Abstract

ObjectiveA 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.MethodsIn 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.ResultsCompared 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.ConclusionPlatelets 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.

Highlights

  • The fatal outcome in one of two multiple sclerosis (MS) patients with idiopathic thrombocytopenic purpura (ITP) prompted our interest in platelet activity and function in the context of MS

  • CaFnioDgdmu6M2rpePSarpe1isxaotpinerenostfspiolant,ePleMtPc,oaunndt,pprloateilnetSabcteitvwateioen mcoanrtkreorls Comparison of platelet count, platelet activation marker CD62P expression, platelet microparticles (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

  • We have reported elevated plasma endothelial microparticles (EMP) in MS, positive for platelet endothelial cell adhesion molecule-1 (CD31/ PECAM-1) [22] and suggested that this increase in EMP may reflect the interaction of activated T-cells with endothelium

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Summary

Introduction

The fatal outcome in one of two multiple sclerosis (MS) patients with idiopathic thrombocytopenic purpura (ITP) prompted our interest in platelet activity and function in the context of MS. Putnam investigated a possible role of venule thrombosis as a factor in central nervous system (CNS) demyelination in 1935 [1], a role for platelets in CNS demyelination was not further considered until a series of papers in the 1960s, such as that of Wright et al [2] For example, Nathanson and Savitsky [3] employed a measure of platelet adhesiveness in 132 subjects, 60 of whom had MS. We employed consecutively recruited patients and measured, in addition to routine tests such as platelet counts, the expression of platelet activation marker P-selectin (CD62p), platelet microparticles (PMP) in plasma, platelet micro-aggregates (PAg), protein S activity, and platelet-associated immunoglobulins IgG and IgM, as described following

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