دانلود رایگان مقاله انگلیسی مکمل های بیومارکرهای سیستم در صرع - الزویر 2018

عنوان فارسی
مکمل های بیومارکرهای سیستم در صرع
عنوان انگلیسی
Complement system biomarkers in epilepsy
صفحات مقاله فارسی
0
صفحات مقاله انگلیسی
7
سال انتشار
2018
نشریه
الزویر - Elsevier
فرمت مقاله انگلیسی
PDF
نوع نگارش
مقالات پژوهشی (تحقیقاتی)
رفرنس
دارد
کد محصول
E9501
رشته های مرتبط با این مقاله
پزشکی
گرایش های مرتبط با این مقاله
مغز و اعصاب
مجله
تشنج - Seizure
دانشگاه
Systems Immunity Research Institute and Division of Psychological Medicine and Clinical Neurology - Cardiff University - UK
کلمات کلیدی
التهاب، پیش بینی کننده، پلاسما، تشنج، صرع، بیومارکرها
doi یا شناسه دیجیتال
https://doi.org/10.1016/j.seizure.2018.05.016
چکیده

ABSTRACT


Purpose: To explore whether complement dysregulation occurs in a routinely recruited clinical cohort of epilepsy patients, and whether complement biomarkers have potential to be used as markers of disease severity and seizure control. Methods: Plasma samples from 157 epilepsy cases (106 with focal seizures, 46 generalised seizures, 5 unclassified) and 54 controls were analysed. Concentrations of 10 complement analytes (C1q, C3, C4, factor B [FB], terminal complement complex [TCC], iC3b, factor H [FH], Clusterin [Clu], Properdin, C1 Inhibitor [C1Inh] plus C-reactive protein [CRP]) were measured using enzyme linked immunosorbent assay (ELISA). Univariate and multivariate statistical analysis were used to test whether combinations of complement analytes were predictive of epilepsy diagnoses and seizure occurrence. Correlation between number and type of anti-epileptic drugs (AED) and complement analytes was also performed. Results: We found: 1) significant differences between all epilepsy patients and controls for TCC (p < 0.01) and FH (p < 0.01) after performing univariate analysis. 2) multivariate analysis combining six analytes (C3, C4, Properdin, FH, C1Inh, Clu) to give a predictive value (area under the curve) of 0.80 for differentiating epilepsy from controls. 3) significant differences in complement levels between patients with controlled seizures (n = 65) in comparison with uncontrolled seizures (n = 87). Levels of iC3b, Properdin and Clu were decreased and levels of C4 were increased in patients with uncontrolled seizures. 4) no correlation was found between the level of complement biomarkers and the number of AEDs taken, but an association between some analyte levels and drug therapy was seen in patients taking sodium valproate, clobazam, and perampanel. Conclusion: This study adds to evidence implicating complement in pathogenesis of epilepsy and may allow the development of better therapeutics and prognostic markers in the future. Replication in a larger sample set is needed to validate the findings of the study.

نتیجه گیری

5. Conclusion


Significant differences were found in a number of complement analytes between patients with epilepsy and controls, controlled and uncontrolled epilepsy, and certain AEDs. Multivariate analyses identified highly predictive models for distinguishing cases from controls and well-controlled from uncontrolled cases. These data adds further evidence to the role of complement dysregulation in the pathogenesis of epilepsy and may allow the development of better prognostic markers and therapeutics in the future.


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