About: Tocilizumab improves oxidative stress and endothelial glycocalyx: A mechanism that may explain the effects of biological treatment on COVID-19

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About: Tocilizumab improves oxidative stress and endothelial glycocalyx: A mechanism that may explain the effects of biological treatment on COVID-19 Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Tocilizumab improves oxidative stress and endothelial glycocalyx: A mechanism that may explain the effects of biological treatment on COVID-19
Creator	Andreadou, Ioanna Boumpas, Dimitrios Ikonomidis, Ignatios Katsimbri, Pelagia Kouretas, Dimitrios Lambadiari, Vaia Parissis, John Pavlidis, George Tsoumani, Maria
source	Elsevier; Medline; PMC
abstract	We investigated the effects of tocilizumab on endothelial glycocalyx, a determinant of vascular permeability, and myocardial function in rheumatoid arthritis(RA). Eighty RA patients were randomized to tocilizumab(n=40) or conventional synthetic disease-modifying antirheumatic drugs(csDMARDs) and glucocorticoids(GC) (n=40) for 3 months. Forty healthy subjects with similar age and sex served as controls. We measured: a)perfused boundary region(PBR) of the sublingual arterial microvessels (increased PBR indicates reduced glycocalyx thickness), b)pulse wave velocity(PWV), c)global LV longitudinal strain(GLS), d)global work index(GWI) using speckle tracking echocardiography and e)C-reactive protein(CRP), malondialdehyde(MDA) and protein carbonyls(PCs) as oxidative stress markers at baseline and post-treatment. Compared to controls, RA patients had impaired glycocalyx and myocardial deformation markers(P<0.05). Compared with baseline, tocilizumab reduced PBR(2.14±0.2 versus 1.97±0.2μm; P<0.05) while no significant differences were observed post-csDMARDs+GC(P>0.05). Compared with csDMARDs+GC, tocilizumab achieved a greater increase of GLS, GWI and reduction of MDA, PCs and CRP(P<0.05). The percent improvement of glycocalyx thickness(PBR) was associated with the percent decrease of PWV, MDA, PCs and the percent improvement of GLS and GWI(P<0.05). Tocilizumab improves endothelial function leading to a greater increase of effective myocardial work than csDMARDs+GC through a profound reduction of inflammatory burden and oxidative stress. This mechanism may explain the effects of tocilizumab on COVID-19. CLINICAL TRIAL REGISTRATION: URL: https://www.clinicaltrials.gov. Unique identifier: NCT03288584
has issue date	2020-08-18(xsd:dateTime)
bibo:doi	10.1016/j.fct.2020.111694
bibo:pmid	32822775
has license	no-cc
sha1sum (hex)	cb4a6d6dd69b2d5109bd8d79bfce4c278942f694
schema:url	https://doi.org/10.1016/j.fct.2020.111694
resource representing a document's title	Tocilizumab improves oxidative stress and endothelial glycocalyx: A mechanism that may explain the effects of biological treatment on COVID-19
has PubMed Central identifier	PMC7434461
has PubMed identifier	32822775
schema:publication	Food Chem Toxicol
resource representing a document's body	covid:cb4a6d6dd69b2d5109bd8d79bfce4c278942f694#body_text
is schema:about of	named entity 'glycocalyx' named entity 'oxidative stress' named entity 'oxidative stress' named entity 'arterial stiffness' named entity 'glycocalyx' named entity 'diastolic' named entity 'glycocalyx' named entity 'glycocalyx' named entity 'sublingual' named entity 'monotherapy' named entity 'endothelial' named entity 'experimental subjects' named entity 'proteoglycans' named entity 'tocilizumab' named entity 'CAD' named entity 'PBR' named entity 'CAR' named entity 'speckle tracking echocardiography' named entity 'pro-inflammatory cytokines' named entity 'arterial stiffness' named entity 'systolic' named entity 'shear stress' named entity 'clinical practice' named entity 'PWV' named entity 'PBR' named entity 'methotrexate' named entity 'eGFR' named entity 'diastolic dysfunction' named entity 'tocilizumab' named entity 'arterial stiffness' named entity 'scintigraphy' named entity 'speckle tracking echocardiography' named entity 'IL-6' named entity 'inflammation' named entity 'papillary muscles' named entity 'smooth muscle' named entity 'fibrosis' named entity 'tocilizumab' named entity 'IL-6' named entity 'angina' named entity 'inflammatory disease' named entity 'GE Healthcare' named entity 'systolic' named entity 'blood pressure' named entity 'systole' named entity 'tocilizumab' named entity 'chronic inflammatory' named entity 'blood pressure' named entity 'reduction of inflammation' named entity 'strain rate' named entity 'systolic' named entity 'PWV' named entity 'pulse wave' named entity 'frame rate' named entity 'cardiovascular risk factors' named entity 'oxygen' named entity 'TGF-β1' named entity 'tocilizumab' named entity 'Sitia' named entity 'valvular heart disease' named entity 'prednisolone' named entity 'haemodynamics' named entity 'RBC' named entity 'femoral' named entity 'Rheumatoid arthritis' named entity 'glycocalyx' named entity 'glycoproteins' named entity 'circulating blood cells' named entity 'perfused' named entity 'Siemens Healthcare Diagnostics' named entity 'tocilizumab' named entity 'Horten' named entity 'endothelial'

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