In aPL syndrome, contributing to the understandingof the pathophysiology of thrombophilia in these patients [36]. Those autoantibodies are strong risk factors for venous thromboembolism in patients with SLE because they induce activated protein C resistance [37]. The other two IgG autoantibodies, namely antithrombin and aPL, are also associated with thrombotic events in aPL syndrome and SLE [32,33,50,51], and are risk factors for myocardial infarction in middle-aged men [52,53]. The pathophysiology of the thromboembolic phenomena associated with CD [10-26] represents a puzzle with multiple constituents: hyperhomocysteinemia; B12
PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/14445666 and \or folate deficiency; methylenetetrahydrofolate reductase mutations; the high homology between blood coagulation factor XIII and tTG; and protein C and S deficiency due to vitamin K deficiency [21-26,54]. The present study unravels a series of autoantibodies, aPL, aPT and mainly aPS/PT, that form part of this puzzle and are suggested to play a pathogenic role in the thrombogenicity of CD. Phosphatidylserine is a regular constituent of the inner leaflet of the cell membrane, which is only exposed on the outside of the cell membrane during apoptosis or because of damaged endothelial cells [55]. It is known that prothrombin and aPL antibodies bind specifically to the surface of apoptotic cells [56,57]. Recently, IekoTable 2 Percentage positivity of autoantibodies in celiac children and their parents compared with pediatric controlsP <0.9 Pediatric controls Celiac disease parents Pediatric celiac disease Optical density cut-off (N = 88) (N = 90) (N = 70) levels ND. 3.3 ***7.8, ** 9.9 11 *3.3 2.2 1.1 4.3 45.7*** 7.1 17.1 11.4 1.4 0 >28 >28 >28 >18 >18 >18 >24 Autoantibodies positivity/ groups aPS/PT IgA aPS/PT IgG aPS/PT IgM Prothrombin IgG Phospholipid IgG Phospholipid IgM Cardiolipin check<0.0001 0***,** 0.23> 0.5> 0.07> 1> 1> 3.
4 14.9 *12.5 ND.*P <0.05,**P <0.01,***P <0.0001; aPS/PT: antiphosphatidylserine/prothrombin; aPT: antiprothrombin; Ig: immunoglobulin.Lerner et al. BMC Medicine 2013, 11:89 http://www.biomedcentral.com/1741-7015/11/Page 5 ofet al. [58] reported that aPS/PT IgG recognizes prothrombin bound to phosphatidylserine on platelets and endothelial cells and, directly or via Fc-gamma receptors, activates a variety of procoagulant agents. However, the complementary aspects of CD are endothelial dysfunction [59], platelet abnormalities [60,61] and increased apoptosis [62]. Thus, it is suggested that intestinal injury, endothelial dysfunction, platelet abnormalities and enhanced apoptosis cause increased exposure of phospholipids or new epitopes, which are the origin <a href="https://www.ncbi.nlm.nih.gov/pubmed/17591728" title=View Abstract(s)">PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/17591728 of aPT, aPL and aPS/PT autoantibodies. Those antibodies might play a pathogenic role in the thrombophilia associated with CD. New light was recently shed on the `inflammation coagulation crosstalks' [63]. Recent studies have
3-(2,4-Dichlorophenoxy)azetidine unveiled molecular underpinnings of the intimate interconnection between both systems. Being a classical inflammatory state, CD can present such crosstalks, resulting in enhanced coagulability in the intestinal arena and on the systemic level. Because there are several pathways of mucosal injury, autoantigens like phospholipids, phosphatidylserine and prothrombin are exposed, inducing the production of aPS/PT, aPL and aPT antibodies. With their
thrombogenic capacities, those autoantibodies
4-((2-Hydroxyethyl)(methyl)amino)benzaldehyde can present the first or an additional hit in the thrombogenic background operating in CD. Because of the increased coagulabili.