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Thromb Haemost 2023; 123(03): 326-335
DOI: 10.1055/a-1951-3402
Stroke, Systemic or Venous Thromboembolism

Inflammatory Markers Differentiate Cerebral Venous Sinus Thrombosis from Mimics

Jiayue Ding   *
1   Department of Neurology, Tianjin Medical University General Hospital, Tianjin, People's Republic of China
,
Liqun Pan   *
2   Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, People's Republic of China
,
Duo Lan   *
2   Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, People's Republic of China
,
Zhiying Chen
3   Department of Neurology, Jiujiang University Affiliated Hospital, Jiujiang, Jiangxi, People's Republic of China
,
Zhongao Wang
2   Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, People's Republic of China
,
Ming Zou
1   Department of Neurology, Tianjin Medical University General Hospital, Tianjin, People's Republic of China
,
Ran Meng
2   Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, People's Republic of China
› Institutsangaben Funding This study was sponsored by the National Key R&D Program of China (2017YFC1308401), the National Natural Science Foundation of China (82171297), the Natural Science Foundation of Beijing Municipality (7212047), the Natural Science Foundation of Tianjin City (19JCYBJC27500), and the Tianjin Key Medical Discipline (Specialty) Construction Project.
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Abstract

Imaging tests always misdiagnose anatomical variants of cerebral sinuses as cerebral venous sinus thrombosis (CVST). Anatomical variants of cerebral sinuses are called CVST mimics. This study aimed to identify the role of inflammatory markers in differentiating CVST from mimics. A total of 146 patients diagnosed as CVST and 93 patients with mimics were recruited in this study. Receiver operating characteristic (ROC) analysis was performed to demonstrate the sensitivity and specificity of inflammatory markers for diagnosing CVST. Rank logistic regression analysis was performed to identify the association of markers to CVST severity and prognosis. CVST presented higher inflammatory reactions compared with mimics, demonstrated by the neutrophil count (5.11 [3.97–6.80] vs. 3.06 [2.34–3.86]), interleukin (IL)-6 (7.42 [3.85–14.22] vs. 2.47 [1.50–4.00]), and neutrophil-to-lymphocyte ratio (NLR; 3.19 [2.18–4.62] vs. 1.66 [1.16–2.22]). ROC analysis showed markers with area under the curve (AUC) >0.8, including IL-6 (optimal cutoff: 3.790; kappa value: 0.499), neutrophil count (3.975; 0.522), and NLR (2.070; 0.476). After propensity score matching, only IL-6 had an AUC >0.8, with an optimal cutoff of 3.060 and a kappa value of 0.636. Ranked logistic regression showed that IL-6 (odds ratio, 95% confidence interval: 1.063, 1.026–1.101; 1.029, 1.009–1.050), cerebrospinal fluid (CSF) immunoglobulin (Ig) A (0.279, 0.110–0.706; 0.398, 0.162–0.974), CSF IgM (22.399, 3.004–167.001; 9.545, 1.382–65.928), and CSF IgG (1.287, 1.124–1.473; 1.232, 1.091–1.392) were independently correlated with the baseline and follow-up mRS. In conclusion, inflammatory markers in CVST were different from those in mimics. These markers, especially IL-6, could not only differentiate CVST from its mimics, but also evaluate CVST severity and prognosis.

Keywords

inflammation - cerebral venous sinus thrombosis - mimics - diagnosis

Author Contributions

J.D., L.P., and R.M. formulated the conception and design of the study, drafted the manuscript, and prepared the figures; L.P., D.L., Z.C., and Z.W. contributed to data acquisition; J.D. and R.M. were responsible for the data interpretation and statistical analysis; M.Z. and R.M. made critical revisions of the manuscript.


* These authors contributed equally to the study.


Supplementary Material



Publikationsverlauf

Eingereicht: 16. Juli 2022

Angenommen: 23. September 2022

Accepted Manuscript online:
27. September 2022

Artikel online veröffentlicht:
15. Dezember 2022

© 2022. Thieme. All rights reserved.

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  • References

  • 1 Saposnik G, Barinagarrementeria F, Brown Jr RD. et al; American Heart Association Stroke Council and the Council on Epidemiology and Prevention. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2011; 42 (04) 1158-1192
    CrossrefPubMedGoogle Scholar
  • 2 Ferro JM, Bousser MG, Canhão P. et al; European Stroke Organization. European Stroke Organization guideline for the diagnosis and treatment of cerebral venous thrombosis - Endorsed by the European Academy of Neurology. Eur Stroke J 2017; 2 (03) 195-221
    CrossrefPubMedGoogle Scholar
  • 3 Ropper AH, Klein JP. Cerebral venous thrombosis. N Engl J Med 2021; 385 (01) 59-64
    CrossrefPubMedGoogle Scholar
  • 4 Liang L, Korogi Y, Sugahara T. et al. Normal structures in the intracranial dural sinuses: delineation with 3D contrast-enhanced magnetization prepared rapid acquisition gradient-echo imaging sequence. AJNR Am J Neuroradiol 2002; 23 (10) 1739-1746
    PubMedGoogle Scholar
  • 5 Chiewvit P, Piyapittayanan S, Poungvarin N. Cerebral venous thrombosis: diagnosis dilemma. Neurol Int 2011; 3 (03) e13
    CrossrefPubMedGoogle Scholar
  • 6 Bai C, Xu Y, Zhou D. et al. The comparative analysis of non-thrombotic internal jugular vein stenosis and cerebral venous sinus stenosis. J Thromb Thrombolysis 2019; 48 (01) 61-67
    CrossrefPubMedGoogle Scholar
  • 7 Bai C, Wang Z, Stone C. et al. Pathogenesis and management in cerebrovenous outflow disorders. Aging Dis 2021; 12 (01) 203-222
    CrossrefPubMedGoogle Scholar
  • 8 Ding J, Guan J, Ji X, Meng R. Cerebral venous sinus stenosis may cause intracranial arterial hypoperfusion. Clin Neuroradiol 2020; 30 (02) 409-411
    CrossrefPubMedGoogle Scholar
  • 9 Nagai M, Terao S, Yilmaz G. et al. Roles of inflammation and the activated protein C pathway in the brain edema associated with cerebral venous sinus thrombosis. Stroke 2010; 41 (01) 147-152
    CrossrefPubMedGoogle Scholar
  • 10 Rashad S, Niizuma K, Sato-Maeda M. et al. Early BBB breakdown and subacute inflammasome activation and pyroptosis as a result of cerebral venous thrombosis. Brain Res 2018; 1699: 54-68
    CrossrefPubMedGoogle Scholar
  • 11 Akbari F, Ghorbani A, Fatehi F. The assessment of proinflammatory cytokines in the patients with the history of cerebral venous sinus thrombosis. Iran J Neurol 2016; 15 (02) 75-79
    PubMedGoogle Scholar
  • 12 Wang L, Duan J, Bian T. et al. Inflammation is correlated with severity and outcome of cerebral venous thrombosis. J Neuroinflammation 2018; 15 (01) 329
    CrossrefPubMedGoogle Scholar
  • 13 Aguiar de Sousa D, Pereira-Santos MC, Serra-Caetano A. et al. Blood biomarkers associated with inflammation predict poor prognosis in cerebral venous thrombosis: a multicenter prospective observational study. Eur J Neurol 2021; 28 (01) 202-208
    CrossrefPubMedGoogle Scholar
  • 14 Duan J, Leng X, Han Z. et al. Identifying biomarkers associated with venous infarction in acute/subacute cerebral venous thrombosis. Aging Dis 2021; 12 (01) 93-101
    CrossrefPubMedGoogle Scholar
  • 15 Yang Q, Duan J, Fan Z. et al. Early detection and quantification of cerebral venous thrombosis by magnetic resonance black-blood thrombus imaging. Stroke 2016; 47 (02) 404-409
    CrossrefPubMedGoogle Scholar
  • 16 Akboga YE, Bektas H, Anlar O. Usefulness of platelet to lymphocyte and neutrophil to lymphocyte ratios in predicting the presence of cerebral venous sinus thrombosis and in-hospital major adverse cerebral events. J Neurol Sci 2017; 380: 226-229
    CrossrefPubMedGoogle Scholar
  • 17 Li S, Liu K, Gao Y. et al. Prognostic value of systemic immune-inflammation index in acute/subacute patients with cerebral venous sinus thrombosis. Stroke Vasc Neurol 2020; 5 (04) 368-373
    CrossrefPubMedGoogle Scholar
  • 18 Coutinho JM, Zuurbier SM, Aramideh M, Stam J. The incidence of cerebral venous thrombosis: a cross-sectional study. Stroke 2012; 43 (12) 3375-3377
    CrossrefPubMedGoogle Scholar
  • 19 Devasagayam S, Wyatt B, Leyden J, Kleinig T. Cerebral venous sinus thrombosis incidence is higher than previously thought: a retrospective population-based study. Stroke 2016; 47 (09) 2180-2182
    CrossrefPubMedGoogle Scholar
  • 20 Silvis SM, de Sousa DA, Ferro JM, Coutinho JM. Cerebral venous thrombosis. Nat Rev Neurol 2017; 13 (09) 555-565
    CrossrefPubMedGoogle Scholar
  • 21 Ding J, Guan J, Rajah G. et al. Clinical and neuroimaging correlates among cohorts of cerebral arteriostenosis, venostenosis and arterio-venous stenosis. Aging (Albany NY) 2019; 11 (23) 11073-11083
    CrossrefPubMedGoogle Scholar
  • 22 Fuchs TA, Brill A, Duerschmied D. et al. Extracellular DNA traps promote thrombosis. Proc Natl Acad Sci U S A 2010; 107 (36) 15880-15885
    CrossrefPubMedGoogle Scholar
  • 23 Esmon CT, Xu J, Lupu F. Innate immunity and coagulation. J Thromb Haemost 2011; 9 (Suppl. 01) 182-188
    CrossrefPubMedGoogle Scholar
  • 24 Engelmann B, Massberg S. Thrombosis as an intravascular effector of innate immunity. Nat Rev Immunol 2013; 13 (01) 34-45
    CrossrefPubMedGoogle Scholar
  • 25 Jerjes-Sanchez C. Venous and arterial thrombosis: a continuous spectrum of the same disease?. Eur Heart J 2005; 26 (01) 3-4
    CrossrefPubMedGoogle Scholar
  • 26 Vazquez-Garza E, Jerjes-Sanchez C, Navarrete A, Joya-Harrison J, Rodriguez D. Venous thromboembolism: thrombosis, inflammation, and immunothrombosis for clinicians. J Thromb Thrombolysis 2017; 44 (03) 377-385
    CrossrefPubMedGoogle Scholar