Fingolimod treatment for multiple sclerosis patie… [Ann Neurol. 2011] – PubMed – NCBI.
Fingolimod treatment for multiple sclerosis patients What do we do with varicella?
Comment on
- PMID:
- 22028236
- [PubMed – indexed for MEDLINE]
Mult Scler. 2011 Nov;17(11):1387-9. doi: 10.1177/1352458511410344. Epub 2011 Jun 7.
Delayed fingolimod-associated asystole.
Espinosa PS, Berger JR.
Source
North Oaks Neurology, Hammond, LA, USA. ps.espinosa@gmail.com
Abstract
Oral fingolimod (Gilenya) is a sphingosine-1-phosphate-receptor modulator that prevents the egress of lymphocytes from lymph nodes. Fingolimod reduces relapses and delays disability progression in patients with relapsing forms of multiple sclerosis (MS). We report a patient with MS who developed asystole and sustained bradycardia 21 hours after the first dose of fingolimod.
PMID:
21652609
[PubMed – indexed for MEDLINE]
Publication Types, MeSH Terms, Substances
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via Delayed fingolimod-associated asystole. [Mult Scler. 2011] – PubMed – NCBI.
Neurology. 2010 Jan 5;74(1):18-26. doi: 10.1212/WNL.0b013e3181beecb7. Epub 2009 Nov 25.
25-Hydroxyvitamin D, dementia, and cerebrovascular pathology in elders receiving home services.
Buell JS, Dawson-Hughes B, Scott TM, Weiner DE, Dallal GE, Qui WQ, Bergethon P, Rosenberg IH, Folstein MF, Patz S, Bhadelia RA, Tucker KL.
Source
Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, 711 Washington St., Boston, MA 02111, USA.
Abstract
BACKGROUND:
Vitamin D deficiency has potential adverse effects on neurocognitive health and subcortical function. However, no studies have examined the association between vitamin D status, dementia, and cranial MRI indicators of cerebrovascular disease (CVD).
METHODS:
Cross-sectional investigation of 25-hydroxyvitamin D [25(OH)D], dementia, and MRI measures of CVD in elders receiving home care (aged 65-99 years) from 2003 to 2007.
RESULTS:
Among 318 participants, the mean age was 73.5 +/- 8.1 years, 231 (72.6%) were women, and 109 (34.3%) were black. 25(OH)D concentrations were deficient (<10 ng/mL) in 14.5% and insufficient (10-20 ng/mL) in 44.3% of participants. There were 76 participants (23.9%) with dementia, 41 of which were classified as probable AD. Mean 25(OH)D concentrations were lower in subjects with dementia (16.8 vs 20.0 ng/mL, p < 0.01). There was a higher prevalence of dementia among participants with 25(OH)D insufficiency (< or =20 ng/mL) (30.5% vs 14.5%, p < 0.01). 25(OH)D deficiency was associated with increased white matter hyperintensity volume (4.9 vs 2.9 mL, p < 0.01), grade (3.0 vs 2.2, p = 0.04), and prevalence of large vessel infarcts (10.1% vs 6.9%, p < 0.01). After adjustment for age, race, sex, body mass index, and education, 25(OH)D insufficiency (< or =20 ng/mL) was associated with more than twice the odds of all-cause dementia (odds ratio [OR] = 2.3, 95% confidence interval [CI] 1.2-4.2), Alzheimer disease (OR = 2.5, 95% CI 1.1-6.1), and stroke (with and without dementia symptoms) (OR = 2.0, 95% CI 1.0-4.0).
CONCLUSIONS:
Vitamin D insufficiency and deficiency was associated with all-cause dementia, Alzheimer disease, stroke (with and without dementia symptoms), and MRI indicators of cerebrovascular disease. These findings suggest a potential vasculoprotective role of vitamin D.
Comment in
25-hydroxyvitamin D, dementia, and cerebrovascular pathology in elders receiving home services. [Neurology. 2010]
via 25-Hydroxyvitamin D, dementia, and cerebrovascular… [Neurology. 2010] – PubMed – NCBI.
Lancet Neurol. 2011 May;10(5):436-45. doi: 10.1016/S1474-4422(11)70045-X. Epub 2011 Mar 31.
Clinical, environmental, and genetic determinants of multiple sclerosis in children with acute demyelination: a prospective national cohort study.
Banwell B, Bar-Or A, Arnold DL, Sadovnick D, Narayanan S, McGowan M, O’Mahony J, Magalhaes S, Hanwell H, Vieth R, Tellier R, Vincent T, Disanto G, Ebers G, Wambera K, Connolly MB, Yager J, Mah JK, Booth F, Sebire G, Callen D, Meaney B, Dilenge ME, Lortie A, Pohl D, Doja A, Venketaswaran S, Levin S, Macdonald EA, Meek D, Wood E, Lowry N, Buckley D, Yim C, Awuku M, Cooper P, Grand’maison F, Baird JB, Bhan V, Marrie RA.
Source
Division of Neurology, Department of Paediatrics, The Hospital for Sick Children, University of Toronto, Toronto, ON, Canada. brenda.banwell@sickkids.ca
Abstract
BACKGROUND:
HLA-DRB1*15 genotype, previous infection with Epstein-Barr virus, and vitamin D insufficiency are susceptibility factors for multiple sclerosis, but whether they act synergistically to increase risk is unknown. We aimed to assess the contributions of these risk factors and the effect of established precursors of multiple sclerosis, such as brain lesions on MRI and oligoclonal bands in CSF at the time of incident demyelination, on development of multiple sclerosis in children.
METHODS:
In our prospective national cohort study, we assessed children who presented with incident CNS demyelination to any of the 16 paediatric health-care facilities or seven regional health-care facilities in Canada. We did univariate and multivariable analyses to assess contributions of HLA-DRB1*15, Epstein-Barr virus, vitamin D status, MRI evidence of brain lesions, and CSF oligoclonal bands as determinants of multiple sclerosis. We used classification and regression tree analyses to generate a risk stratification algorithm for clinical use.
FINDINGS:
Between Sept 1, 2004, and June 30, 2010, we screened 332 children of whom 302 (91%) were eligible and followed-up for a median of 3·14 years (IQR 1·61-4·51). 63 (21%) children were diagnosed with multiple sclerosis after a median of 127 days (99-222). Although the risk of multiple sclerosis was increased with presence of one or more HLA-DRB1*15 alleles (hazard ratio [HR] 2·32, 95% CI 1·25-4·30), reduced serum 25-hydroxyvitamin D concentration (HR per 10 nmol/L decrease 1·11, 1·00-1·25), and previous Epstein-Barr-virus infection (HR 2·04, 0·99-4·20), no interactions between these variables were detected on multivariate analysis. Multiple sclerosis was strongly associated with baseline MRI evidence of one or more brain lesion (HR 37·9, 5·26-273·85) or CSF oligoclonal bands (6·33, 3·35-11·96), suggesting established disease. One patient diagnosed with multiple sclerosis had a normal MRI scan, and therefore sensitivity of an abnormal MRI scan for multiple sclerosis diagnosis was 98·4%.
INTERPRETATION:
Risk of multiple sclerosis in children can be stratified by presence of HLA-DRB1*15 alleles, remote Epstein-Barr virus infection, and low serum 25-hydroxyvitamin D concentrations. Similar to previous studies in adults, brain lesions detected on MRI and CSF oligoclonal bands in children are probable precursors to the clinical onset of multiple sclerosis. Children with a normal MRI are very likely to have a monophasic illness.
FUNDING:
Canadian Multiple Sclerosis Scientific Research Foundation.
Copyright © 2011 Elsevier Ltd. All rights reserved.
Comment in
Risk of multiple sclerosis in children with acute demyelination. [Lancet Neurol. 2011]
via Clinical, environmental, and genetic determina… [Lancet Neurol. 2011] – PubMed – NCBI.