Background Systemic sclerosis (SSc) is an autoimmune condition characterized by microvascular, skin and multi-organ involvement. As it usual arises in the reproductive years, a number of these patients plans (or achieves) a pregnancy. Several studies (1,2) showed increased sterility, risk of preterm delivery and fetal growth complications in these pregnancies, but less is known about the patophysiological mechanisms underlying these phenomena, neither the potentially pathogenetic role of certain anticorpal patterns (3).
Objectives To assess the outcome and the relationship between anti-centromere pattern and placental structural abnormalities in a group of SSc with recent labor.
Methods We retrospectively enrolled 20 SSc patients (mean age 34±7 years) who delivered in our University Hospital within 48 months. For each patient we performed focused visits collecting clinical and laboratory data. After delivery, placentas were analyzed according to a validated villous tree alterations score (presence of sclerotic/fibrotic villi; dilated chorionic plate vessels), used as a thrombotic index in extended protocols (4). The placental features were subsequently compared by a Student t-test. To establish a correlation between the SSc subtype and the placental abnormalities, we assessed the obtained data by a non-parametric X2 test.
Results The mean gestational duration was 37±4 weeks. The incidence of preterm delivery, 15%; baby delivered small for gestational age, 10%; no intra-uterine growth retardation was detected. Among the SSc women, 30% showed a diffuse subset of SSc disease with anti-Scl70 positivity, whereas 70% had a lcSSc subtype with anti-centromere pattern. None was positive for anticardiolipin antibodies, nor for other thrombofilic conditions. Placental abnormal findings were noticed in the totality of lcSSc patient (sclerotic 93% and fibrotic 86%villi; dilated vessels 71%), as opposed to the dcSSc patients (respectively, 17%, 33% and 50%) (p<0.01). Assuming the anti-centromere positivity linked to the placental thrombotic findings, the X2 overall analysis showed a p<0.01 (6 dof). The statistical significance was kept even after the lcSSc comparison with the three placental abnormalities subgroups (p<0.05).
Conclusions Anti Scl-70 is generally associated to a more severe kind of SSc disease, but in many papers the anti-centromere pattern has been indicated as a negative pronostic factor regarding the microvascular damage (5) and, potentially, the placental effectiveness (3). Placental histologic findings of our cohort could reflect the microvascular remodeling, strongly associated to the centromeric antibodies pattern. The pathophysiologic role of these antibodies is still unknown, but an interaction with several centromeric proteins, thus preventing the physiological mitotic process, has been described. In this study, anti-centromere antibodies appear strictly related to typical thrombotic changes in placental tissue: to our knowledge, this association has not been previously reported.
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Disclosure of Interest None Declared
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