Vitamin B12 maintains normal folate metabolism which is essential for cell multiplication during pregnancy. No good data are available on what constitutes vitamin B12 deficiency in pregnancy, nevertheless vitamin B12 deficiency is frequently reported in pregnancy due to inadequate dietary intake of vitamin B12 and a physiological decline of maternal vitamin B12 concentrations. This decline can be explained by the increased maternal metabolic rate and active transport by the placenta to the fetus. If the mother is deficient during pregnancy, the baby may have low serum vitamin B12 concentrations at birth [1]. Vitamin B12 deficiency during pregnancy is associated with preeclampsia, fetal growth restriction, preterm labor, neural tube defects, neonatal megaloblastic anemia and neonatal neurological symptoms. It has been suggested to improve vitamin B12 status of women in the periconceptional period by supplementation of vitamin B12, but no randomized studies on the outcome of such supplementation have been published.
We report on a woman with an Lp(a) lipoprotein level above the 99th centile of the population distribution of concentrations, who at the age of 43 had had deep vein thrombosis causing a pulmonary embolus and whose brother, who also had a very high level, had suffered a cerebral infarction at the age of 43. She had given birth to three children, all with very low birth weight, one of whom died when 3 months old. The placentas had been small and ischemic. The concurrence of a very high Lp(a) lipoprotein level, familial thromboembolic disease and recurrent placental ischemia with delivery of children with low birth weight suggests the possibility that a very high Lp(a) lipoprotein concentration may predispose to placental insufficiency, presumably arising from pathological changes in maternal uterine vessels in the placental bed. If confirmed, a very high Lp(a) lipoprotein level may be a factor to consider in women who have repeated pregnancies with placental insufficiency and who give birth to children with low birth weight.
Objective: Descriptive study on maternal serum vitamin B12 and folic acid in term pregnancy and in umbilical cord blood that was performed in an inner city hospital with a mixed ethnic population in the region of Flanders in Belgium. Materials and Methods: A prospective cohort study that took place from April 1 until May 31, 2011. Plasma folic acid and vitamin B12 were measured in maternal and umbilical cord blood from all term uncomplicated deliveries in a single regional hospital. Data on age, previous obstetric history, ethnicity, nutritional intake, and use of vitamin supplements were registered. Results: Data were collected from 110 patients, mean maternal serum vitamin B12 was 243.9 pmol/l and mean folic acid level was 43.0 nmol/l. Using a cutoff of respectively 150 pmol/l for vitamin B12 and 7.1 nmol/l for folic acid, 13% of the women were classified as vitamin B12-deficient and 23% were deficient for folic acid. Vitamin B12 deficiency was only seen in autochthonous Belgian women. A correlation between the maternal and umbilical cord levels was noted (R = 0.7 for vitamin B12, R = 0.85 for folic acid), but none of the umbilical cord levels demonstrated deficiency. Number of previous pregnancies and intake of supplements had no influence. Conclusion: Pregnant women in Antwerp, Belgium, frequently show vitamin B12 and folic acid deficiency, although a correlation exists with lower umbilical cord levels, the present limited data did not demonstrate any case of deficiency in umbilical cord blood. The frequency is highest in the autochthonous population and is not influenced by intake of vitamin supplements.
Uromucoid (Tamm-HorsfalΓs mucoprotein) was not detected in amniotic fluid from pregnancies with gestational age 12–18 weeks, but was detected in 5 of 9 samples of amniotic fluid from full-term pregnancies, and in urine from all full-term infants investigated 1st day of life. This suggests that uromucoid excretion under normal conditions esthablished near term. Change from intrauterine to extrauterine life may rapidly induce uromucoid excretion, as this protein was found in premature infants (32–34 weeks of gestation) at the 2nd day of life. Healthy newborn infants had a lower uromucoid concentration in urine than children 7–13 years old. In newborns with uncomplicated prematurity, idiopathic respiratory distress syndrome and full-term asphyxiated newborns, the uromucoid concentration in urine during the 1st week of life was not different from healthy newborn infants. Though uromucoid is found to be the major constituent of hyaline casts, the excretion of casts did not correlate to the uromucoid concentration.
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