Contributions
Abstract: P991
Type: Poster Sessions
Abstract Category: Clinical aspects of MS - Paediatric MS
Background: Multiple sclerosis (MS) risk is modified by HLA-DRB1*15 genotype, race, vitamin D status and location of residence during childhood. Geographic residence is associated with ultraviolet radiation exposure, and consequently with its impact on dermal pigmentation.
Objectives: To determine whether HLA-DRB1*15 status, 25-hydroxyvitamin D (25(OH)D) levels measured at baseline, and skin tone are associated with MS outcome in children with acquired demyelinating syndromes (ADS).
Methods: 71 children with incident ADS were enrolled at a single site (43° latitude) and completed demographic questionnaires. Non-sun exposed upper inner arm melanin content was measured using the DSM II ColorMeter device. 25(OH)D concentrations were measured in serum obtained within 60 days of symptom onset and compared to lab-reported normative values. Vitamin D insufficiency was defined as [25(OH)D] less than 75 nmol/l (30 ng/dl). HLA-DRB1*15 alleles were quantified using allele-specific PCR amplification. Statistical analysis was performed using Spearman correlation models and Wilcoxon or Kruskal-Wallis tests as appropriate.
Results: 24 (33.8%) children were diagnosed with MS, and 47 remain monophasic (monoADS). HLA-DRB1*15 status did not differ between the groups (p=0.91). Children diagnosed with MS had lower 25(OH)D levels at baseline (mean=51.1, SD=18.7) than the monoADS children (mean=63.6, SD=24.4; p=0.03). Non-sun exposed skin tone measured in the upper inner arm did not differ between children diagnosed with MS (melanin index, mean=44.2, SD=11.3) and monoADS (mean=43.6, SD=8.8; p=0.87). Interestingly 25(OH)D levels correlated with upper inner arm melanin index in the MS group (rho= -0.45, p=0.03) but not in children with monoADS (rho= -0.21, p=0.16).
Conclusions: The association of vitamin D insufficiency with MS outcome in children with ADS appears to relate, in part, to skin pigmentation. Further work is required to delineate the complex interplay between dietary vitamin D ingestion, extent of sun exposure and pigmentation of sun-exposed skin, seasonal vitamin D concentrations, and genetic influences of vitamin D pathways with MS risk.
Disclosure: Candice Dunn, Julia O´Mahony, Neda Ebrahimi, Heather Hanwell: nothing to disclose.
Dr. Marrie receives research funding from: CIHR, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn's and Colitis Canada, National Multiple Sclerosis Society, CMSC.
Dr. Bar-Or has participated as a speaker in meetings sponsored by and received consulting fees and/or grant support from: Atara Biotherapeutics, Biogen Idec, Celgene/Receptos, Genentech/Roche, GlaxoSmithKline, MAPI, Medimmune, Merck/EMD Serono, Novartis, Sanofi-Genzyme.
Dr. Banwell has served as a consultant for Novartis and as a non-remunerated advisor on clinical trial design for Biogen-IDEK, Sanofi, Teva Neuroscience and Novartis and has received funding from Canadian Multiple Sclerosis Research Foundation, National MS Society and Pcori.
Dr. Yeh: Novartis- speaker's honorarium, Teva unrestricted funding for an educational symposium, Juno Therapeutics, Scientific Advisory Panel. ACI, relapse adjudication. Funding sources: OIRM, MSSC/MSSF, NMSS, SickKids Foundation, CBMH, Guthy Jackson Foundation, CHAK, CMSC, SCN.
Abstract: P991
Type: Poster Sessions
Abstract Category: Clinical aspects of MS - Paediatric MS
Background: Multiple sclerosis (MS) risk is modified by HLA-DRB1*15 genotype, race, vitamin D status and location of residence during childhood. Geographic residence is associated with ultraviolet radiation exposure, and consequently with its impact on dermal pigmentation.
Objectives: To determine whether HLA-DRB1*15 status, 25-hydroxyvitamin D (25(OH)D) levels measured at baseline, and skin tone are associated with MS outcome in children with acquired demyelinating syndromes (ADS).
Methods: 71 children with incident ADS were enrolled at a single site (43° latitude) and completed demographic questionnaires. Non-sun exposed upper inner arm melanin content was measured using the DSM II ColorMeter device. 25(OH)D concentrations were measured in serum obtained within 60 days of symptom onset and compared to lab-reported normative values. Vitamin D insufficiency was defined as [25(OH)D] less than 75 nmol/l (30 ng/dl). HLA-DRB1*15 alleles were quantified using allele-specific PCR amplification. Statistical analysis was performed using Spearman correlation models and Wilcoxon or Kruskal-Wallis tests as appropriate.
Results: 24 (33.8%) children were diagnosed with MS, and 47 remain monophasic (monoADS). HLA-DRB1*15 status did not differ between the groups (p=0.91). Children diagnosed with MS had lower 25(OH)D levels at baseline (mean=51.1, SD=18.7) than the monoADS children (mean=63.6, SD=24.4; p=0.03). Non-sun exposed skin tone measured in the upper inner arm did not differ between children diagnosed with MS (melanin index, mean=44.2, SD=11.3) and monoADS (mean=43.6, SD=8.8; p=0.87). Interestingly 25(OH)D levels correlated with upper inner arm melanin index in the MS group (rho= -0.45, p=0.03) but not in children with monoADS (rho= -0.21, p=0.16).
Conclusions: The association of vitamin D insufficiency with MS outcome in children with ADS appears to relate, in part, to skin pigmentation. Further work is required to delineate the complex interplay between dietary vitamin D ingestion, extent of sun exposure and pigmentation of sun-exposed skin, seasonal vitamin D concentrations, and genetic influences of vitamin D pathways with MS risk.
Disclosure: Candice Dunn, Julia O´Mahony, Neda Ebrahimi, Heather Hanwell: nothing to disclose.
Dr. Marrie receives research funding from: CIHR, Research Manitoba, Multiple Sclerosis Society of Canada, Multiple Sclerosis Scientific Foundation, Crohn's and Colitis Canada, National Multiple Sclerosis Society, CMSC.
Dr. Bar-Or has participated as a speaker in meetings sponsored by and received consulting fees and/or grant support from: Atara Biotherapeutics, Biogen Idec, Celgene/Receptos, Genentech/Roche, GlaxoSmithKline, MAPI, Medimmune, Merck/EMD Serono, Novartis, Sanofi-Genzyme.
Dr. Banwell has served as a consultant for Novartis and as a non-remunerated advisor on clinical trial design for Biogen-IDEK, Sanofi, Teva Neuroscience and Novartis and has received funding from Canadian Multiple Sclerosis Research Foundation, National MS Society and Pcori.
Dr. Yeh: Novartis- speaker's honorarium, Teva unrestricted funding for an educational symposium, Juno Therapeutics, Scientific Advisory Panel. ACI, relapse adjudication. Funding sources: OIRM, MSSC/MSSF, NMSS, SickKids Foundation, CBMH, Guthy Jackson Foundation, CHAK, CMSC, SCN.