Liver disease late in pregnancy without pre-eclampsia.

We describe the case of a first twin pregnancy in a 27 year old patient, who experienced acute onset epigastric and right upper quadrant pain at a gestational age of 32 weeks and 2 days. She was diagnosed with acute liver and renal failure and possible disseminated intravascular coagulopathy (DIC) syndrome without pre-eclampsia. Early labor induction was mandatory to save both mother and foetuses. In this overview we describe the differential diagnosis of severe pregnancy related liver injury in the third trimester of pregnancy without pre-eclampsia. (Acta gastroenterol. belg., 2017, 80, 53-57).

Platelet activation and vascular damage in gestational hypertension.

Increased plasma fibronectin levels are a highly sensitive and specific predictor of gestational hypertension. Of a total of 105 apparently healthy normotensive primigravid women seen at the outpatient clinic, 10 with increased plasma levels of fibronectin (mean +/- 2 SD), were compared with 14 controls. Parameters of early vascular damage (laminin, preprocollagen III), platelet activation (beta-thromboglobulin, platelet factor 4), and coagulation (thrombin-antithrombin III complexes, fibrinopeptide A) were measured at regular (weekly or monthly) intervals. Abnormal values of laminin (p less than 0.005) and fibronectin (p less than 0.0001) were found up to 4 weeks before the onset of clinical disease. Levels of beta-thromboglobulin (p less than 0.0001) were also elevated at least 4 weeks before the appearance of clinical symptoms. Our results show that increased levels of laminin, fibronectin, and platelet activation, as indicated by beta-thromboglobulin levels, are preclinical features of gestational hypertension and indicate that vascular damage has occurred. Fibrin formation would appear to occur later.

Predictive value of increased plasma levels of fibronectin in gestational hypertension.

Blood pressure, proteinuria, and plasma fibronectin and plasminogen activator inhibitor-1 levels were measured in 120 apparently healthy normotensive primigravid women during the first, second, and third trimesters of pregnancy and 2 days post partum. Thirty-two women developed hypertension (diastolic blood pressure greater than or equal to 90 mm Hg) that in 17 women was associated with proteinuria (greater than 0.3 gm/day). Fibronectin levels were 83% +/- 22% of normal (mean +/- SD) during the first trimester and 75% +/- 20% at term in the healthy women but increased from 94% +/- 36% to 187% +/- 36% in the women who developed gestational hypertension (with or without proteinuria) (p less than 0.0001). Plasminogen activator inhibitor-1 levels increased from 26 +/- 19 ng/ml to 110 +/- 86 ng/ml in healthy women and from 32 +/- 35 ng/ml to 290 +/- 90 ng/ml in hypertensive women (p less than 0.001). Increased levels of fibronectin at 25 to 36 weeks of pregnancy (greater than or equal to mean + 2 SD of the healthy women, or greater than 140%) were found in 31 of the 32 women with gestational hypertension with or without proteinuria and in 5 of the 88 healthy women (sensitivity 96%, specificity 94%). Fibronectin levels increased 3.6 +/- 1.9 weeks earlier than the onset of hypertension and/or proteinuria. Increased levels of plasminogen activator inhibitor-1 at 25 to 32 weeks (greater than or equal to 280 ng/ml) were found in 16 of the 32 women who developed gestational hypertension with or without proteinuria and in 4 of the 88 healthy women (sensitivity 50%, specificity 95%). We conclude that increased fibronectin levels are the best predictor of gestational hypertension with or without proteinuria and that its level in plasma increases several weeks before the development of hypertension.

Fibrinolytic response to venous occlusion and fibrin fragment D-dimer levels in normal and complicated pregnancy.

The fibrinolytic response to venous occlusion was assessed in 29 women with normal or complicated pregnancy, by measurements of total t-PA and free t-PA with specific ELISAs. The release of t-PA from the vessel wall was 11 +/- 9 ng/ml in non-pregnant women (mean +/- SD, n = 6) but was markedly reduced throughout pregnancy. Following venous occlusion, free t-PA increased by 12 +/- 11 ng/ml in non-pregnant women but remained below the detection limit of 2 ng/ml towards the end of pregnancy. A markedly reduced t-PA release with absence of free t-PA was also observed during late pregnancy in patients with insulin-dependent diabetes mellitus, intra-uterine growth retardation and pre-eclampsia. Plasma levels of fragment D-dimer of cross-linked fibrin were measured with a specific ELISA in 79 pregnant women. D-dimer levels were 129 +/- 36 ng/ml (mean +/- SD, n = 8) in non-pregnant women and increased to 400 +/- 170 ng/ml (n = 25) and 440 +/- 220 ng/ml (n = 22) during the second and third trimester of pregnancy respectively. Significantly higher levels than observed in uncomplicated third trimester pregnancies were found in 3 out of 6 diabetic and in 2 out of 7 pre-eclamptic women. It is concluded that the t-PA release after venous occlusion is significantly reduced during pregnancy. In addition, released t-PA is rapidly inhibited. The levels of fragment D-dimer increase during pregnancy, suggesting that, notwithstanding the marked impairment of the fibrinolytic response to venous occlusion, the fibrinolytic system remains functionally active.