Effect of vitamin A supplementation to mother and infant on morbidity in infancy. Effect of postpartum maternal or neonatal vitamin A supplementation on infant mortality among infants born to HIV-negative mothers in Zimbabwe. Vitamin a status of pregnant women and effect of post partum vitamin a supplementation. Randomized controlled safety and efficacy trial of 2 vitamin A supplementation schedules in Tanzanian infants. Maternal vitamin A or beta-carotene supplementation in lactating bangladeshi women benefits mothers and infants but does not prevent subclinical deficiency. Impact of a single megadose of vitamin A at delivery on breastmilk of mothers and morbidity of their infants. Vitamin a supplementation does not affect infants' immune responses to polio and tetanus vaccines. Effectiveness of an early supplementation scheme of high-dose vitamin A versus standard WHO protocol in Gambian mothers and infants: a randomised controlled trial. The effects of maternal and infant vitamin A supplementation on vitamin A status: a randomised trial in Kenya. High dose vitamin A supplementation of breast-feeding Indonesian mothers: effects on the vitamin A status of mother and infant.
To assess the impact of Vitamin A supplementation to the mother soon after delivery and to the infant at six months on morbidity in infancy.
                Randomized double blind placebo controlled field trial.
                51 villages in two contiguous Primary Health Centers in Villupuram Health Unit District of Tamil Nadu, South India.
                909 newly delivered mother-and-infant pairs.
                Both mother and infant received Vitamin A (300,000 IU for mothers and 200,000 IU for children) in 311 instances (AA); mother received Vitamin A but infant received Placebo in 301 instances (AP); and both mother and infant received Placebo in the remaining 297 instances (PP).
                Incidence of diarrhea and Acute Respiratory Infection (ARI); distributions of infants by frequency of episodes and number of infected days.
                233 in the AA Group and 228 each in the AP and PP Groups were followed up regularly. The incidence of diarrhea in these infants was 97.4%, 96.9% and 94.7% in the three groups, mean number of diarrheal episodes was 4.4, 4.6 and 4.2 and median number of days in infancy with diarrhea was 26, 26 and 22 days, respectively. For ARI, the incidences were 96.6%, 95.6% and 96.1%, means were 4.8, 5.1 and 4.8 episodes, and the medians were 32, 34 and 34 days, respectively.
                Prophylactic administration of mega doses of Vitamin A to the mother soon after delivery and to the infant at six months do not have any beneficial impact on the incidence of diarrhea and ARI in infancy. Young infants are at risk of vitamin A deficiency. Supplementation of breastfeeding mothers improves the vitamin A status of their infants, but there are no data regarding its effect on infant mortality, and data on the effect of directly supplementing infants during the first few weeks of life are conflicting.
                The objective was to measure the effect on infant mortality of supplementing neonates and their HIV-negative mothers with single, large doses of vitamin A during the immediate postpartum period.
                A randomized, placebo-controlled, 2-by-2 factorial design trial was conducted in 14,110 mothers and their infants; 9208 of the mothers were HIV-negative at delivery, remained such during the postpartum year, and were retained in the current analysis. The infants were randomly assigned within 96 h of delivery to 1 of 4 treatment groups: mothers and infants received vitamin A (Aa), mothers received vitamin A and infants received placebo (Ap), mothers received placebo and infants received vitamin A (Pa), and both mothers and infants received placebo (Pp). The vitamin A dose in the mothers was 400,000 IU and in the infants was 50,000 IU. The mother-infant pairs were followed to 12 mo.
                Hazard ratios (95% CI) for 12 mo mortality among infants in the maternal-supplemented and infant-supplemented groups were 1.17 (0.87, 1.58) and 1.08 (0.80, 1.46), respectively. Hazard ratios (95% CI) for the Aa, Ap, and Pa groups compared with the Pp group were 1.28 (0.83, 1.98), 1.27 (0.82, 1.97), and 1.18 (0.76, 1.83), respectively. These data indicate no overall effect. Serum retinol concentrations among a subsample of women were similar to reference norms.
                Postpartum maternal or neonatal vitamin A supplementation may not reduce infant mortality in infants of HIV-negative women with an apparently adequate vitamin A status. To assess the Vitamin A status of pregnant women in their third trimester using maternal serum retinol levels as the indicator; and (ii) To assess the impact of postpartum Vitamin A supplementation on the Vitamin A status of exclusively breastfed infants.
                Prospective randomized single blind controlled study.
                Teaching Hospital.
                109 apparently healthy primi and second gravida women registered at the antenatal clinic were included in the study and followed up for three months postpartum. Serum retinol levels of pregnant mothers in their third trimester (35-37 weeks) and cord blood levels after delivery were estimated. Mothers were then assigned to two groups. The experimental group included 53 mothers who received a single dose of 2 lakh units of Vitamin A orally. The control group had 56 mothers who did not receive Vitamin A. Mothers and infants were followed up for three months. The serum retinol of infants and the breast milk retinol levels were estimated at the end of three months and the results were compared. The growth of the infants was also monitored.
                Subclinical Vitamin A deficiency was seen in 29.67% of pregnant women. At the end of three months, 69.6% of mothers in the control group had breast milk retinol levels below 30 mg/dl, as opposed to 36.1% in the experimental group. Forty five per cent of infants in the control group had subclinical vitamin A deficiency compared to none in the experimental group. There was no difference in the growth of infants in the two groups. However, the infant serum and the breast milk retinol levels were significantly higher in the supplemented group.
                There is a high prevalence of inapparent Vitamin A deficiency (29.7%) in pregnant women in their third trimester from lower socio-economic strata. Postpartum Vitamin A supplementation had a beneficial impact on the infant serum retional and the breast milk retinol level but no effect on infant growth. Vitamin A supplementation reduces morbidity and mortality in children living in areas endemic for vitamin A deficiency. Routine vitamin A supplementation usually starts only at age 9 mo, but high rates of illness and mortality are seen in the first months of life.
                The objective of the study was to evaluate the safety and efficacy of vitamin A supplementation at the same time as routine vaccination in infants aged 1-3 mo.
                We recruited 780 newborn infants and their mothers to a randomized double-blind controlled trial in Ifakara in southern Tanzania. In one group, mothers received 60,000 microg vitamin A palmitate shortly after delivery, and their infants received 7500 microg at the same time as vaccinations given at approximately 1, 2, and 3 mo of age. In the other group, mothers received a second 60,000-microg dose when their infant was aged 1 mo, and their infants received 15,000 microg at the same time as the routine vaccinations. VAD was defined as a modified relative dose-response test result of >or=0.060.
                High-dose vitamin A supplementation was well tolerated. The relative risk of VAD at 6 mo in the high-dose group compared with the lower dose group was 0.91 (95% CI: 0.76, 1.09; P=0.32). Serum retinol and incidence of illness did not differ significantly between the 2 groups. Some vitamin A capsules degraded toward the end of the study.
                Doubling the doses of vitamin A to mothers and their young infants is safe but unlikely to reduce short-term morbidity or to substantially enhance the biochemical vitamin A status of infants at age 6 mo. The stability of vitamin A capsules merits further investigation. The effects of maternal postpartum vitamin A or beta-carotene supplementation on maternal and infant serum retinol concentrations, modified relative dose-response (MRDR) ratios and breast milk vitamin A concentrations were assessed during a community-based trial in Matlab, Bangladesh. At 1-3 wk postpartum, women were randomly assigned to receive either (1) a single dose of 200,000 international units [60,000 retinol equivalents (RE)] vitamin A followed by daily placebos (n = 74), (2) daily doses of beta-carotene [7.8 mg (1300 RE)] (n = 73) or (3) daily placebos (n = 73) until 9 mo postpartum. Compared to placebos, vitamin A supplementation resulted in lower maternal MRDR ratios (i.e., increased liver stores) and higher milk vitamin A concentrations at 3 mo, but these improvements were not sustained. The beta-carotene supplementation acted more slowly, resulting in milk vitamin A concentrations higher than the placebo group only at 9 mo. Irrespective of treatment group, over 50% of women produced milk with low vitamin A concentrations (</=1.05 micromol/L or </=0.28 micromol/g fat) throughout the study. Overall, mean maternal serum retinol concentrations were not affected by supplementation. Compared to the placebo group, the mean MRDR ratio of 6-mo-old infants was higher in the vitamin A group. Infants (33%) had serum retinol concentrations <0.70 micromol/L and 88% had MRDR ratios >/=0. 06. We conclude that while both interventions were beneficial, neither was sufficient to correct the underlying subclinical vitamin A deficiency in these women nor to bring their infants into adequate vitamin A status. To evaluate the effect of vitamin A supplementation 24 h after delivery on breastmilk retinol concentration.
                Fifty low income women were randomly assigned to a single oral dose of 209 micromol of Vitamin A or none at delivery. Maternal serum and breastmilk retinol levels and infant morbidity and anthropometry were serially assessed.
                Mean (95% CI) serum retinol levels increased in the supplemented mothers at 2.77 (2.3, 3.2) compared to 1.15 (0.9, 1.4) micromol/l in controls (P < 0.05) and remained at a significantly higher level of 1.59 (1.4, 1.8) micromol/l compared to 1.33 (1.8, 1.5) micromol/l in the control group (P < 0.001) up to a period of three months. Breastmilk retinol concentration was also greater at 24 h after supplementation, mean (CI) 11.34 (9.0, 13.7) micromol/l, compared to 2.95 (2.3, 3.6) micromol/l in the control group (P < 0.0001), and remained higher for the next six months at 1.06 (0.9, , 1.3) micromol/l compared to 0.73 (0.6, 0.8) micromol/l in the control group (P < 0.02). Infants of the supplemented mothers had reduced mean duration of respiratory tract infection of 3.1 (2.7, 3.5) days compared to 3.7 (3.3, 4.2) days (P < 0.03) and mean incidence of febrile illness 0.1 (0.1, 0.1) compared to control infants 0.3 (0.3, 0.3) days, (P < 0.002).
                Vitamin A supplementation of malnourished mothers maintains higher breastmilk retinol concentration for at least six months and reduces the duration of respiratory tract infection and febrile illness in their breastfed infants. It has been suggested that administering vitamin A with the measles vaccine may reduce the vaccine's immunogenicity. This trial examined the effect of supplementing vitamin A during the early months of life on infants' immune responses to tetanus and polio vaccines. Young infants (n = 1085) were enrolled and individually randomized into 1 of 4 groups in a factorial, double-blind, placebo-controlled trial. Three vitamin A supplementation strategies were investigated: 1) supplementation of breast-feeding mothers with 60 mg retinol equivalent (RE) vitamin A within 4 wk of delivery; 2) Expanded Program on Immunization (EPI)-linked supplementation of infants with 7.5 mg RE vitamin A at 6, 10, and 14 wk; and 3) combined mother and child supplementations. A 4th group in which mother and child were given placebos served as controls. Blood samples were collected from each child at 6 wk and 6 mo of age to measure antipolio antibody titer, antitetanus toxoid antibodies, and avidity of antibodies to tetanus. Of the infants randomized into the 4 arms of the study, 767 (71%) completed follow-up at 6 mo of age. Follow-up rates were similar in all 4 arms (69-72%, P = 0.8). Antibody titers were relatively high in all 4 groups at both 6 wk and 6 mo of age, with no differences among the groups. We found no evidence that vitamin A supplementation affects infants' antibody responses to tetanus toxoid or oral polio vaccine delivered at EPI contacts. Most developing countries have adopted a standard WHO dosing schedule for vitamin A supplementation. However, in 2002 the International Vitamin A Consultative Group (IVACG) Annecy Accord recommended a new high-dose regimen for mothers and infants. Our aim was to test whether the new high-dose regimen of vitamin A supplementation would increase maternal and infant plasma vitamin A, reduce infant Helicobacter pylori infection and nasopharyngeal pneumococcal carriage, and improve infant gut epithelial integrity.
                In an area of moderate vitamin A deficiency in rural Gambia, 220 mother-infant pairs were enrolled in a randomised double-blind trial between September, 2001, and October, 2004, that compared the IVACG high dose with the WHO dose. The primary endpoints were levels of maternal and infant plasma vitamin A, H pylori infection, pneumococcal carriage, and gut epithelial integrity. The trial is registered as ISRCTN 98554309.
                197 infants completed follow-up to 12 months (99 high dose and 98 WHO dose). There were no adverse events at dosing. No differences were found in the primary outcomes for high-dose versus WHO schedule: maternal vitamin A concentration at 2 months +0.02 micromol/L (95% CI -0.10 to 0.15); infant vitamin A at 5 months +0.01 micromol/L (-0.06 to 0.08); H pylori infection at 12 months -0.3% (-14.7 to 14.2); maternal pneumococcal carriage at 12 months -2.0% (-13.7 to 9.7); infant pneumococcal carriage at 12 months -4.1% (-15.8 to 7.6); infant gut mucosal damage at 12 months 5.2% (-8.7 to 19.2). There were more clinic attendances by the high-dose group in the first 6 months of life (p=0.018).
                Our results do not lend support to the proposal to increase the existing WHO standard dosing schedule for vitamin A in areas of moderate vitamin A deficiency. Caution is urged for future studies because trials have shown possible adverse effects of higher doses of vitamin A, and potential negative interactions with the expanded programme on immunisation (EPI) vaccines. Postpartum vitamin A supplementation of mothers and infants is recommended, but the efficacy has been questioned. In this double-blind, placebo-controlled trial, Kenyan mother-infant pairs were randomised to maternal vitamin A (400,000 IU) or placebo <24 h postpartum, and infant vitamin A (100,000 IU) or placebo at 14 weeks. Milk retinol was determined at weeks 4, 14 and 26, and maternal and infant serum retinol at weeks 14 and 26. Infant retinol stores were assessed at week 26, using a modified relative dose response (MRDR) test. Among 564 women, serum retinol at 36 weeks gestation was 0.81 (SD 0.21) micromol/l, and 33.3% were<0.7 micromol/l. Maternal serum retinol was not different between groups, but milk retinol was higher in the vitamin A group: (0.67 v. 0.60 micromol/l; 0.52 v. 0.44 micromol/l; 0.50 v. 0.44 micromol/l at 4, 14 and 26 weeks, respectively). When expressed per gram fat, milk retinol was higher in the vitamin A group only at 4 weeks. Infant serum retinol was not different between groups. However, although most infants had deficient vitamin A stores (MRDR>0.06%) at 26 weeks, vitamin A to infants, but not mothers, resulted in a lower proportion of infants with deficient vitamin A stores (69 v. 78 %). High-dose postpartum vitamin A supplementation failed to increase serum retinol and infant stores, despite modest effects on milk retinol. Infant supplementation, however, increased stores. There is a need for a better understanding of factors affecting absorption and metabolism of vitamin A. For regions where vitamin A deficiency is common, high dose vitamin A supplementation of lactating mothers is currently recommended, but the effects of this intervention have not been carefully evaluated. We conducted a randomized, double-blind trial in which 153 Indonesian mothers 1-3 wk postpartum received either a capsule containing 312 mumol of vitamin A as retinyl palmitate or a placebo. Mothers' serum retinol concentrations in the vitamin A group tended to be lower than in the placebo group at baseline but higher at 3 mo postpartum (1.39 vs. 1.24 mumol/L, P = 0.03) and 6 mo postpartum (1.23 vs. 1.08 mumol/L, P < 0.01). The milk retinol concentrations of the vitamin A group were higher than those of the placebo group by 0.48 to 1.18 mumol/L at 1-8 mo postpartum (P < 0.05). Among the infants at 6 mo of age, the prevalences of low serum retinol concentration (< 0.52 mumol/L) were 36 and 15% in the placebo and vitamin A groups, respectively (P < 0.005), and the prevalences of low vitamin A stores (assessed by relative dose response) were 23 and 10%, respectively (P < 0.03). High dose vitamin A supplementation of lactating mothers is an efficacious way to improve the vitamin A status of both mother and breast-fed infant.