5296
`
`Late Breaking News
`
`5 (p=0.004) years, patients in the early treatment group performed
`better in the PASAT. Conclusions: The 5-year results of the BENEFIT
`study provide further evidence supporting early initiation of
`treatment with IFNB-lb in patients with a first event suggestive of MS.
`Supported by: Bayer Schering Pharma AG, Berlin, Germany.
`
`P902
`
`Randomized, prospective, rater-blinded, four-year, pilot study to
`compare the effect of daily versus every-other-day glatiramer
`acetate 20 mg subcutaneous injections in relapsing-remitting
`multiple sclerosis
`Omar Khan, Christina Caon, !mad Zak, Zahid Latif, Ramya Penmesta,
`Fen Bao, Samia Ragheb, Alan Hudson, Alex Tselis
`
`Wayne State University School o( Medicine, Detroit, Michigan, USA
`
`Background: The recommended dose of GA in RRMS is 20 mg subcu(cid:173)
`taneous (SC) daily (QD) although the optimal dose remains unknown.
`There is considerable interest in alternate dosing regimens of GA in
`RRMS. Daily SC injectable therapy can be challenging for long-term
`patient compliance. Objective: We conducted a pilot trial to compare
`the effect of GA 20 mg SC daily versus every other day (QOD) in
`RRMS. The primary endpoint was based on a composite of clinical,
`MRI, and immunologic outcomes. Methods: Treatment naive RRMS
`patients were randomized to GA 20 mg SC QD or QOD and followed
`prospectively for 2 years. After 2 years, patients in each group were
`given the option to continue or switch to the other group, and fol(cid:173)
`lowed for an additional 2 years. EDSS was recorded every 6 months by
`a rater blinded to dosing allocation. Brain MRI scans were obtained at
`baseline, and years 2 and 4. Blood for immunologic testing was
`obtained at baseline and multiple time points after randomization.
`Results: 30 patients were randomized to GA 20 mg SC given QD or
`QOD. Both groups were well-matched for age, disease duration, EDSS,
`relapse rate, T2W and gadolinium (Gd) enhancing lesions. After
`2 years, there were no differences in the relapse rate, disease progres(cid:173)
`sion, Change in T2W lesion volume, or Gd enhancing lesions
`between the two groups. In vitro proliferation of GA-responsive T-cells
`and Thl/Th2 cytokine expression did not differ between the two
`groups at any time point after randomization. After 2 years, all
`patients in the QD group opted to switch to QOD. After a total of
`4 years of prospective follow-up, there was no difference between the
`QD-QOD cross over group and the always QOD group. Additional
`data on imaging and immunologic outcomes will be presented.
`Conclusions: This pilot study suggests that GA 20 mg SC adminis(cid:173)
`tered QD or QOD may be equally effective in RRMS. This may have
`implications for the long-term use of GA. However, large multi-center
`studies are warranted to confirm our findings and to identify the opti(cid:173)
`mal dose of GA in RRMS.
`
`Epidemiology I Genetics
`
`P903
`
`IMSGC. Results: Two of these seven SNPs also demonstrated evidence
`for association with multiple sclerosis; rs12708716 from the C-type
`lectin domain family 16, member A (CLEC16A) gene (p=l.6x10-16
`)
`and rs763361 from the CD226 gene (p=5.4x10-8
`). In each case the
`allele associated with increased risk for multiple sclerosis was identi(cid:173)
`cal to that showing evidence for association with type 1 diabetes.
`Conclusions: These findings thereby suggest two additional multiple
`sclerosis susceptibility genes and lend support to the notion of
`autoimmune susceptibility genes.
`Supported by: The National Multiple Sclerosis Society (USA)
`(AP 3758-A-16, RG 2899, FG-1718-Al), grants from the NINDS
`the NIAID (POl
`(NS049477, NS032830, NS26799), AI067152,
`AI039671), a National Multiple Sclerosis Society (USA) Collaborative
`Research Award (CA 1001-A-14), and the Penates Foundation. We
`acknowledge use of DNA from the British 1958 Birth Cohort collec(cid:173)
`tion, funded by the Medical Research Council grant G0000934 and
`the Wellcome Trust grant 068545/Z/02.
`
`P904
`
`Infections and vaccinations and the risk of multiple sclerosis:
`a population-based study
`Sreeram Ramagopalan 1
`, William Valdar1
`, David Dyment', Gabriele
`, Irene Yee2
`, Gavin Giovannoni 1
`DeLuca1
`, George Ebers 1
`, Dessa
`Sadovnick2
`
`'University o( Ox(ord, Ox(ord, United Kingdom; 2 University o( British
`Columbia, Vancouver, British Columbia, United Kingdom
`
`Background: Genetic and environmental factors have important
`roles in multiple sclerosis (MS) susceptibility. Several studies have
`attempted to correlate exposure to viral illness with the subsequent
`development of MS. Objective: Here in a population based Canadian
`cohort, we investigate the relationship between prior clinical
`infection or vaccination and the risk of MS. Methods: Using the lon(cid:173)
`gitudinal Canadian database, 14362 MS index cases and 7671 spouse
`controls were asked about history of measles, mumps, rubella,
`varicella and infectious mononucleosis as well as details about vacci(cid:173)
`nation with measles, mumps,rubella, hepatitis B and influenza vac(cid:173)
`cines. Comparisons were made between cases and spouse controls.
`Results: Spouse controls and stratification by sex appear to correct for
`ascertainment bias because with a single exception we found no sig(cid:173)
`nificant differences between cases and controls for all viral exposures
`and vaccinations. However 699 cases and 165 controls reported a
`history of infectious mononucleosis (chi 2 = 97.9, 1 d.f., p<O.OOl)
`(corrected odds ratio 2.06, 95% confidence interval 1.71-2.48).
`Conclusions: Historically reported measles, mumps, rubella, varicella
`and vaccination for hepatitis B, influenza, measles, mumps and rubel(cid:173)
`la are not associated with increased risk of MS later in life. A clinical
`history of infectious mononucleosis is conspicuously associated with
`increased MS
`susceptibility. These findings support studies
`implicating Epstein Barr virus in MS disease susceptibility but a
`co-association between MS susceptibility and clinically apparent
`infectious mononucleosis cannot be excluded.
`Supported by: Multiple Sclerosis Society of Canada Scientific
`Research Foundation.
`
`The expanding genetic overlap between multiple sclerosis and
`type 1 diabetes
`Maria Ban, for the International Multiple Sclerosis Genetics
`Consortium
`
`Imaging
`
`Clinical Neurosciences, University o( Cambridge, Cambridge, United
`Kingdom
`
`P905
`
`Background: A familial clustering of autoimmune disease is well
`recognised and suggests that some susceptibility genes may predis(cid:173)
`pose to autoimmunity in general whereas other genes lead to specific
`disease. Objective: To investigate if variants of established relevance
`in type 1 diabetes might also be relevant in multiple sclerosis.
`Methods: We tested seven single nucleotide polymorphisms (SNPs)
`that are known to be associated with type 1 diabetes in a large multi(cid:173)
`ple sclerosis dataset consisting of 2,369 trio families, 5,737 cases and
`10,296 unrelated controls. Samples were recruited from across
`six countries: Australia, Belgium, Norway, Sweden, United Kingdom
`(UK) and the United States of America (USA) that are within the
`
`Predictive value of magnetic resonance imaging for future clinical
`outcome
`Bouke Boden, Ivo van den Elskamp, Bernard Uitdehaag, Frederik
`Barkhof
`
`Vrije Universiteit Medical Centre, Amsterdam, Netherlands
`
`Background: Although only weak correlations between MRI and
`clinical findings have been found, MRI variables are widely used as
`secondary outcome measures in MS-related clinical trials. Better
`knowledge of these possible relationships is clinically important and
`could help patient selection in future trials in MS. Objective: To
`
`Multiple Sclerosis 2008; 14: 529 5-5298
`
`http:/ /msj.sagepub.com
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