Antiphospholipid Syndrome
in Pregnancy
Rheum Dis Clin N Am 33 (2007) 287–297
Guillermo Ruiz-Irastorza, MD, PhD
a,
Munther A. Khamashta, MD, FRCP, PhD
b,*
a
Department of Internal Medicine, Hospital de Cruces,
University of the Basque Country, 48903-Bizkaia, Spain
b
Lupus Research Unit, The Rayne Institute, St. Thomas’ Hospital,
King’s College University, London SE1 7EH, UK
Obstetric complications, together with thrombosis, are the major clinical
manifestations of the antiphospholipid syndrome (APS). There is a strong
relationship between antiphospholipid antibodies (aPL) and pregnancy
loss
[1]. A recent meta-analysis has analyzed the relationship between the
different aPL (lupus anticoagulant [LA], anticardiolipin antibodies [aCL]
and anti–beta2 glycoprotein I antibodies [anti-B2GPI)] with recurrent fetal
loss in women without known autoimmune diseases
[2]. LA has shown the
strongest association with recurrent fetal losses before 24 weeks’ gestation
(odds ratio [OR] 7.79, 95% confidence interval [CI] 2.30 to 26.45). Data
were insufficient to analyze the association of LA with early (
!13 weeks)
miscarriage. Both IgG and IgM aCL also were clearly related with recurrent
losses before 24 weeks (OR 3.57, 95% CI 2.26 to 5.65 and OR 5.61, 95% CI
1.26 to 25.03, respectively). IgG aCL also showed an association with early
miscarriage (OR 3.56, 95% CI 1.48 to 8.59). On the contrary, anti-B2GPI
failed to show a similar relationship with any form of recurrent miscarriage.
Pregnant women with APS are at increased risk for miscarriage and
thrombotic events
[1]. In fact, both features are connected, and previous adverse
obstetric events may herald the occurrence of thrombotic complications
[3]
. However, pregnancies in women with aPL are subject to other
types of additional complications, such as systemic and pulmonary hypertension,
prematurity, and intrauterine growth restriction.
APS is defined from the laboratory point of view by the persistent positivity
of aPL. Until recently, the Sapporo criteria for the classification of
* Corresponding author.
E-mail address:
munther.khamashta@kcl.ac.uk (M.A. Khamashta).
0889-857X/07/$ - see front matter
2007 Elsevier Inc. All rights reserved.
doi:10.1016/j.rdc.2007.02.003
rheumatic.theclinics.com
Rheum Dis Clin N Am
33 (2007) 287–297