By Pier Luigi Meroni
This e-book, a part of the sequence infrequent illnesses of the Immune process, deals complete, updated assurance of the pathophysiology and administration of the antiphospholipid syndrome (APS). Immunologic and genetic elements are mentioned and the pathogenic mechanisms answerable for such phenomena as APS-mediated thrombosis and being pregnant loss/complications are defined. the most scientific manifestations, class standards and diagnostic instruments are pointed out, and shut cognizance is paid to the character of the involvement of varied organs or organ platforms in APS. particular chapters describe the therapy of the several indicators, cures of worth in warding off recurrences, and cutting edge remedy methods. The authors are senior specialists within the box who're aided via more youthful fellows, making sure that the ebook is additionally educationally orientated. this useful quantity may be a important device for postgraduates in education and pros wishing to increase their wisdom of this particular syndrome.
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Additional resources for Antiphospholipid Antibody Syndrome: From Bench to Bedside
J Thromb Haemost 9(Suppl 1):275–282 19. Blank M et al (2002) Bacterial induction of autoantibodies to beta2-glycoprotein-I accounts for the infectious etiology of antiphospholipid syndrome. J Clin Invest 109:797–804 20. Tincani A et al (1996) The anti-beta2-glycoprotein I activity in human anti-phospholipid syndrome sera is due to monoreactive low-affinity autoantibodies directed to epitopes located on native beta2-glycoprotein I and preserved during species’ evolution. J Immunol 157: 5732–5738 21.
However, two main reasons supported the search for additional pathogenic mechanisms: (a) Vascular events in APS patients are affecting both arterial and venous vessels, while abnormal protein C and fibrinolysis may account mainly for venous events. (b) It is still not clear whether aPL react in a significant manner with the PL-binding proteins (β2GPI and PT) in fluid phase. In fact, all aPL are low-avidity antibodies suggesting that complex formation in the fluid phase requires stechiometric antigen-antibody ratios that are uncommon in patients .
Altogether, these findings suggest that a local acute inflammatory response might have a role in experimental aPL-mediated fetal loss. In spite of the experimental results, the role of inflammation in determining APS pregnancy complications still remains a debated issue. In APS placentas a strong infiltration of complement components, as well as histopathological findings of deciduitis and villous infiltration, has been found more frequently compared to normal controls [42–45]. On the contrary, further ex vivo examinations of APS placentas and subsequent in vivo studies, using another model of fetal resorption and growth retardation, injected with small amount of human aPL IgG (10–50 μg/ mouse) before implantation, failed to show any sign of acute placental 4 The Pathogenic Mechanisms for Antiphospholipid Antibodies (aPL) in pregnancy loss 41 inflammatory events and complement deposition .