Clinical Improvement and Successful Pregnancy in a Preeclamptic Patient With Antiphospholipid Syndrome Treated With Pravastatin

Lefkou, Eleftheria; Mamopoulos, Apostolos; Fragakis, Nikolaos; Dagklis, Themistoklis; Vosnakis, Christos; Nounopoulos, Efthimios; Rousso, David; Girardi, Guillermina

doi:10.1161/hypertensionaha.114.03115

Cited by 52 publications

(43 citation statements)

References 11 publications

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“…37 Although this seems an impressive gain in gestation (which did not occur for any of our participants), there are reasons to view this case with caution. Although she had antiphospholipid syndrome and a past history of severe preeclampsia (both strong risk factors for subsequent preeclampsia), the diagnosis of preeclampsia was made on the basis of hypertension and borderline proteinuria (360 mg per 24 hours).…”

Section: Discussionmentioning

confidence: 68%

Effects of Pravastatin on Human Placenta, Endothelium, and Women With Severe Preeclampsia

et al. 2015

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Abstract-Preeclampsia is a major pregnancy complication where excess placental release of soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin causes maternal endothelial and multisystem organ injury. Clinical trials have commenced examining whether pravastatin can be used to treat preeclampsia. However, the preclinical evidence supporting pravastatin as a treatment is limited to animal models, with almost no studies in human tissues. Therefore, we examined whether pravastatin reduced sFlt-1 and soluble endoglin secretion and decreased endothelial dysfunction in primary human tissues. Pravastatin reduced sFlt-1 secretion from primary endothelial cells, purified cytotrophoblast cells, and placental explants obtained from women with preterm preeclampsia. It increased soluble endoglin secretion from endothelial cells but did not change secretion from placental explants. The regulation of sFlt-1 by pravastatin seemed to be mediated via the 3-hydroxy-3-methylglutaryl-coenzyme A reductase cholesterol synthesis pathway. Pravastatin also reduced markers of endothelial dysfunction, including vascular cell adhesion molecule-1 expression and leukocyte adhesion on endothelial cells and increased endothelial cell migration and invasion. We also treated 4 patients with preterm preeclampsia presenting at <30 weeks of gestation with daily pravastatin. Pravastatin seemed to stabilize blood pressure, proteinuria, and serum uric acid levels. Furthermore, serum sFlt-1 levels decreased. We collected the placentas at delivery and found that pravastatin reduced sFlt-1 secretion. These results indicate that pravastatin reduced sFlt-1 and soluble endoglin production and decreased endothelial dysfunction in primary human tissues. We also present pilot data, suggesting that pravastatin can stabilize clinical and biochemical features of preterm preeclampsia. Our data obtained in human tissues support the concept that pravastatin is a candidate therapeutic for preeclampsia. Clinical Trial Registration-URL: http://www.anzctr.org.au. Unique identifier: ACTRN12613000268741.

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Section: Discussionmentioning

confidence: 68%

Effects of Pravastatin on Human Placenta, Endothelium, and Women With Severe Preeclampsia

et al. 2015

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“…Therefore, animal models and the similarities between PE and CVD provide a strong basis for the use of statins in the prevention of placental insufficiency in APS in humans. We have previously reported the clinical improvement in a preeclamptic APS patient treated with pravastatin (30). Similarly, a recent study has reported the successful use of pravastatin in preventing intrauterine fetal death (IUFD) in a case of massive perivillous fibrin deposition in the placenta (31).…”

Section: Resultsmentioning

confidence: 84%

“…Three pregnancies ended in stillbirth at 25 to 26 weeks. Preterm cesarean delivery (C-section) was performed in 7 women due to fetal distress and or maternal health concerns (median C-section time, 26.3 weeks; IQR, [26][27][28][29][30][31][32]. One neonate died 3 hours after birth.…”

Section: Resultsmentioning

confidence: 99%

Pravastatin improves pregnancy outcomes in obstetric antiphospholipid syndrome refractory to antithrombotic therapy

Lefkou¹,

Mamopoulos²,

Dagklis³

et al. 2016

Journal of Clinical Investigation

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164

143

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“…In cases of severe PE, an induced pre-term delivery is the standard approach. However, pravastatin may lead to a clinical improvement in PE [124]. MgSO 4 treatment was shown to be highly effective, enabling a prolonged pregnancy and the prevention of platelet count decrease.…”

Section: Therapymentioning

confidence: 99%

Immunology of hepatic diseases during pregnancy

2016

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The mother's immune system has to adapt to pregnancy accepting the semi-allograft fetus and preventing harmful effects to the developing child. Aberrations in feto-maternal immune adaptation may result in disease of the mother, such as liver injury. Five pregnancy-associated liver disorders have been described so far, however, little is known concerning immune alterations promoting the respective disease. These liver disorders are pre-eclampsia, hemolysis, elevated liver enzymes, low platelet count (HELLP), acute fatty liver, hyperemesis gravidarum, and intrahepatic cholestasis of pregnancy. On the other hand, pre-existing autoimmune liver injury of the mother can be affected by pregnancy. This review intends to summarize current knowledge linking feto-maternal immunology and liver inflammation with a special emphasis on novel potential biomarkers.

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Clinical Improvement and Successful Pregnancy in a Preeclamptic Patient With Antiphospholipid Syndrome Treated With Pravastatin

Cited by 52 publications

References 11 publications

Effects of Pravastatin on Human Placenta, Endothelium, and Women With Severe Preeclampsia

Effects of Pravastatin on Human Placenta, Endothelium, and Women With Severe Preeclampsia

Pravastatin improves pregnancy outcomes in obstetric antiphospholipid syndrome refractory to antithrombotic therapy

Immunology of hepatic diseases during pregnancy

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