MS). Methods: Prospective cohort study of 87 patients with relapsing-remitting MS originally included in a randomized placebo-controlled trial of omega-3 fatty acids in MS (the OFAMS Study). Serum levels of cotinine (biomarker of tobacco use) were analyzed at baseline and every 6 months for 2 years. MRI activity was assessed at baseline and monthly for 9 months and after 12 and 24 months. Results: Fifty-three patients (61%) had serum cotinine levels ≥85 nmol/L on ≥60% of the measurements and were considered tobacco users and 34 (39%) had cotinine levels <85 nmol/L, consistent with non–tobacco use. There was no association between tobacco use and the occurrence of new gadolinium-enhancing T1 lesions, new or enlarging T2 lesions, or their aggregate (combined unique activity). Furthermore, there was no association between cotinine levels and MRI activity for the tobacco users, and tobacco users did not have more relapses or Expanded Disability Status Scale progression. Conclusion: Our results indicate that tobacco use does not directly influence MRI activity or relapse rate in MS. This may implicate that the reported association between smoking and MS disease progression could be mediated through other mechanisms.nb_NO
dc.language.isoengnb_NO
dc.publisherIOP Publishingnb_NO
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/deed.no*
dc.titleNo association of tobacco use and disease activity in multiple sclerosisnb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.source.pagenumber5nb_NO
dc.source.volume3nb_NO
dc.source.journalNeurology: Neuroimmunology and neuroinflammationnb_NO
dc.source.issue4nb_NO
dc.identifier.doi10.1212/NXI.0000000000000260
dc.identifier.cristin1420567
dc.description.localcode© 2016 American Academy of Neurology. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License 4.0 (CC BY-NC-ND), which permits downloading and sharing the work provided it is properly cited. The work cannot be changed in any way or used commercially.nb_NO
cristin.unitcode194,65,10,0
cristin.unitcode194,65,1,0
cristin.unitnameInstitutt for laboratoriemedisin, barne- og kvinnesykdommer
cristin.unitnameDMF fakultetsadministrasjon
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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Attribution-NonCommercial-NoDerivatives 4.0 Internasjonal
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