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To investigate whether genotypic differences can be identified between MS patients developing 'liver injury' (defined as ALT levels five times the upper normal limit and above) compared to those not developing liver injury after exposure to beta-interferon for MS.
PURPOSE: To investigate whether genotypic differences can be identified between MS patients who develop liver injury compared to those who do not develop injury in response to beta-interferon therapy.
OBJECTIVE: To determine whether elevated liver enzyme tests (ALT > 5 times the upper limit of normal) in response to beta-interferon therapy in MS patients is associated with genetic polymorphisms.
METHOD OF RECRUITMENT:
Patients will be identified through a clinic database and chart reviews. An introductory letter will be mailed to potential participants, inviting them to volunteer. A follow-up phone call will be made to determine interest and consent into study.
Saliva will be collected for genetic analyses and a questionnaire will be administered
Observational Model: Case Control, Time Perspective: Retrospective
MS Clinic UBC Hospital
Not yet recruiting
University of British Columbia
Published on BioPortfolio: 2014-08-27T03:13:54-0400
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A form of multiple sclerosis characterized by a progressive deterioration in neurologic function which is in contrast to the more typical relapsing remitting form. If the clinical course is free of distinct remissions, it is referred to as primary progressive multiple sclerosis. When the progressive decline is punctuated by acute exacerbations, it is referred to as progressive relapsing multiple sclerosis. The term secondary progressive multiple sclerosis is used when relapsing remitting multiple sclerosis evolves into the chronic progressive form. (From Ann Neurol 1994;36 Suppl:S73-S79; Adams et al., Principles of Neurology, 6th ed, pp903-914)
A non-glycosylated form of interferon beta-1 that has a serine at position 17. It is used in the treatment of both RELAPSING-REMITTING MULTIPLE SCLEROSIS and CHRONIC PROGRESSIVE MULTIPLE SCLEROSIS.
An autoimmune disorder mainly affecting young adults and characterized by destruction of myelin in the central nervous system. Pathologic findings include multiple sharply demarcated areas of demyelination throughout the white matter of the central nervous system. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia, and bladder dysfunction. The usual pattern is one of recurrent attacks followed by partial recovery (see MULTIPLE SCLEROSIS, RELAPSING-REMITTING), but acute fulminating and chronic progressive forms (see MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE) also occur. (Adams et al., Principles of Neurology, 6th ed, p903)
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Multiple protein bands serving as markers of specific ANTIBODIES and detected by ELECTROPHORESIS of CEREBROSPINAL FLUID or serum. The bands are most often seen during inflammatory or immune processes and are found in most patients with MULTIPLE SCLEROSIS.
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