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Introduction: Increased BMI has been identified as a risk factor for most pregnancy complications, but the underlying metabolic factors mediating the detrimental effects of BMI are largely unknown. We aimed to compare metabolic profiles in overweight/obese women (body mass index [BMI] ≥ 25 kg/m2) and normal weight/underweight women (BMI < 25 kg/m2) across gestation. We also explored how gestational weight gain (GWG) affected maternal metabolic profiles. Material and methods: Exploratory nested case–control study based on a prospective longitudinal cohort of women who were healthy prior to pregnancy and gave birth at Oslo University Hospital from 2002 to 2008. The sample consisted of 48 women who were overweight/obese and 59 normal‐weight/underweight women. Plasma samples from four time points in pregnancy (weeks 14–16, 22–24, 30–32 and 36–38) were analyzed by nuclear magnetic resonance spectroscopy and 91 metabolites were measured. Linear regression models were fitted for each of the metabolites at each time point. Results: Overweight or obese women had higher levels of lipids in very‐low‐density lipoprotein (VLDL), total triglycerides, triglycerides in VLDL, total fatty acids, monounsaturated fatty acids, saturated fatty acids, leucine, valine, and total branched‐chain amino acids in pregnancy weeks 14–16 compared to underweight and normal‐weight women. Docosahexaenoic acid and degree of unsaturation were significantly lower in overweight/obese women in pregnancy weeks 36–38. In addition, overweight or obese women had higher particle concentration of XXL‐VLDL and glycoprotein acetyls (GlycA) at weeks 14–16 and 30–32. GWG did not seem to affect the metabolic profile, regardless of BMI group when BMI was treated as a dichotomous variable, ≥25 kg/m2 (yes/no). Conclusions: Overweight or obese women had smaller pregnancy‐related metabolic alterations than normal‐weight/underweight women. There was a trend toward higher triglyceride and VLDL particle concentration in overweight/obese women. As this was a hypothesis‐generating study, the similarities with late‐onset pre‐eclampsia warrant further investigation. The unfavorable development of fatty acid composition in overweight/obese women, with possible implication for the offspring, should also be studied further in the future. [ABSTRACT FROM AUTHOR]

Background: Ferroptosis plays a key role in placental development and physiology, and abnormal ferroptosis has been implicated in trophoblast injury leading to preeclampsia (PE). We hypothesize that leukocytes isolated from PE exhibit increased ferroptosis and that extracellular vesicles contain long non‐coding (lnc) RNA/mRNAs that modulate oxidative stress and iron toxicity in vascular endothelial cells. Methods: We measured the expression of key regulators of ferroptosis in leukocytes and extracellular vesicles as well as circulating biomarkers of iron homeostasis and oxidative stress in plasma from women with/without PE at different timepoints during pregnancy. For markers that were dysregulated, we assessed their temporal correlation with established markers of disease activity and marker of endothelial activation. For markers dysregulated in early pregnancy, we assessed their ability to predict the development of PE. Results: We found decreased lncRNA/mRNAs in leukocytes, but not extracellular vesicles, in PE that may modulate oxidative stress and iron toxicity. This decrease in anti‐ferroptotic markers does not appear to be related to maternal disease activity or plasma oxidative stress status but rather to attenuated anti‐inflammatory expression in these cells. Circulating ferritin was elevated in PE, supporting the hypothesis that PE represents a disbalance in iron homeostasis. Low lncRNA taurine upregulated gene 1 RNA levels in leukocytes at 22–24 weeks were strongly associated with the development of PE. Conclusions: Our findings suggest that maternal leukocytes in PE show decreased anti‐ferroptotic activity that correlates with anti‐inflammatory expression. Moreover, some of these changes in ferroptotic activity appear to precede the development of PE. [ABSTRACT FROM AUTHOR]

Background: Women with a history of gestational diabetes mellitus and preeclampsia are at increased risk of cardiovascular disease later in life, but the mechanism remains unclear. The aim of the study was to evaluate the association between CXC chemokine ligand 16 and indices of glucose metabolism, dyslipidemia and systemic inflammation in gestational diabetes mellitus and preeclampsia. Methods: This sub-study of the population-based prospective cohort included 310 women. Oral glucose tolerance test was performed during pregnancy and 5 years later along with lipid analysis. CXC chemokine ligand 16 was measured in plasma (protein) and peripheral blood mononuclear cells (messenger RNA) during pregnancy and at follow-up. Results: Circulating CXC chemokine ligand 16 was higher in gestational diabetes mellitus women early in pregnancy and at follow-up, while higher in preeclampsia women late in pregnancy compared to control women. Messenger RNA of CXC chemokine ligand 16 in peripheral blood mononuclear cells were lower in gestational diabetes mellitus and preeclampsia women compared to control women. Increased circulating CXC chemokine ligand 16 level was associated with a higher apolipoprotein B and low-density lipoprotein cholesterol in gestational diabetes mellitus women but not in normal pregnancy at follow-up. Conclusion: Our study shows that women with gestational diabetes mellitus and preeclampsia had a dysregulated CXC chemokine ligand 16 during pregnancy, and in gestational diabetes mellitus, the increase in CXC chemokine ligand 16 early in pregnancy and after 5 years was strongly associated with their lipid profile. [ABSTRACT FROM AUTHOR]

Acute fatty liver of pregnancy (AFLP) is a serious, but rare condition with substantial maternal and perinatal mortality and morbidity. It occurs in the third trimester or early postpartum period. The medical history, physical examination and laboratory tests are often sufficient to make the diagnosis, and liver biopsy is rarely indicated. We present a 33-year-old woman with the diagnosis AFLP. Her case is presented to draw attention to AFLP as a differential diagnosis to liver diseases in pregnancy, especially the HELLP syndrome (haemolysis, elevated liver enzymes and low platelets). Appropriate diagnosis and prompt delivery is essential to optimal maternal and fetal outcome in both the AFLP and HELLP syndromes, and this should be followed by intensive care treatment of the dysfunctional maternal multiorgan system.

Background: Cardiomyopathy is a condition with heart failure caused by a reduction in the contractility of the heart. Peripartum cardiomyopathy is a rare, but serious condition, characterised by development of heart failure during the last month of pregnancy or the first five months after delivery., Material and Methods: We present a case in which a woman pregnant with twins developed heart failure a few days after giving birth. We give a short report of symptoms, clinical signs, diagnosis, treatment and prognosis for subsequent pregnancies., Results and Interpretation: The condition was initially diagnosed and treated as pneumonia, but despite treatment and improvement in her laboratory tests, her condition worsened. The symptoms were dyspnoea, peripheral oedemas and pulmonary oedema. Peripartum cardiomyopathy was diagnosed after echocardiography. Treatment of heart failure with diuretics, nitroglycerine, angiotensin-converting enzyme inhibitor and beta blocker was given with good results. This case is presented in order to draw attention to a rare, but serious condition in pregnancy or the postnatal period which easily can be misjudged or mistreated.