Abstract

ology (CVUE), was observed. The frequency of maternal complications in scleroderma patients is not increased compared with healthy controls, except for renal crisis [1]. Prematurity and preterm births are amajor problem. In a recent study, pretermbirths occurred in 29% of scleroderma pregnancies [3]. Detailed descriptions of placental findings in scleroderma are limited and include chronic villitis associated with decidual vasculopathy, placental infarcts, abruption, as well as normal placentas [2]. In a recent study of 13 placentas from 8 women with scleroderma, decidual vasculopathy was observed in 5 placentas and was associated with poor perinatal outcome [4]. Decidual vasculopathy reflects pathological deviations from normal placentation, such as fibrinoid necrosis of vessel walls, with or without foamy macrophages (atherosis), vasculitis, and presence of small muscularized thick-walled blood vessels [5]. In the present case PMD, and not decidual vasculopathy, was the most prominent placental finding. PMD is associated with IUGR. The typical features of PMD, that were also observed in this case, are stem villi with excessive proliferation of mesenchymatous tissue, with foci of myxoid degeneration, and large stromalmacrophages and vessels with fibromuscular sclerosis and thrombosis [6]. In conclusion, PMD, decidual vasculopathy, and other placental lesions associated with compromised uteroplacental perfusion may appear in scleroderma and are correlated with poor perinatal outcome.

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