Antiphospholipid Antibody Syndrome: From Bench to Bedside - download pdf or read online

By Pier Luigi Meroni

ISBN-10: 3319110438

ISBN-13: 9783319110431

ISBN-10: 3319110446

ISBN-13: 9783319110448

This publication, a part of the sequence infrequent illnesses of the Immune method, deals complete, updated insurance of the pathophysiology and administration of the antiphospholipid syndrome (APS). Immunologic and genetic features are mentioned and the pathogenic mechanisms chargeable for such phenomena as APS-mediated thrombosis and being pregnant loss/complications are defined. the most medical manifestations, type standards and diagnostic instruments are pointed out, and shut recognition is paid to the character of the involvement of varied organs or organ platforms in APS. particular chapters describe the therapy of different indicators, cures of price in averting recurrences, and leading edge remedy methods. The authors are senior specialists within the box who're aided via more youthful fellows, making sure that the ebook can also be educationally orientated. this convenient quantity may be a important software for postgraduates in education and pros wishing to increase their wisdom of this particular syndrome.

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Extra info for Antiphospholipid Antibody Syndrome: From Bench to Bedside

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J Thromb Haemost 4:295–306 2. Gómez-Puerta JA, Cervera R (2014) Diagnosis and classification of the antiphospholipid syndrome. J Autoimmun 48:20–25 4 The Pathogenic Mechanisms for Antiphospholipid Antibodies (aPL) in pregnancy loss 43 3. Meroni PL, Borghi MO, Raschi E et al (2011) Pathogenesis of antiphospholipid syndrome: understanding the antibodies. Nat Rev Rheumatol 7:330–339 4. Pierangeli SS, Chen PP, Raschi E et al (2008) Antiphospholipid antibodies and the antiphospholipid syndrome: pathogenic mechanisms.

The best association was reported for antibodies detected by the PS-PT assay, suggesting that the pathogenic antibodies may react with a conformational epitope(s) expressed by PT when complexed with anionic PL in the presence of calcium ions [6]. 3 Why We Break the Tolerance Against Beta2GPI? The mechanism(s) through which the tolerance towards β2GPI is lost is still matter of research, and several hypotheses have been suggested. There is sound evidence that aPL can be detectable in the course of viral, bacterial, and parasitic infections as a transient phenomenon [7, 8].

Platelet activation by aPL has been supported by ex vivo studies since elevated levels of thromboxane (TX, the major eicosanoid metabolic breakdown product) have been found in the urine of APS patients [26]. 2 Involvement of Monocytes aPL upregulate TF expression on peripheral blood monocytes. In particular, monocyte TF expression is increased in patients with APS and correlates with the expression of β2GPI. Accordingly, cell-surface TF on monocytes is higher in APS patients than in subjects without thrombotic events.

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Antiphospholipid Antibody Syndrome: From Bench to Bedside by Pier Luigi Meroni

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