Polona Žigon

University Medical Centre Ljubljana

Dr. Polona Žigon is a senior scientist at the Department of Rheumatology, University Medical Center Ljubljana, Slovenia, and is a teaching assistant at the Faculty of Mathematics, Natural Sciences, and Information Technologies, University of Primorska, Slovenia. She obtained an MSc in Clinical Biochemistry in 2008 and a Ph.D. in Biomedicine in 2014 at the Faculty of Pharmacy, University of Ljubljana. During her post-graduate studies, she completed a six-month research internship in the School of Medicine, Hokkaido University Sapporo, Japan. She is a member of the Slovene Chamber Laboratory Medicine, a working member of EMEUNET, and a member of the Autoimmunity Network. Her research in the field of systemic autoimmune diseases resulted in more than thirty original scientific articles published in peer-reviewed journals, six book chapters, and one patent application.

Polona Žigon

1books edited

3chapters authored

Latest work with IntechOpen by Polona Žigon

Antiphospholipid syndrome (APS) is an acquired autoimmune disorder in which the immune system mistakenly produces antiphospholipid antibodies that attack tissues in the body. These antibodies can lead to the formation of blood clots in arteries and veins. During pregnancy, APS can also lead to miscarriage and stillbirth. Classification criteria require a clinical event (i.e., thrombosis or pregnancy complication) and persistent positive blood test results at least three months apart that detect lupus anticoagulant, anti-cardiolipin antibodies, or anti-β2-glycoprotein-1 antibodies. This book addresses important clinical aspects of APS, including stroke and APS, obstetric manifestations of APS, and bleeding complications in APS. It also discusses the diagnostic utility of a novel autoantibody against β2-glycoprotein I/HLA class II complexes as a promising biomarker for APS. Finally, this book also reviews the latest findings in the field of extracellular vesicles in APS and provides explanations of their role in the pathogenesis of APS.

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