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. 2008 Jun 27:5:27.
doi: 10.1186/1742-2094-5-27.

Evidence of platelet activation in multiple sclerosis

William A Sheremata  1 , Wenche Jy, Lawrence L Horstman, Yeon S Ahn, J Steven Alexander, Alireza Minagar
Affiliations

Evidence of platelet activation in multiple sclerosis

William A Sheremata et al. J Neuroinflammation. .

Abstract

Objective: A fatality in one multiple sclerosis (MS) patient due to acute idiopathic thrombocytopenic purpura (ITP) and a near fatality in another stimulated our interest in platelet function abnormalities in MS. Previously, we presented evidence of platelet activation in a small cohort of treatment-naive MS patients.

Methods: In this report, 92 normal controls and 33 stable, untreated MS patients were studied. Platelet counts, measures of platelet activation [plasma platelet microparticles (PMP), P-selectin expression (CD62p), circulating platelet microaggragtes (PAg)], as well as platelet-associated IgG/IgM, were carried out. In addition, plasma protein S activity was measured.

Results: Compared to controls, PMP were significantly elevated in MS (p < 0.001) and CD62p expression was also markedly elevated (p < 0.001). Both are markers of platelet activation. Platelet-associated IgM, but not IgG, was marginally elevated in MS (p = 0.01). Protein S in MS patients did not differ significantly from normal values.

Conclusion: Platelets are significantly activated in MS patients. The mechanisms underlying this activation and its significance to MS are unknown. Additional study of platelet activation and function in MS patients is warranted.

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Figures

Figure 1
Figure 1
Comparison of platelet count, platelet activation marker CD62P expression, PMP, and protein S between controls and MS patients. (A) Mean platelet counts did not differ between the MS and control groups. (B) Elevation of platelet activation marker CD62p in the MS group was highly significant, *P < 0.001. Not shown or included in the analysis was one extremely high value (60.6), possibly a technical error. (C) PMP counts in the MS patients were significantly higher than controls, *p < 0.001. Not shown or included in the analysis was one very high outlying value (25.2). (D) Protein S activity (% control) did not differ significantly between MS and controls. All values are expressed as mean ± SD. The institutional control values (mean ± SD) of platelet count and protein S activity were obtained from the laboratory of University of Miami Hospital and Clinics, and are not shown as individual dots because the numbers are too large.
Figure 2
Figure 2
Comparison of platelet-associated IgG and IgM between controls and MS patients. Results are expressed as percentage of platelets positive for the indicated immunoglobulin, where positive is defined as >3SD above the mean for normal subjects in this laboratory by the procedure referenced in the methods section. (A) Results for platelet-associated IgG showed no significant difference between the MS group and controls. Value were, ± SD: 2.7 ± 1.3 for controls vs. 3.4 ± 2.7. (B) In contrast, mean platelet associated IgM was significantly higher in the MS group, *p < 0.01. Values were, ± SD: 3.4 ± 1.3 for controls vs. 7.8 ± 6.5 for MS. Not shown or included in analysis were 2 very high outlying values (55.9, 65.9).
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