Antiphospholipid syndrome in obstetrics

Lupus ◽  
2018 ◽  
Vol 27 (1_suppl) ◽  
pp. 28-31 ◽  
Author(s):  
M Kemp ◽  
W Thomas

Antiphospholipid syndrome (APS) covers a spectrum of clinical manifestations ranging from recurrent pregnancy loss and obstetric complications from placental dysfunction through to thrombotic disease. This article will focus on the common manifestations of the pregnancy-related complications of APS. This includes clinical manifestations, diagnosis and management, as general practitioners will need to be able to recognize the disorder and will also have patients under their care receiving treatment for APS.

2010 ◽  
Vol 115 (6) ◽  
pp. 1256-1262 ◽  
Author(s):  
Panayiotis D. Ziakas ◽  
Matthaios Pavlou ◽  
Michael Voulgarelis

2007 ◽  
Vol 9 (30) ◽  
pp. 1-15 ◽  
Author(s):  
Silvia S. Pierangeli ◽  
Mariano E. Vega-Ostertag ◽  
Emilio B. González

Antiphospholipid (aPL) antibodies (Abs) are associated with thrombosis and pregnancy loss in antiphospholipid syndrome (APS), a disorder initially characterised in patients with systemic lupus erythematosus (SLE) but now known to occur in the absence of other autoimmune disease. There is strong evidence that aPL Abs are pathogenic in vivo, from studies of animal models of thrombosis, endothelial cell activation and pregnancy loss. In recent years, progress has been made in characterising the molecular basis of this pathogenicity, which includes direct effects on platelets, endothelial cells and monocytes as well as activation of complement. This review summarises the clinical manifestations of APS and current modalities of treatment, and explains recent advances in understanding the molecular events triggered by aPL Abs on target cells in coagulation pathways as well as effects of aPL Abs on complement activation. Based on this information and on additional scientific evidence using in vitro and in vivo models, new potential targeted therapies for treatment and/or prevention of thrombosis in APS are proposed and discussed.


2002 ◽  
Vol 266 (2) ◽  
pp. 61-66 ◽  
Author(s):  
M. F. Diejomaoh ◽  
M. M. Al-Azemi ◽  
A. Bandar ◽  
P. E. Egbase ◽  
J. Jirous ◽  
...  

1998 ◽  
Vol 79 (05) ◽  
pp. 924-927 ◽  
Author(s):  
Tatsuya Atsumi ◽  
Rafael Caliz ◽  
Olga Amengual ◽  
Munther A. Khamashta ◽  
Graham R. V. Hughes

SummaryA role for Fcγ receptor in the pathophysiology of thrombosis in APS has been hypothesized. The polymorphism of this receptor, FcγRIIA H/R131, is associated with the binding affinity for human IgG2 (i.e. FcγRIIA-H131 isoform has a higher affinity than FcγRIIA-R131). Since anti-β2 glycoprotein I antibodies (anti β2GPI), which play a major pathogenic role in APS, show IgG2 dominant distribution, we investigated the prevalence of receptor isoforms in patients with anti-phospholipid antibodies (aPL) by a PCR-RFLP method. We studied 100 Caucasian patients with aPL (57 primary APS, 32 secondary APS to SLE and 11 other diseases with aPL) and 41 healthy controls. H131/H131, H131/R131 and R131/R131 genotypes were found in 21 (21%), 50 (50%) and 29 (29%) in the patient group, and 9 (22%), 23 (56%) and 9 (22%) in control group, respectively. Thus there was no statistically significant difference in the prevalence of each genotype in these groups. None of the clinical manifestations of primary APS (arterial/venous thrombosis, recurrent pregnancy loss and thrombocytopenia) was significantly correlated with any FcγRIIA genotype. In conclusion, FcγRIIA polymorphism did not correlate with the manifestations of APS, and FcγRIIA genotype is not a genetic marker of APS.


Sign in / Sign up

Export Citation Format

Share Document