Towards a More Stable Understanding of Pregnancy Micronutrient Metabolism

There is an urgent need to better understand the micronutrient demands of pregnancy due to the complex physiological adaptations during the gestational period and the importance of micronutrients in maternal-fetal health. However, the rigorous study of micronutrients in pregnancy is significantly lacking due to a number of issues including the exclusion of pregnant people in research, methodological barriers to studying micronutrients, and the multidisciplinary expertise required for such studies. Stable isotopes present a unique methodological opportunity to quantify pregnancy-related changes in the absorption, distribution, metabolism and excretion of micronutrients. However, we demonstrate here through a rapid review of the published literature that this approach is dramatically underutilized outside of calcium. In this perspective we discuss the use of stable isotopes to study micronutrient physiology and our experiences in addressing the need for more studies in this area. Lastly, we discuss how we might overcome major barriers to move towards a better understanding of micronutrient physiology in pregnancy.

Krüppel-like factor 17 upregulates uterine corin expression and promotes spiral artery remodeling in pregnancy

Spiral artery remodeling is an important physiological process in the pregnant uterus which increases blood flow to the fetus. Impaired spiral artery remodeling contributes to preeclampsia, a major disease in pregnancy. Corin, a transmembrane serine protease, is up-regulated in the pregnant uterus to promote spiral artery remodeling. To date, the mechanism underlying uterine corin up-regulation remains unknown. Here we show that Krüppel-like factor (KLF) 17 is a key transcription factor for uterine corin expression in pregnancy. In cultured human uterine endometrial cells, KLF17 binds to theCORINpromoter and enhances the promoter activity. Disruption of theKLF17gene in the endometrial cells abolishesCORINexpression. In mice,Klf17is up-regulated in the pregnant uterus.Klf17deficiency prevents uterineCorinexpression in pregnancy. Moreover,Klf17-deficient mice have poorly remodeled uterine spiral arteries and develop gestational hypertension and proteinuria. Together, our results reveal an important function of KLF17 in regulatingCorinexpression and uterine physiology in pregnancy.

Pulmonary Edema in Pregnancy

Pulmonary edema is characterized by the movement of excess fluid into the alveoli of the lungs. Although the alterations of cardiovascular and pulmonary physiology in pregnancy may predispose patients to pulmonary edema, it is never normal and constitutes severe maternal morbidity. The etiologies of pulmonary edema are diverse, ranging from disease processes independent of pregnancy to pathophysiology unique to the gravid state. The causes of pulmonary edema can be broadly classified as either cardiogenic or noncardiogenic, which constitutes the first important branch point in the diagnosis and management of the disease. The treatment of pulmonary edema in pregnancy parallels that in the nonpregnant population with an emphasis on maintaining the physiologic alterations of pregnancy through supportive care, including mechanical ventilation if needed. In all cases of pulmonary edema, the decision to proceed with delivery to improve the maternal status should be considered within the context of the etiology and anticipated disease course, the gestational age, and the goals of care. This review contains 3 figures, 4 tables, and 60 references. Key Words: Pulmonary edema, respiratory alkalosis, acute respiratory distress syndrome (ARDS), cardiogenic pulmonary edema, transfusion-related acute lung injury (TRALI), transfusion-associated circulatory overload (TACO), mechanical ventilation, extra corporeal membrane oxygenation (ECMO).

Pulmonary Edema in Pregnancy

Pulmonary edema is characterized by the movement of excess fluid into the alveoli of the lungs. Although the alterations of cardiovascular and pulmonary physiology in pregnancy may predispose patients to pulmonary edema, it is never normal and constitutes severe maternal morbidity. The etiologies of pulmonary edema are diverse, ranging from disease processes independent of pregnancy to pathophysiology unique to the gravid state. The causes of pulmonary edema can be broadly classified as either cardiogenic or noncardiogenic, which constitutes the first important branch point in the diagnosis and management of the disease. The treatment of pulmonary edema in pregnancy parallels that in the nonpregnant population with an emphasis on maintaining the physiologic alterations of pregnancy through supportive care, including mechanical ventilation if needed. In all cases of pulmonary edema, the decision to proceed with delivery to improve the maternal status should be considered within the context of the etiology and anticipated disease course, the gestational age, and the goals of care. This review contains 3 figures, 4 tables, and 60 references. Key Words: Pulmonary edema, respiratory alkalosis, acute respiratory distress syndrome (ARDS), cardiogenic pulmonary edema, transfusion-related acute lung injury (TRALI), transfusion-associated circulatory overload (TACO), mechanical ventilation, extra corporeal membrane oxygenation (ECMO).

Hypomagnesaemia and pregnancy

Hypomagnesaemia is common in pregnancy, particularly in developing countries and low-income communities. Despite the frequent therapeutic use of magnesium in pregnancy, and the evidence regarding the association of hypomagnesaemia with adverse pregnancy outcomes in animal studies, it remains unclear whether hypomagnesaemia is associated with complications in human pregnancy. Three case reports of pregnancies complicated by moderate–severe hypomagnesaemia are presented and magnesium physiology in pregnancy is discussed. The evidence as to whether hypomagnesaemia may represent a direct cause, a consequence of other disease processes or an epiphenomenon in adverse pregnancies outcomes is reviewed.