Uterine artery Doppler flow velocity waveform analysis following uterine fibroid embolisation.

The objective was to evaluate the relation of uterine artery Doppler flow pulsatility index (PI) with total uterine volume reduction following bilateral embolisation of uterine fibroids by injection of polyvinyl alcohol particles. Doppler flow velocity was examined before and within 8 days after embolisation (n = 13). Uterine size was assessed by magnetic resonance imaging (MRI) before, and at 3 and 6 months after, the procedure. Mean PI values (mean of right and left side) obtained before embolisation were negatively related to uterine size (r = -0.68, p = 0.010) but not to uterine volume reduction after the procedure. Mean PI values after the procedure were related to the percentage decrease in uterine volume both at 3 (r = 0.74, p = 0.004) and 6 months (p = 0.73, p = 0.005). Doppler ultrasound measures of the uterine arteries may be used to evaluate reduction of uterine size following fibroid embolisation.

Hemostatic variables as independent predictors for fetal growth retardation in preeclampsia.

BACKGROUND: Preeclampsia is a major contributor to perinatal disease and fetal growth retardation (FGR). It has been suggested that increased intravascular coagulation, fibrin deposition in spiral arteries and hypoperfusion of the placenta are involved in these pregnancy complications. METHODS: Multiple variables of the hemostatic system and lipid metabolism, as well as clinical features, were entered into univariate and multivariate models in order to examine the association with preeclampsia and FGR. RESULTS: Two hundred women with preeclampsia and 97 normotensive pregnant women were examined. Plasma levels of the thrombin-antithrombin complex (TAT), tissue factor pathway inhibitor free antigen (TFPI-Fag), protein S free antigen, plasminogen activator inhibitor type-1 (PAI-1) activity and serum levels of triglycerides were significantly increased, whereas plasma levels of antithrombin (AT), fibrinogen, C4b-binding protein (C4b-BP), PAI-2 antigen and serum HDL-cholesterol levels were decreased in the presence of preeclampsia. In the multivariate regression analysis, high TFPI-Fag plasma levels were associated with the presence of preeclampsia. The presence of FGR was in the univariate analysis associated with decreased PAI-1 activity and lower concentrations of fibrin, fibrinogen, factor VII antigen and PAI-2 antigen, as well as with evidence of macroscopic placental infarction. In a multivariate regression model, low maternal weight, placental infarction and low PAI-2 levels were predictors for low birth weight. In a logistic regression model, with the presence or absence of FGR as the dependent variable, male sex of the infant, placental infarction, low PAI-1 activity and factor VII antigen or PAI-2 antigen levels were independent predictors. CONCLUSIONS: Our results are consistent with activated coagulation in the placental vessels in preeclampsia. A low concentration of PAI-2 antigen in plasma emerged as the most consistent risk factor for preeclampsia and FGR.

Plasma concentrations of Lp(a) lipoprotein and TGF-beta1 are altered in preeclampsia.

This study was performed to investigate the possible association between preeclampsia and the plasma concentrations of Lp(a) lipoprotein and TGF-beta1 in a large series of patients. Additionally, correlation between the concentrations of these molecules and the severity of preeclampsia or fetal growth retardation was evaluated. Following clinical examination and biochemical analyses, both electroimmunoassay and RIA technique were used for quantitative determinations of plasma Lp(a) lipoprotein. ELISA technique was used to measure the active form of TGF-beta1 in plasma of pregnant normotensive and preeclamptic women. We examined 154 women with preeclampsia (preeclampsia group) and 76 healthy, pregnant normotensive women (control group). The preeclampsia group was further divided into the following subgroups: mild preeclampsia, severe preeclampsia and preeclampsia with fetal growth retardation. Plasma levels of Lp(a) lipoprotein were lower in the total preeclampsia group as well as in all preeclampsia subgroups (5.45+/-7.41, 5.58+/-8.02, 5.08+/-5.38, and 4.32+/-5.28 mg/dl in the total preeclampsia group, and in subgroups with mild preeclampsia, severe preeclampsia, and preeclampsia with fetal growth retardation, respectively) than in the control group (7.84+/-9.26 mg/dl) as determined by quantitative electroimmunoassay. Corresponding results were obtained with a radioimmunoassay (166.03+/-200.2 U/l in the total preeclampsia group vs. 229.18+/-257.7 U/l in controls). There was good correlation between the two methods used for Lp(a) lipoprotein measurement. The differences between controls and the total preeclampsia group as well as each preeclampsia subgroup were statistically significant by a non-parametric test (one-way Kruskal-Wallis test). Plasma concentrations of the active form of TGF-beta1 were increased in all preeclampsia subgroups as well as in the total group (5.63+/-1.68 ng/ml) compared to controls (4.67+/-1.33 ng/ml). This increase in TGF-beta1 was statistically highly significant. Plasma concentrations of Lp(a) lipoprotein and the active form of TGF-beta1 did not differ significantly between the preeclampsia subgroups. The outcome of this study may suggest involvement of both parameters in the pathophysiology of preeclampsia and may substantiate the notion of a multifactorial etiology of the disease.

High levels of Lp(a) lipoprotein in a family with cases of severe pre-eclampsia.

We report a family with two cases of severe pre-eclampsia/eclampsia in which very high levels of Lp(a) lipoprotein were found. The serum level of Lp(a) lipoprotein is genetically determined and the Lp(a) apolipoprotein has a close homology to plasminogen. Very high levels of Lp(a) lipoprotein might interfere with the fibrinolytic/thrombolytic process in man. A previous report suggested that a high maternal serum Lp(a) lipoprotein level can cause fetal growth retardation, and it is proposed that very high levels might lead to increased deposition of fibrin in the uterine spiral arteries in pregnancy, which is central in the pathogenesis of pre-eclampsia. If confirmed, a very high Lp(a) lipoprotein level could be one risk factor for pre-eclampsia that is genetically determined.

Parenchymal pulmonary endometriosis.

Parenchymal pulmonary endometriosis is an extremely rare but well described condition. We present four new cases, and discuss the examination and treatment of these patients. We conclude that the condition may be underdiagnozed, and that it is a relatively harmless disorder. We propose treatment with progesterone as the first choice of treatment. None of our patients needed surgical treatment.

Zygosity, placental membranes and Weinberg's rule in a Danish consecutive twin series.

The usual assumption that monochorionic twins are monozygotic has recently been questioned, based on blood group discordance in 3 of 12 monochorionic pairs. Therefore, this study evaluates the validity of zygosity diagnosis based on examination of placental membranes, and at the same time evaluates Weinberg's differential rule in a Danish consecutive twin series. All twin pairs, 265 like-sexed and 87 unlike-sexed pairs, born at Odense University Hospital, Denmark, from 1 January 1980 through 31 August 1988, were ascertained. In 229 like-sexed pairs, zygosity was determined by serological methods, and in 190 of these, the fetal membranes could be reliably classified. Fifty-nine monochorionic twin pairs were identified and none of those pairs were discordant for any genetic markers. Therefore, we conclude that monochorionic twins can be considered monozygotic. The distribution of monozygotic and dizygotic pairs was in accordance with Weinberg's rule.

Atrial natriuretic peptide during the menstrual cycle.

Plasma atrial natriuretic peptide levels were found to decrease from 82.5 pg/ml in the follicular phase to 55.8 pg/ml in the luteal phase in 10 normal menstruating women. The reduced level of plasma atrial natriuretic peptide could be a compensatory response to the natriuretic effect of the increased plasma progesterone in the luteal phase.

[Intrauterine tachycardia--differential diagnosis from fetal death]. / Intrauterin takykardi--differentaldiagnose til fosterdød.

A case of intrauterine tachycardia is presented. The case was primarily diagnosed as one of foetal death. The correct diagnosis was established by ultrasonic scanning. During the neonatal period, the Wolff-Parkinson-White syndrome was diagnosed. This is a common cause of intrauterine tachycardia.