Tissue factor levels and high ratio of fibrinopeptide A:D‐dimer as a measure of endothelial procoagulant disorder in pre‐eclampsia

Bellart, Jordi; Gilabert, Rosa; Anglés, A.; Piera, Verónica; Miralles, Ramón; Monasterio, J; Cabero, L.

doi:10.1111/j.1471-0528.1999.tb08330.x

Cited by 47 publications

(31 citation statements)

References 20 publications

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“…A variety of agents known to induce or sustain inflammation, like TNF-a, IL-1 and CRP, are potent stimulators of TF expression 21 . The plasma level and the monocyte expression of TF are increased in overt pre-eclampsia demonstrating that enhanced expression of TF is a part of the inflammatory response in this disease as well 6,22 . Accordingly, it is reasonable to interpret our finding of unaltered plasma level of TF early in preeclamptic pregnancies to indicate an absence of enhanced systemic inflammatory activity.…”

Section: Discussionmentioning

confidence: 99%

Absence of enhanced systemic inflammatory response at 18 weeks of gestation in women with subsequent pre-eclampsia

Djurovic¹

2002

BJOG: An International Journal of Obstetrics and Gynaecology

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Objective To compare indicators of systemic inflammatory response in the second trimester in women who developed pre-eclampsia with normal pregnancies. Design Prospective nested case control study derived from a cohort of 2190 pregnant women. Blood samples were obtained at 18 weeks of gestation. The following inflammatory parameters were measured: tumour necrosis factor-a (TNF-a), plasminogen activator inhibitor-1 (PAI-1), interleukin-1h (IL-1h), IL-6, IL-10, microCRP and tissue factor (TF). Setting Institute of Medical Genetics, University of Oslo, and Department of Medical Genetics, Ullevål University Hospital and Departments of Obstetrics and Gynecology, Aker University Hospital, Oslo, Norway. Sample The cases were 71 women who subsequently developed pre-eclampsia. The controls were 71 healthy, pregnant women matched for age, parity and first trimester body mass index (BMI). Methods Venous blood was drawn from fasting subjects into 5 mL test tubes containing EDTA. Samples were analysed for inflammatory parameters : IL-1-h, IL-6, IL-10, TNF-a, PAI-1, TF (ELISA-technique) and CRP (latex-enhanced immunonephelometric assay), strictly according to the manufacturer's recommendation. Main outcome measures The matched case and control subjects were compared by the paired two-tailed Wilcoxon signed rank test. All P values were two-tailed and P < 0.05 was deemed statistically significant. Results We found no differences in plasma concentrations of PAI-1, IL-1h, IL-6, IL-10, microCRP, TNF-a or TF at 18 weeks of gestation between women who subsequently developed pre-eclampsia and matched control women. Conclusion In contrast to findings from women with overt pre-eclampsia, the present study indicates that there are no indications of intensified systemic inflammatory response at 18 weeks of gestation in women who later develop pre-eclampsia.

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Section: Discussionmentioning

confidence: 99%

Absence of enhanced systemic inflammatory response at 18 weeks of gestation in women with subsequent pre-eclampsia

Djurovic¹

2002

BJOG: An International Journal of Obstetrics and Gynaecology

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“…Moreover, the FPA/D-dimer ratio also remains constant throughout pregnancy, suggesting a constant coagulation/ fibrinolysis balance [28]. In contrast, a high FPA/D-dimer ratio, suggestive of hypofibrinolysis, was observed in women with pre-eclampsia [38], thus highlighting the importance of coagulation/fibrinolysis balance during normal pregnancy and lending further support to the concept that haemostasis in normal pregnancy may indeed be a balancing act.…”

Section: A Balancing Act?mentioning

confidence: 92%

Haemostasis in normal pregnancy: a balancing act?

Holmes

Wallace

2005

Biochemical Society Transactions

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Pregnancy is a risk factor for venous thrombosis and the incidence of venous thromboembolism during normal pregnancy is 6-fold higher during pregnancy than in the general female population of child-bearing age. This incidence is, however, remarkably low given the increases in markers of haemostatic activation observed during normal pregnancy. During normal healthy pregnancy there are substantial changes in the haemostatic system, many of which are procoagulant and supposed to be in preparation for the haemostatic challenge of delivery. Normal haemostasis requires a balance between coagulation and fibrinolysis to maintain the integrity of the vasculature, and complex physiological changes are evident during pregnancy which appear to ensure a constant coagulation/fibrinolysis balance. This balance is maintained, at least partly, by an increase in fibrinolytic activity, but decreases in other factors such as factor XI and monocyte tissue factor expression may also serve to counterbalance procoagulant changes.

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“…Given that PE is accompanied by coagulopathies, it is probably not surprising that d -dimer levels are raised in PE (741–745), although this is true for many conditions (746), and some of the assays would bear improvement (747, 748). Needless to say, however, raised d -dimer levels are also a strong marker for infection (749, 750).…”

Section: Proteomic and Similar Biomarkers – Circulating And Placentalmentioning

confidence: 99%

A Dormant Microbial Component in the Development of Preeclampsia

Kell

Kenny

2016

Front. Med.

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Preeclampsia (PE) is a complex, multisystem disorder that remains a leading cause of morbidity and mortality in pregnancy. Four main classes of dysregulation accompany PE and are widely considered to contribute to its severity. These are abnormal trophoblast invasion of the placenta, anti-angiogenic responses, oxidative stress, and inflammation. What is lacking, however, is an explanation of how these themselves are caused. We here develop the unifying idea, and the considerable evidence for it, that the originating cause of PE (and of the four classes of dysregulation) is, in fact, microbial infection, that most such microbes are dormant and hence resist detection by conventional (replication-dependent) microbiology, and that by occasional resuscitation and growth it is they that are responsible for all the observable sequelae, including the continuing, chronic inflammation. In particular, bacterial products such as lipopolysaccharide (LPS), also known as endotoxin, are well known as highly inflammagenic and stimulate an innate (and possibly trained) immune response that exacerbates the inflammation further. The known need of microbes for free iron can explain the iron dysregulation that accompanies PE. We describe the main routes of infection (gut, oral, and urinary tract infection) and the regularly observed presence of microbes in placental and other tissues in PE. Every known proteomic biomarker of “preeclampsia” that we assessed has, in fact, also been shown to be raised in response to infection. An infectious component to PE fulfills the Bradford Hill criteria for ascribing a disease to an environmental cause and suggests a number of treatments, some of which have, in fact, been shown to be successful. PE was classically referred to as endotoxemia or toxemia of pregnancy, and it is ironic that it seems that LPS and other microbial endotoxins really are involved. Overall, the recognition of an infectious component in the etiology of PE mirrors that for ulcers and other diseases that were previously considered to lack one.

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Tissue factor levels and high ratio of fibrinopeptide A:D‐dimer as a measure of endothelial procoagulant disorder in pre‐eclampsia

Cited by 47 publications

References 20 publications

Absence of enhanced systemic inflammatory response at 18 weeks of gestation in women with subsequent pre-eclampsia

Absence of enhanced systemic inflammatory response at 18 weeks of gestation in women with subsequent pre-eclampsia

Haemostasis in normal pregnancy: a balancing act?

A Dormant Microbial Component in the Development of Preeclampsia

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