The effects of thrombomodulin and activated protein C on the pathogenesis of multiple sclerosis

dc.authorid0000-0003-2866-555X
dc.authorid0000-0002-1483-997X
dc.contributor.authorBalkuv, Ece
dc.contributor.authorVaroglu, Asuman Orhan
dc.contributor.authorIsik, Nihal
dc.contributor.authorIsbilen, Banu
dc.contributor.authorDuruyen, Saadettin
dc.contributor.authorBaşaran, Recep
dc.contributor.authorKocer, Abdulkadir
dc.date.accessioned2025-05-10T19:43:02Z
dc.date.issued2016
dc.departmentİstanbul Medeniyet Üniversitesi
dc.description.abstractBackground: Various molecules of the coagulation cascade are thought to have varying roles in the pathophysiology of multiple sclerosis (MS). We aimed to find new information about the effects of the coagulation cascade molecules to develop new therapeutic strategies for MS. Materials and methods: Patients with MS were chosen from among patients who were followed up at our hospital. We examined the thrombomodulin (TM) and activated protein C (APC) serum levels in patients with MS and the healthy controls. The patient groups were determined as relapsing-remitting MS (RRMS) or secondary progressive MS (SPMS) according to the McDonald criteria and between ages of 18 and 70. Results: A total of 244 participants, 122 patients with multiple sclerosis and 122 healthy volunteers were included in the study. There was no statistically significant difference in the APC and TM levels between the patients and the healthy controls (p > 0.05), between the patients with RRMS and SPMS (p > 0.05), and between the first day of acute relapse and 10th day of methylprednisolone therapy in the patients with RRMS (p=0.334; p=0.363). We detected a statistically positive correlation only between the expanded disability status scale (EDSS) scores and TM levels in the patient group (p=0.009). Conclusion: Treatment with methylprednisolone decreases EDSS score in RRMS relapse. The increase in EDSS is related to level of TM. The changes in level of TM and APC may be indicator for prognosis of MS or treatment modalities to MS. (C) 2016 Elsevier B.V. All rights reserved.
dc.identifier.doi10.1016/j.msard.2016.05.017
dc.identifier.endpage135
dc.identifier.issn2211-0348
dc.identifier.issn2211-0356
dc.identifier.pmid27456888
dc.identifier.scopus2-s2.0-84973439817
dc.identifier.scopusqualityQ2
dc.identifier.startpage131
dc.identifier.urihttps://doi.org/10.1016/j.msard.2016.05.017
dc.identifier.urihttps://hdl.handle.net/20.500.14730/10479
dc.identifier.volume8
dc.identifier.wosWOS:000382345200025
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherElsevier Sci Ltd
dc.relation.ispartofMultiple Sclerosis and Related Disorders
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WOS_20250302
dc.subjectMultiple sclerosis
dc.subjectThrombomodulin
dc.subjectActivated protein C
dc.subjectCoagulation cascade factor
dc.subjectNeuroinflammation
dc.subjectNeuroprotection
dc.titleThe effects of thrombomodulin and activated protein C on the pathogenesis of multiple sclerosis
dc.typeArticle

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