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Genetic susceptibility to MS: a second stage analysis in Canadian MS families.

https://arctichealth.org/en/permalink/ahliterature193481
Source
Neurogenetics. 2001 Jul;3(3):145-51
Publication Type
Article
Date
Jul-2001
Author
D A Dyment
C J Willer
B. Scott
H. Armstrong
A. Ligers
J. Hillert
D W Paty
S. Hashimoto
V. Devonshire
J. Hooge
L. Kastrukoff
J. Oger
L. Metz
S. Warren
W. Hader
C. Power
A. Auty
A. Nath
R. Nelson
M. Freedman
D. Brunet
J E Paulseth
G. Rice
P. O'Connor
P. Duquette
Y. Lapierre
G. Francis
J P Bouchard
T J Murray
V. Bhan
C. Maxner
W. Pryse-Phillips
M. Stefanelli
A D Sadovnick
N. Risch
G C Ebers
Author Affiliation
The Wellcome Trust Center for Human Genetics, Oxford, UK.
Source
Neurogenetics. 2001 Jul;3(3):145-51
Date
Jul-2001
Language
English
Publication Type
Article
Keywords
Canada
Family
Female
Genetic Linkage
Genetic markers
Genetic Predisposition to Disease
Genome, Human
HLA-DR Antigens - genetics
HLA-DRB1 Chains
Humans
Linkage Disequilibrium
Male
Multiple Sclerosis - genetics
Nuclear Family
Software
Abstract
Four published genome screens have identified a number of markers with increased sharing in multiple sclerosis (MS) families, although none has reached statistical significance. One hundred and five markers previously identified as showing increased sharing in Canadian, British, Finnish, and American genome screens were genotyped in 219 sibling pairs ascertained from the database of the Canadian Collaborative Project on Genetic Susceptibility to MS (CCPGSMS). No markers examined met criteria for significant linkage. Markers located at 5p14 and 17q22 were analyzed in a total of 333 sibling pairs and attained mlod scores of 2.27 and 1.14, respectively. The known HLA Class II DRB1 association with MS was confirmed (P
PubMed ID
11523565 View in PubMed
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The Mayo Clinic-Canadian Cooperative trial of sulfasalazine in active multiple sclerosis.

https://arctichealth.org/en/permalink/ahliterature203919
Source
Neurology. 1998 Nov;51(5):1342-52
Publication Type
Article
Date
Nov-1998
Author
J H Noseworthy
P. O'Brien
B J Erickson
D. Lee
D. Sneve
G C Ebers
G P Rice
A. Auty
W J Hader
A. Kirk
P. Duquette
J. Carter
G. Francis
L. Metz
E. Shuster
Author Affiliation
Mayo Clinic/Mayo Foundation, Rochester, MN 55905, USA.
Source
Neurology. 1998 Nov;51(5):1342-52
Date
Nov-1998
Language
English
Publication Type
Article
Keywords
Adult
Anti-Inflammatory Agents, Non-Steroidal - therapeutic use
Brain - pathology
Canada
Disabled Persons
Disease Progression
Double-Blind Method
Female
Follow-Up Studies
Humans
Magnetic Resonance Imaging
Male
Minnesota
Multiple Sclerosis - drug therapy - physiopathology
Placebos
Recurrence
Sulfasalazine - therapeutic use
Survival Analysis
Time Factors
Abstract
To determine whether sulfasalazine is better than placebo in slowing disability progression in MS.
In this randomized, double-blind, placebo-controlled phase III trial, 199 patients with active relapsing-remitting (n = 151) or progressive (n = 48) MS were evaluated at 3-month intervals for a minimum of 3 years (94% completed 3 years of follow-up; mean follow-up, 3.7 years). MRI studies were performed at 6-month intervals on a subset of 89 patients.
Sulfasalazine failed to slow or prevent disability progression as measured by the primary outcome (confirmed worsening of the Expanded Disability Status Scale [EDSS] score by at least 1.0 point on two consecutive 3-month visits). Sulfasalazine influenced favorably a number of secondary outcomes during the first 18 months of the trial (e.g., annualized relapse rate, proportion of relapse-free patients; progressive subgroup only: rate of EDSS progression at 1 and 2 years, median time to EDSS progression) but these positive findings were not sustained into the second half of the trial.
Sulfasalazine does not prevent EDSS score progression in the subset of MS patients studied by this protocol. Treatments may improve relapse-related outcomes in MS, at least temporarily, without providing sustained slowing of EDSS progression. Phase III MS trials should be of sufficient length to determine a meaningful impact on disease course.
Notes
Comment In: Neurology. 1999 Jul 22;53(2):43710430451
PubMed ID
9818858 View in PubMed
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