Decidual arteriopathy in hypertension and diabetes in pregnancy: immunofluorescent studies

J L Kitzmiller, N Watt, S G Driscoll
American Journal of Obstetrics and Gynecology 1981 December 1, 141 (7): 773-9
Lesions of the uteroplacental vasculature may be involved in the pathogenesis of "placental insufficiency" in pregnancies complicated by hypertension, diabetes, systemic lupus erythematosus, and idiopathic fetal growth retardation. The decidual arteries of the placental bed of normotensive, hypertensive, and diabetic women were studied by histologic examination and direct immunofluorescence for immunoglobulins and complement. Decidual tissue was obtained by curettage and snap frozen immediately after delivery of the placenta in 21 normal pregnant control subjects, 73 nondiabetic women with hypertensive disorders, and 41 women with insulin-dependent diabetes. Lesions of fibrinoid necrosis and/or atherosis were observed in some of the decidual arteries of 53% of women with preeclampsia (primary or superimposed) and also in a proportion of women with stable chronic hypertension or normotensive diabetes. Thus, fibrinoid necrosis/atherosis of the decidual arteries is not specific for preeclampsia. Immunoglobulins and complement were detected in arteries with lesions in subjects of all clinical groups. The findings do not support the concept that immunoprotein deposition in pathologic decidual arteries is related to a hypothetical immunologic reaction specific for preeclampsia. In preeclampsia, vascular deposition of immunoglobulin and complement may be related to local intravascular coagulation.

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