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      Effect of Fingolimod on Platelet Count Among Multiple Sclerosis Patients

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          Abstract

          Background:

          While many studies have previously focused on fingolimod's effect on immune cells, the effect it has on circulating and local central nervous system platelets (Plts) has not yet been investigated. This study will elucidate what effects fingolimod treatment has on multiple sclerosis (MS) patients’ plasma Plt levels. In addition, it will propose possible reasoning for these effects and suggest further investigation into this topic.

          Methods:

          This quasi-experimental study used patients from the Isfahan Multiple Sclerosis Society to produce a subject pool of 80 patients, including 14 patients who ceased fingolimod use due to complications. The patients had their blood analyzed to determine Plt levels both 1-month prior to fingolimod treatment and 1-month after fingolimod treatment had been started.

          Results:

          The mean level of Plts before initiation of fingolimod therapy (Plt1) among these MS patients was 256.53 ± 66.26. After 1-month of fingolimod treatment, the Plt level yielded an average of 229.96 ± 49.67 (Plt2). This number is significantly lower than the average Plt count before treatment ( P < 0.01).

          Conclusions:

          MS patients taking oral fingolimod treatment may be at risk for side-effects caused by low Plt levels. This may not be a factor for patients with higher or normal Plt levels. However, a patient with naturally low Plt levels may experience a drop below the normal level and be at risk for excessive bleeding. In addition to these possible harmful side-effects, the decreased Plt population may pose positive effects for MS patients.

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          Most cited references 28

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          Platelets contribute to the pathogenesis of experimental autoimmune encephalomyelitis.

          Multiple sclerosis (MS) and its mouse model, experimental autoimmune encephalomyelitis (EAE), are inflammatory disorders of the central nervous system (CNS). The function of platelets in inflammatory and autoimmune pathologies is thus far poorly defined. We addressed the role of platelets in mediating CNS inflammation in EAE. We found that platelets were present in human MS lesions as well as in the CNS of mice subjected to EAE but not in the CNS from control nondiseased mice. Platelet depletion at the effector-inflammatory phase of EAE in mice resulted in significantly ameliorated disease development and progression. EAE suppression on platelet depletion was associated with reduced recruitment of leukocytes to the inflamed CNS, as assessed by intravital microscopy, and with a blunted inflammatory response. The platelet-specific receptor glycoprotein Ibα (GPIbα) promotes both platelet adhesion and inflammatory actions of platelets and targeting of GPIbα attenuated EAE in mice. Moreover, targeting another platelet adhesion receptor, glycoprotein IIb/IIIa (GPIIb/IIIa), also reduced EAE severity in mice. Platelets contribute to the pathogenesis of EAE by promoting CNS inflammation. Targeting platelets may therefore represent an important new therapeutic approach for MS treatment.
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            Physiology and pathophysiology of sphingolipid metabolism and signaling.

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              Platelets Recognize Brain-Specific Glycolipid Structures, Respond to Neurovascular Damage and Promote Neuroinflammation

              Platelets respond to vascular damage and contribute to inflammation, but their role in the neurodegenerative diseases is unknown. We found that the systemic administration of brain lipid rafts induced a massive platelet activation and degranulation resulting in a life-threatening anaphylactic-like response in mice. Platelets were engaged by the sialated glycosphingolipids (gangliosides) integrated in the rigid structures of astroglial and neuronal lipid rafts. The brain-abundant gangliosides GT1b and GQ1b were specifically recognized by the platelets and this recognition involved multiple receptors with P-selectin (CD62P) playing the central role. During the neuroinflammation, platelets accumulated in the central nervous system parenchyma, acquired an activated phenotype and secreted proinflammatory factors, thereby triggering immune response cascades. This study determines a new role of platelets which directly recognize a neuronal damage and communicate with the cells of the immune system in the pathogenesis of neurodegenerative diseases.
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                Author and article information

                Journal
                Int J Prev Med
                Int J Prev Med
                IJPVM
                International Journal of Preventive Medicine
                Medknow Publications & Media Pvt Ltd (India )
                2008-7802
                2008-8213
                2015
                23 December 2015
                : 6
                Affiliations
                [1 ]Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
                [2 ]Isfahan Neurosciences Research Centre, Affiliated to Isfahan University of Medical Sciences, Isfahan, Iran
                [3 ]Department of Neurology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
                [4 ]Multiple Sclerosis and Neuroimmunology Research Center, Isfahan, Iran
                [5 ]Department of Molecular Biology, Cell Biology, and Biochemistry, Brown University, Providence, Rhode Island 02912, USA
                [6 ]Department of Neuroscience, Brown University, Providence, Rhode Island 02912, USA
                [7 ]Department of Electrical and Computer Engineering, Isfahan University of Technology, Isfahan, Iran
                [8 ]Department of Immunology, School of Medicine, Kashan University of Medical Sciences, Kashan, Iran
                Author notes
                Correspondence to: Dr. Mehrdad Farrokhi, Department of Immunology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran. E-mail: mehrdadfarokhi72@ 123456yahoo.com
                Article
                IJPVM-6-125
                10.4103/2008-7802.172539
                4736130
                26900439
                Copyright: © 2015 Farrokhi M.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                Categories
                Original Article

                Health & Social care

                multiple sclerosis, fingolimod, platelet

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