Case of soluble fms‐like tyrosine kinase 1 apheresis in severe pre‐eclampsia developed at 15 weeks’ gestation

Nakakita, Baku; Mogami, Haruta; Kondoh, Eiji; Tsukamoto, Tatsuo; Yanagita, Motoko; Konishi, Ikuo

doi:10.1111/jog.12760

Cited by 15 publications

(9 citation statements)

References 8 publications

(7 reference statements)

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“…The new insights into the pathogenesis of this clinical condition will provide great opportunity to improve the care of preeclamptic women before delivery and undoubtedly will lead 1 day to the development of novel strategies for prevention and treatment of the disease. Pipeline clinical trials based on elimination of serum sFlt-1 by means of apheresis yielded promising results indicating that the remedy for this prevalent dangerous entity is within reach ( Nakakita et al, 2015 ; Easterling, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

Preeclampsia: Novel Mechanisms and Potential Therapeutic Approaches

et al. 2018

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Preeclampsia is a serious complication of pregnancy where it affects 5–8% of all pregnancies. It increases the morbidity and mortality of both the fetus and pregnant woman, especially in developing countries. It deleteriously affects several vital organs, including the kidneys, liver, brain, and lung. Although, the pathogenesis of preeclampsia has not yet been fully understood, growing evidence suggests that aberrations in the angiogenic factors levels and coagulopathy are responsible for the clinical manifestations of the disease. The common nominator of tissue damage of all these target organs is endothelial injury, which impedes their normal function. At the renal level, glomerular endothelial injury leads to the development of maternal proteinuria. Actually, peripheral vasoconstriction secondary to maternal systemic inflammation and endothelial cell activation is sufficient for the development of preeclampsia-induced hypertension. Similarly, preeclampsia can cause hepatic and neurologic dysfunction due to vascular damage and/or hypertension. Obviously, preeclampsia adversely affects various organs, however it is not yet clear whether pre-eclampsia per se adversely affects various organs or whether it exposes underlying genetic predispositions to cardiovascular disease that manifest in later life. The current review summarizes recent development in the pathogenesis of preeclampsia with special focus on novel diagnostic biomarkers and their relevance to potential therapeutic options for this disease state. Specifically, the review highlights the renal manifestations of the disease with emphasis on the involvement of angiogenic factors in vascular injury and on how restoration of the angiogenic balance affects renal and cardiovascular outcome of Preeclamptic women.

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Section: Discussionmentioning

confidence: 99%

Preeclampsia: Novel Mechanisms and Potential Therapeutic Approaches

et al. 2018

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“…In a human case of very early-onset PE (15 weeks of gestation), sFlt-1 apheresis was performed 13 times in of the interval from 19 to 23 weeks of gestation; however, at 23 weeks and 3 days-cesarean section had to be performed due to maternal respiratory failure and fetal distress. This study indicates sFlt-1 functions to protect the placenta and fetus in PE and that removal may have negative consequences [ 180 ].…”

Section: Therapeutic Approachesmentioning

confidence: 99%

“…Although preliminary studies suggest that the extracorporeal removal of circulating sFlt1 in PE prolongs pregnancy and improves the maternal symptoms of PE [ 34 ], this strategy should be considered very carefully, as sFlt1 also plays an essential role in protecting the fetus [ 27 , 180 ]. Additionally, a recent study in mice also suggests that reducing PlGF levels has a protective effect against the development of preeclampsia [ 54 ].…”

Section: Future Perspectivesmentioning

confidence: 99%

Pathogenesis of Preeclampsia and Therapeutic Approaches Targeting the Placenta

et al. 2020

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Preeclampsia (PE) is a serious pregnancy complication, affecting about 5–7% of pregnancies worldwide and is characterized by hypertension and damage to multiple maternal organs, primarily the liver and kidneys. PE usually begins after 20 weeks’ gestation and, if left untreated, can lead to serious complications and lifelong disabilities—even death—in both the mother and the infant. As delivery is the only cure for the disease, treatment is primarily focused on the management of blood pressure and other clinical symptoms. The pathogenesis of PE is still not clear. Abnormal spiral artery remodeling, placental ischemia and a resulting increase in the circulating levels of vascular endothelial growth factor receptor-1 (VEGFR-1), also called soluble fms-like tyrosine kinase-1 (sFlt-1), are believed to be among the primary pathologies associated with PE. sFlt-1 is produced mainly in the placenta during pregnancy and acts as a decoy receptor, binding to free VEGF (VEGF-A) and placental growth factor (PlGF), resulting in the decreased bioavailability of each to target cells. Despite the pathogenic effects of increased sFlt-1 on the maternal vasculature, recent studies from our laboratory and others have strongly indicated that the increase in sFlt-1 in PE may fulfill critical protective functions in preeclamptic pregnancies. Thus, further studies on the roles of sFlt-1 in normal and preeclamptic pregnancies are warranted for the development of therapeutic strategies targeting VEGF signaling for the treatment of PE. Another impediment to the treatment of PE is the lack of suitable methods for delivery of cargo to placental cells, as PE is believed to be of placental origin and most available therapies for PE adversely impact both the mother and the fetus. The present review discusses the pathogenesis of PE, the complex role of sFlt-1 in maternal disease and fetal protection, and the recently developed placenta-targeted drug delivery system for the potential treatment of PE with candidate therapeutic agents.

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“…Furthermore, serum levels of soluble fms-like tyrosine kinase 1 (sFlt1) were very high (8.41 ng/mL) at 18 weeks of gestation. Subsequently, we classified this case as extremely early onset preeclampsia [ 4 ]. Nifedipine and magnesium sulfate were administered.…”

Section: Casementioning

confidence: 99%

Noninvasive Positive-Pressure Ventilation for Preeclampsia-Induced Pulmonary Edema: 3 Case Reports and a Literature Review

Hamada

Chigusa

Kondoh

et al. 2018

Case Reports in Obstetrics and Gynecology

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Pulmonary edema caused by severe preeclampsia can be an indication for pregnancy termination. We aimed to investigate whether noninvasive positive-pressure ventilation (NPPV) was useful for preeclampsia-induced pulmonary edema. Three cases of preeclampsia-induced pulmonary edema managed with NPPV in our institute were reviewed retrospectively. A literature review was conducted regarding NPPV usage during pregnancy. NPPV was initiated at 30, 20, and 24 weeks of gestation in the 3 cases. In all cases, NPPV slowed the progression of pulmonary edema and succeeded in delaying pregnancy termination by 17 days on average. Maternal outcomes were positive, and no intubation was required. Between 1994 and 2017, there were 11 articles describing 12 cases in which NPPV was applied for pulmonary edema during pregnancy. However, there has been no case of NPPV management of preeclampsia-induced pulmonary edema thus far. Maternal and fetal outcomes were positive in these 12 cases. NPPV may contribute to prolonging pregnancy in patients with poor oxygenation due to preeclampsia-induced pulmonary edema. However, patients should be closely monitored, and the decision to intubate or terminate the pregnancy should be made without delay when the maternal or fetal condition worsens.

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Case of soluble fms‐like tyrosine kinase 1 apheresis in severe pre‐eclampsia developed at 15 weeks’ gestation

Cited by 15 publications

References 8 publications

Preeclampsia: Novel Mechanisms and Potential Therapeutic Approaches

Preeclampsia: Novel Mechanisms and Potential Therapeutic Approaches

Pathogenesis of Preeclampsia and Therapeutic Approaches Targeting the Placenta

Noninvasive Positive-Pressure Ventilation for Preeclampsia-Induced Pulmonary Edema: 3 Case Reports and a Literature Review

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