Türk Nöroloji Dergisi (Sep 2021)

Could Serum Endocan Be a Vascular Endothelial Marker in Relapsing-Remitting Multiple Sclerosis?

  • Arife Çimen Atalar,
  • Mesrure Köseoğlu,
  • Nurettin Yavuz,
  • Yüksel Erdal,
  • Osman Oğuz,
  • Ufuk Emre

DOI
https://doi.org/10.4274/tnd.2021.81073
Journal volume & issue
Vol. 27, no. 3
pp. 257 – 262

Abstract

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Objective: Multiple sclerosis (MS) is a chronic degenerative and inflammatory disease leading to axonal damage and demyelination in the central nervous system. Although the pathogenesis is still controversial, it is accepted that there is an immune-mediated inflammatory response. Endothelial cell specific molecule-1 (ESM-1) (endocan) is expressed by endothelial cells under the control of cytokines, and increases in inflammatory processes involving the vascular endothelium. In this study, we aimed to compare serum endocan levels along with other hematologic inflammatory markers [such as C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR)] in patients with relapsing-remitting MS (RRMS) and healthy controls. We also aimed at investigating the role of vascular endothelial dysfunction in RRMS. Materials and Methods: We enrolled 64 patients with RRMS in the remission period, and 37 healthy controls in the study. We investigated hematologic parameters (ESR, CRP) and serum ESM-1 levels by enzyme-linked immunosorbent assay. Results were compared between two groups statistically. Results: The CRP and ESR had no significant difference between patients and controls (p=0.861 and p=0.76 respectively). Serum endocan levels of the patient group were significantly higher than the healthy controls (p=0.045). RRMS patients with or without treatment and comorbid diseases showed no significant difference in serum endocan levels (p=0.565 and p=0.169 respectively). The predictive value of endocan was 62.0%, cut-off value was 9124.7326 pg/l, sensitivity was 68.8%, and specificity was 54.1%. Conclusion: We demonstrated higher serum endocan levels in patients with RRMS in remission period, confirming the role of vascular inflammation. Further studies including larger patient cohorts are needed to support our results.

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