Platelet activity and hypercoagulation in type 2 diabetes

dc.contributor.authorPretorius, Leshaen_ZA
dc.contributor.authorThomson, Greig J. A.en_ZA
dc.contributor.authorAdams, Rozanne C. M.en_ZA
dc.contributor.authorNell, Theo A.en_ZA
dc.contributor.authorLaubscher, Willem A.en_ZA
dc.contributor.authorPretorius, Etheresiaen_ZA
dc.identifier.citationPretorius, L., et al. 2018. Platelet activity and hypercoagulation in type 2 diabetes. Cardiovascular Diabetology, 17:141, doi:10.1186/s12933-018-0783-zen_ZA
dc.identifier.issn1475-2840 (online)
dc.descriptionCITATION: Pretorius, L., et al. 2018. Platelet activity and hypercoagulation in type 2 diabetes. Cardiovascular Diabetology, 17:141, doi:10.1186/s12933-018-0783-z.en_ZA
dc.descriptionThe original publication is available at https://cardiab.biomedcentral.comen_ZA
dc.description.abstractBackground: A strong correlation exists between type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD), with CVD and the presence of atherosclerosis being the prevailing cause of morbidity and mortality in diabetic populations. T2DM is accompanied by various coagulopathies, including anomalous clot formation or amyloid fibrin(ogen), the presence of dysregulated inflammatory molecules. Platelets are intimately involved in thrombus formation and particularly vulnerable to inflammatory cytokines. Methods: The aim of this current study was therefore to assess whole blood (hyper)coagulability, platelet ultrastructure and receptor expression, as well as the levels of IL-1β, IL-6, IL-8 and sP-selectin in healthy and diabetic individuals. Platelet morphology was assessed through scanning electron microscopy (SEM), while assessment of GPIIb/IIIa receptor expression was performed with confocal microscopy and flow cytometry with the addition of FITC-PAC-1 and CD41-PE antibodies. IL-1β, IL-6 and IL-8 and sP-selectin levels were assessed using a multiplex assay. Results: In T2DM there is significant upregulation of circulating inflammatory markers, hypercoagulation and platelet activation, with increased GPIIb/IIIa receptor expression, as seen with flow cytometry and confocal microscopy. Analyses showed that these receptors were additionally shed onto microparticles, which was confirmed with SEM. Conclusions: Cumulatively, this provides mechanistic evidence that pathological states of platelets together with amyloid fibrin(ogen) in T2DM, might underpin an increased risk for cardiovascular events.en_ZA
dc.format.extent11 pages : illustrationsen_ZA
dc.publisherBMC (part of Springer Nature)en_ZA
dc.subjectType 2 diabetesen_ZA
dc.subjectNon-insulin-dependent diabetesen_ZA
dc.subjectBlood -- Coagulationen_ZA
dc.subjectPlatelet ultrastructureen_ZA
dc.titlePlatelet activity and hypercoagulation in type 2 diabetesen_ZA
dc.description.versionPublisher's versionen_ZA
dc.rights.holderAuthors retain copyrighten_ZA

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