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

By Pier Luigi Meroni

This publication, a part of the sequence infrequent illnesses of the Immune method, bargains accomplished, up to date 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 medical manifestations, class standards and diagnostic instruments are pointed out, and shut consciousness is paid to the character of the involvement of varied organs or organ platforms in APS. particular chapters describe the remedy of different indicators, remedies of worth in averting 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 e-book is additionally educationally orientated. this useful quantity can be a important software for postgraduates in education and execs wishing to increase their wisdom of this particular syndrome.

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Blood 105:1540–1545 Thiagarajan P, Shapiro SS (1998) Lupus anticoagulants and antiphospholipid antibodies. 1 Introduction Arterial and/or venous thrombosis in association with the persistent presence of antiphospholipid antibodies (aPL) is the hallmark of the antiphospholipid antibody syndrome (APS). aPL can be detected by solid-phase assays (anticardiolipin [aCL] and/or anti-β2 glycoprotein I [β2GPI]) and/or by a functional assay (lupus anticoagulant [LA]) [1]. Besides their diagnostic value, aPL are also pathogenic autoantibodies that mediate the vascular manifestations in association with an additional second hit (two hits theory) [2].

1 and Fig. 2 summarize the main pathogenic mechanisms that have been reported in the literature [2, 22]. Still open is the question why some aPL-positive patients develop both arterial and venous events and why others can display arterial or venous thrombosis only. 5 Interference of aPL with Fluid-Phase Coagulation Cascade The evidence of aPL interference with fluid-phase components of coagulation has been provided mostly by in vitro models [2, 22]. aPL can bind some members of the serine protease (SP) family, which enlists proteins involved in hemostasis (procoagulant factors such as thrombin, PT, FVIIa, FIXa, and FXa and natural anticoagulants as protein C) and in fibrinolysis (plasmin and tissue plasminogen activator (tPA)).

D’Ippolito The Human Implantation and Placentation Human implantation and placentation represent a complex process based on subsequent steps. In particular, trophoblast cells play a key role in placental development. After implantation, they differentiate into villous and extravillous trophoblast cells (VTC and EVTC, respectively) [6]. VTC support the maternal-fetal exchange of nutrients and the endocrine functions of the placenta. EVTC invade the maternal endometrium and, through the formation of cellular plugs, gradually erode local spiral arteries to provide access to the maternal blood.

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