Increased tissue damage and lesion volumes in African Americans with multiple sclerosis
- PMID: 20089944
- DOI: 10.1212/WNL.0b013e3181cff6fb
Increased tissue damage and lesion volumes in African Americans with multiple sclerosis
Abstract
Background: African American (AA) patients with multiple sclerosis (MS) have more rapid disease progression and poorer responses to disease-modifying therapies than white American (WA) patients with MS.
Objectives: To investigate brain MRI characteristics in AA compared to WA in a cohort of consecutive patients with MS.
Methods: We studied 567 patients with MS (age: 45.1 +/- SD 9.8 years, disease duration: 13.4 +/- 8.6 years), comprised of 488 WA and 79 AA. All patients obtained clinical and quantitative MRI evaluation. The majority of patients, 96% of AA and 94% of WA, were on disease-modifying therapies. The MRI measures included T1-, T2-, and gadolinium contrast-enhancing (CE) lesion volumes (LV) and CE number, global and tissue-specific brain atrophy, and magnetization transfer ratio (MTR) in lesions and normal-appearing gray matter (NAGM) and white matter (NAWM). The associations between race and clinical and MRI measurements were assessed in regression analysis.
Results: The MTR values in lesions and in NAGM and NAWM were significantly lower in AA compared to WA. The AA group had 31% greater T2-LV and 101% greater T1-LV compared to WA. The MS Severity Score for AA (mean +/- SD = 4.3 +/- 2.9) was greater than for WA (3.8 +/- 2.5), despite a shorter disease duration in AA, indicating more aggressive clinical disease.
Conclusions: African American patients showed increased tissue damage, as measured by magnetization transfer ratio, and presented higher lesion volumes compared to white Americans. The greater tissue damage and faster lesion volume accumulation may explain the rapid clinical progression in African American patients.
Comment in
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Does race matter for multiple sclerosis?Neurology. 2010 Feb 16;74(7):532-3. doi: 10.1212/WNL.0b013e3181d0374f. Epub 2010 Jan 20. Neurology. 2010. PMID: 20089941 No abstract available.
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