Retinal artery and vein thrombotic occlusion during pregnancy: markers for familial thrombophilia and adverse pregnancy outcomes

Abstract

BackgroundOcular vascular occlusion (OVO), first diagnosed during or immediately after giving birth, often reflects superposition of the physiologic thrombophilia of pregnancy on previously undiagnosed underlying familial or acquired thrombophilia associated with spontaneous abortion, eclampsia, or maternal thrombosis.Specific aimWe describe OVO, first diagnosed during pregnancy or immediately postpartum, in three young females (ages 32, 35, 40) associated with previously undiagnosed familial thrombophilia.ResultsBranch retinal artery occlusion (BRAO) occurred at 9 and 13 weeks gestation in two females, aged 32 and 35. Central retinal vein occlusion occurred immediately postpartum in a 40-year-old. One of the two females with BRAO subsequently developed eclampsia, and one had a history of unexplained first trimester spontaneous abortion. All three females were found to have previously unexplained familial thrombophilia. The two females with BRAO had low first trimester free protein S 42 (41%), lower normal limit (50%), and one of these two had high factor VIII (165%, upper normal limit 150%). The woman with central retinal vein occlusion had high factor XI (169%, upper normal limit 150%). Enoxaparin (40–60 mg/day) was started and continued throughout pregnancy in both females with BRAO to prevent maternal–placental thrombosis, and of these two females, one had an uncomplicated pregnancy course and term delivery, and the second was at gestational week 22 without complications at the time of this manuscript. There were no further OVO events in the two females treated with enoxaparin or in the untreated patient with postpartum eclampsia.ConclusionOVO during pregnancy may be a marker for familial or acquired thrombophilia, which confers increased thrombotic risk to the mother and pregnancy, associated with spontaneous abortion or eclampsia. OVO during pregnancy, particularly when coupled with antecedent adverse pregnancy outcomes, should prompt urgent thrombophilia evaluation and institution of thromboprophylaxis to prevent adverse maternal and fetal–placental thrombotic events.

The lncRNA TUG1 modulates proliferation in trophoblast cells via epigenetic suppression of RND3

“…Pre-eclampsia (PE), which is characterized by new-onset hypertension and proteinuria, is a pregnancy-specific syndrome. 1 It is the major trigger of fetal morbidity and pregnancy-induced mortality, and it affects 3–5% of pregnancies worldwide, including in developing countries such as China. 2 , 3 …”

The Lnc RNA SPRY4-IT1 Modulates Trophoblast Cell Invasion and Migration by Affecting the Epithelial-Mesenchymal Transition

“…Preeclampsia (PE) is a pregnancy-specific disease characterized by the occurrence of hypertension and proteinuria after 20 weeks of gestation in previously normotensive women1. It afflicts 3–5% of pregnancies and remains a leading cause of maternal mortality and morbidity worldwide, especially in developing countries23.…”

“…Among these characteristics, poor spiral artery remodelling has been considered to be a crucial early defect that causes PE and foetal growth restriction6. In pregnancy, to establish appropriate nutrient and oxygen supplies for the foetus, the extra-villous trophoblasts (EVTs) migrate through the endometrium, invade the uterine decidua, meeting only little resistance, and remodel the spiral arteries; this process is critical for the success of pregnanc789.…”

Circular RNA hsa_circ_0026552 inhibits the proliferation, migration and invasion of trophoblast cells via the miR‑331‑3p/TGF‑βR1 axis in pre‑eclampsia

“…PE is a specific gestational disorder characterized by the manifestation of hypertension and proteinuria after 20 weeks of conception ( 1 , 2 ) and is the primary cause of increased fetal morbidity and gestation-induced mortality, affecting ~3 to 8% of pregnant women globally ( 3 – 5 ). PE is defined according to the International Society for the Study of Hypertension in Pregnancy as systolic (≥140 mmHg) and diastolic (≥90 mmHg) blood pressure ( 6 ) with proteinuria of ≥30 mg/mol protein or without proteinuria or with austere clinical characteristics after 20 weeks of pregnancy in women that previously had a normal blood pressure ( 6 ).…”