Guttorm Haugen

Fetal Liver-Sparing Cardiovascular Adaptations Linked to Mother’s Slimness and Diet

Fetal adaptations to impaired maternoplacental nutrient supply include altered regional blood flow. Whether such responses operate within the normal range of maternal body composition or diet is unknown, but any change in fetal liver perfusion could alter hepatic development, with long-term consequences for the risk of cardiovascular and metabolic disease. In 381 low-risk pregnancies, we found that the fetuses of slimmer mothers with lower body fat stores and those eating an unbalanced diet had greater liver blood flow and shunted less blood away from the liver through the ductus venosus at 36 weeks gestation. Consequences of such “liver-sparing” may underlie the increased cardiovascular risk of people whose mothers were slimmer and had lower body fat stores in pregnancy.

Portal and umbilical venous blood supply to the liver in the human fetus near term.

To determine the contribution of the umbilical (UV) and portal (PV) veins to blood supply to the human fetal liver in a low‐risk population near term, and to assess the distribution between the left and right lobes.

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.

Markers of intravascular coagulation and fibrinolysis in preeclampsia: association with intrauterine growth retardation

Background. Alterations in blood coagulation and fibrinolysis are believed to play an important role in the pathogenesis of preeclampsia. Hypercoagulability may be associated with features seen in preeclampsia, such as fibrin deposition in various organs, consumptive thrombocytopenia, and placental hypoperfusion, insufficiency and infarction.

Fetal growth versus birthweight: the role of placenta versus other determinants.

Introduction Birthweight is used as an indicator of intrauterine growth, and determinants of birthweight are widely studied. Less is known about determinants of deviating patterns of growth in utero. We aimed to study the effects of maternal characteristics on both birthweight and fetal growth in third trimester and introduce placental weight as a possible determinant of both birthweight and fetal growth in third trimester. Methods The STORK study is a prospective cohort study including 1031 healthy pregnant women of Scandinavian heritage with singleton pregnancies. Maternal determinants (age, parity, body mass index (BMI), gestational weight gain and fasting plasma glucose) of birthweight and fetal growth estimated by biometric ultrasound measures were explored by linear regression models. Two models were fitted, one with only maternal characteristics and one which included placental weight. Results Placental weight was a significant determinant of birthweight. Parity, BMI, weight gain and fasting glucose remained significant when adjusted for placental weight. Introducing placental weight as a covariate reduced the effect estimate of the other variables in the model by 62% for BMI, 40% for weight gain, 33% for glucose and 22% for parity. Determinants of fetal growth were parity, BMI and weight gain, but not fasting glucose. Placental weight was significant as an independent variable. Parity, BMI and weight gain remained significant when adjusted for placental weight. Introducing placental weight reduced the effect of BMI on fetal growth by 23%, weight gain by 14% and parity by 17%. Conclusion In conclusion, we find that placental weight is an important determinant of both birthweight and fetal growth. Our findings indicate that placental weight markedly modifies the effect of maternal determinants of both birthweight and fetal growth. The differential effect of third trimester glucose on birthweight and growth parameters illustrates that birthweight and fetal growth are not identical entities.

Plasma concentrations of Lp(a) lipoprotein and TGF‐β1 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‐β1 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‐β1 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‐β1 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‐β1 was statistically highly significant. Plasma concentrations of Lp(a) lipoprotein and the active form of TGF‐β1 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.

Dietary supplementation with l-arginine or placebo in women with pre-eclampsia

Background.  To investigate the effect of dietary intake of the NO‐donor l‐arginine on the diastolic blood pressure in women with pre‐eclampsia.

Pregnancy outcome in renal allograft recipients in Nor

Background. To study the influence of pre‐conceptional health status and immunosuppressive drug regimen on pregnancy outcome in renal allograft recipients.

Acute maternal social dysfunction, health perception and psychological distress after ultrasonographic detection of a fetal structural anomaly

Please cite this paper as: Kaasen A, Helbig A, Malt U, Næs T, Skari H, Haugen G. Acute maternal social dysfunction, health perception and psychological distress after ultrasonographic detection of a fetal structural anomaly. BJOG 2010;117:1127–1138.

Increased levels of intercellular adhesion molecules and vascular cell adhesion molecules in pre‐eclampsia

Objective To investigate the correlation between soluble forms of the intercellular adhesion molecule (SICAM‐1) and vascular cell adhesion molecule (sVCAM‐1) and the severity of pre‐eclampsia or its possible consequences for fetal growth.