ABSTRACT
Background: Term small for gestational age (SGA) babies are at risk for developing iron deficiency anemia. The association between maternal and infant iron stores is not clear. Objective: To assess proportion of term SGA neonates developing iron deficiency anemia by 10 weeks of age, and measure correlation between iron profile and hepcidin of babies at birth and at 10 weeks of age with maternal iron profile. Design: Prospective cohort study conducted from November, 2018 to April, 2020. Participants: 120 term SGA babies and their mothers. Intervention: Hemogram, iron profile and serum hepcidin (every fourth case) estimated in mother, cord blood and baby at 10 weeks. Babies developing anemia at 6 weeks detected by hemogram and ferritin were started on iron supplementation and excluded from the study. Outcome: Proportion of babies developing iron deficiency anemia at 10 weeks of age. Results: 35 (29.2%) of 120 term SGA babies developed anemia (hemoglobin <9 g/dL) at 6 weeks. Proportion of infants who developed iron deficiency anemia (hemoglobin <9 g/dL and serum ferritin <40 µ/dL) at 6 and 10 weeks of age was 14.2% and 23.3%, respectively. No significant correlation was found bet-ween hemoglobin, iron and hepcidin of the baby in cord blood and at 10 weeks of age with that of mothers. Serum hepcidin in babies at birth (137.5 ng/mL) were higher than maternal values (128 ng/mL). Conclusion: A significant proportion of term SGA infants developed anemia during early infancy, irrespective of maternal iron status.
ABSTRACT
Summary In this trial, 200 mothers, who were positive for hepatitis-B e antigen (HBeAg) and who had hepatitis-B virus (HBV) DNA level >200,000 IU/mL, were randomly assigned to receive usual care without antiviral therapy or to receive tenofovir (TDF) at an oral dose of 300 mg/d from 30 to 32 weeks of gestation until postpartum week 4; the participants were followed until postpartum week 28. All the infants received immunoprophylaxis. The primary outcomes were the rates of mother-to-child transmission and birth defects. The secondary outcomes were the safety of TDF, the percentage of mothers with an HBV DNA level of <200,000 IU/mL at delivery, and loss or seroconversion of HBeAg or hepatitis B surface antigen at postpartum week 28. At delivery, 68% of the mothers in the TDF group (66 of 97 women), as compared with 2% in the control group (2 of 100), had an HBV DNA level <200,000 IU/mL. At postpartum week 28, the rate of mother-to-child transmission was significantly lower in the TDF group than in the control group, both in the intention-to-treat analysis (5% vs. 18%, P=0.007) and the per-protocol analysis (0 vs. 7%, P=0.01). The maternal and infant safety profiles were similar in the TDF group and the control group, including birth defect rates (2% vs. 1%, P=1.00), although more mothers in the TDF group had an increase in the creatine kinase level. After the discontinuation of TDF, alanine aminotransferase elevations above the normal range occurred more frequently in mothers in the TDF group than in those in the control group (45% vs. 30%, P=0.03). The authors concluded that in HBeAg-positive mothers with an HBV DNA level >200,000 IU/mL during the third trimester, the rate of mother-to-child transmission was lower among those who received TDF therapy than among those who received usual care without antiviral therapy.
ABSTRACT
Vascular malformations of uterus are a rare cause of delayed post partum hemorrhage (PPH).We discuss a case of a combined pseudoaneurysm with arteriovenous malformation as a cause of secondary PPH, which was diagnosed on doppler sonography and confirmed on angiography. It was successfully managed with uterine artery embolization.