Predictive Values of Coagulation/Fibrinolysis Parameters for the Termination of Pregnancy Complicated by Severe Preeclampsia

Kobayashi, Takao; Tokunaga, Naoki; Sugimura, Motoi; Kanayama, Naohiro; Terao, Toshihiko

doi:10.1055/s-2001-14072

Cited by 30 publications

(35 citation statements)

References 9 publications

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“…Severe pre-eclampsia was found to be associated higher levels of CRP than mild preeclampsia in line with previous studies. Kabayashi et al 27 reported that D-Dimer levels and changes of platelet counts are useful predictive markers with optimal time for the termination of pregnancy in patients with severe pre-eclampsia. 7 Mother delivering at term had circulating PCT concentrations similar to those observed in the apparently healthy adult population.…”

Section: Discussionmentioning

confidence: 99%

An Analysis of C‐Reactive Protein, Procalcitonin, and D‐Dimer in Pre‐Eclamptic Patients

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Özgünen

Güzel

et al. 2012

American J Rep Immunol

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Problem The aim of this study was to evaluate serum procalcitonin (PCT), C‐reactive protein (CRP), and plasma D‐Dimer levels in mild and severe pre‐eclampsia. Method of study Serum PCT, CRP, and D‐Dimer levels were analyzed in 64 cases with pre‐eclampsia as the study group and 33 healthy pregnant women in the third trimester as the control group. Pre‐eclamptic group consisted of mild (n = 31) and severe pre‐eclamptic subgroup (n = 33). Laboratory results were compared between the groups and diagnostic usefulness of these parameters were evaluated. Results PCT, CRP, and D‐Dimer levels were significantly higher in study group than the control group (P = 0.001). PCT, CRP, and D‐Dimer were significantly higher in the patients with severe pre‐eclampsia than mild pre‐eclampsia. There were significant positive correlations between these markers and mean arterial pressure (MAP). Logistic regression analysis using the control and pre‐eclampsia group showed that higher PCT (OR, 15.68; 95%‐CI, 3.15–78.10), CRP (OR, 14.29; 95%‐CI, 3.08–66.34), and D‐Dimer levels (OR, 4.97; 95%‐CI, 1.22–20.29) were found to be risk factors significantly associated with pre‐eclampsia. Conclusions This study results confirm that evidence of a possible exaggerated systemic inflammatory response in pre‐eclampsia especially in severe pre‐eclampsia.

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Section: Discussionmentioning

confidence: 99%

An Analysis of C‐Reactive Protein, Procalcitonin, and D‐Dimer in Pre‐Eclamptic Patients

Güleç

Özgünen

Güzel

et al. 2012

American J Rep Immunol

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“…Thrombin activation can also lead to deposition of fibrin in multiple organ systems, which is a major contributor to the pathology of pre-eclampsia. 2 Excessive thrombin generation can be assessed by measuring the concentration of thrombin–antithrombin complexes, 138 antithrombin III activity 139 or by a thrombin generation assay. 140 In some patients, pre-eclampsia and/or HELLP syndrome can be considered as thrombotic microangiopathy-like disorders, in light of the similarities in clinical presentation and pathology observed in multiple organs (thrombocytopenia, haemolysis, endothelial injury, complement activation and deposition of thrombin and/or fibrin in arterioles and capillaries of the brain, kidneys and liver).…”

Section: Pathogenetic Mechanismsmentioning

confidence: 99%

Pre-eclampsia part 1: current understanding of its pathophysiology

et al. 2014

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Pre-eclampsia is characterized by new-onset hypertension and proteinuria at ≥20 weeks of gestation. In the absence of proteinuria, hypertension together with evidence of systemic disease (such as thrombocytopenia or elevated levels of liver transaminases) is required for diagnosis. This multisystemic disorder targets several organs, including the kidneys, liver and brain, and is a leading cause of maternal and perinatal morbidity and mortality. Glomeruloendotheliosis is considered to be a characteristic lesion of pre-eclampsia, but can also occur in healthy pregnant women. The placenta has an essential role in development of this disorder. Pathogenetic mechanisms implicated in pre-eclampsia include defective deep placentation, oxidative and endoplasmic reticulum stress, autoantibodies to type-1 angiotensin II receptor, platelet and thrombin activation, intravascular inflammation, endothelial dysfunction and the presence of an antiangiogenic state, among which an imbalance of angiogenesis has emerged as one of the most important factors. However, this imbalance is not specific to pre-eclampsia, as it also occurs in intrauterine growth restriction, fetal death, spontaneous preterm labour and maternal floor infarction (massive perivillous fibrin deposition). The severity and timing of the angiogenic imbalance, together with maternal susceptibility, might determine the clinical presentation of pre-eclampsia. This Review discusses the diagnosis, classification, clinical manifestations and putative pathogenetic mechanisms of pre-eclampsia.

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“…A wide variety of hemostatic disturbances have been described in pre‐eclampsia. They include thrombocytopenia as well as consumption of coagulation factors and inhibitors [2–5], with evidence of thrombin generation [3–5] and inhibited fibrinolysis [5–7]. However, the changes in the circulating levels of tissue factor pathway inhibitor (TFPI) in pre‐eclampsia need to be clarified.…”

Section: Introductionmentioning

confidence: 99%