Prevention of anaemia in inner city toddlers by an iron supplemented cows' milk formula

There are few data to support the use of follow-on formulas in infants from the age of 6 months. In a prospective trial in a deprived inner city area of Birmingham 100 infants who were already receiving pasteurised cows' milk by 6 months of age were enrolled and randomised either to receive a follow-on formula or to continue on cows' milk from 6 months until 18 months. At 18 months of age the follow-on formula group returned to cows' milk and both groups were followed up until 24 months. Iron status, growth, and nutritional status were analysed at intervals of six months. At enrollment, no differences in haematological status were evident. However, by 12 months of age, 31% of the cows' milk group were anaemic (haemoglobin concentration < 110 g/l) compared with only 3% of those receiving follow-on formulas. At 18 months, 33% of the cows' milk group were anaemic compared with only 2% of the follow-on formula group and by 24 months of age none of the follow-on formula group was anaemic, whereas 26% in the cows' milk group still had a haemoglobin of < 110 g/l. Mean corpuscular volume was significantly smaller and ferritin significantly lower in the cows' milk group at 12, 18, and 24 months. Dietary iron intake was higher in the follow-on formula group at 12 and 18 months but not at 24 months, when both groups were back on cows' milk. Infants and toddlers at high risk of iron deficiency are therefore unlikely to become anaemic if receiving a follow-on formula, although the relative merits of follow-on formula compared with an ordinary infant formula remain uncertain.     

Prevention of anaemia in inner city toddlers by an iron supplemented cows' milk formula.

There are few data to support the use of follow-on formulas in infants from the age of 6 months. In a prospective trial in a deprived inner city area of Birmingham 100 infants who were already receiving pasteurised cows'' milk by 6 months of age were enrolled and randomised either to receive a follow-on formula or to continue on cows'' milk from 6 months until 18 months. At 18 months of age the follow-on formula group returned to cows'' milk and both groups were followed up until 24 months. Iron status, growth, and nutritional status were analysed at intervals of six months. At enrollment, no differences in haematological status were evident. However, by 12 months of age, 31% of the cows'' milk group were anaemic (haemoglobin concentration < 110 g/l) compared with only 3% of those receiving follow-on formulas. At 18 months, 33% of the cows'' milk group were anaemic compared with only 2% of the follow-on formula group and by 24 months of age none of the follow-on formula group was anaemic, whereas 26% in the cows'' milk group still had a haemoglobin of < 110 g/l. Mean corpuscular volume was significantly smaller and ferritin significantly lower in the cows'' milk group at 12, 18, and 24 months. Dietary iron intake was higher in the follow-on formula group at 12 and 18 months but not at 24 months, when both groups were back on cows'' milk. Infants and toddlers at high risk of iron deficiency are therefore unlikely to become anaemic if receiving a follow-on formula, although the relative merits of follow-on formula compared with an ordinary infant formula remain uncertain.     

Iron deficiency and iron deficiency anaemia during infancy and childhood

The present definition of iron deficiency and iron deficiency anaemia is under debate. Our present figures for the prevalence of iron deficiency in infants and toddlers are thus disputed.

Conclusion: Better understanding of the regulation of iron metabolism and requirement during the critical early period of growth and development is needed for relevant control of iron deficiency anaemia.     

Severe iron deficiency anaemia and ischaemic stroke in children

Iron deficiency anaemia (IDA) has a peak prevalence of 4-8% in children aged 1-3 years of age and is known to be associated with developmental delay, lethargy, irritability and cognitive problems. Rarely, IDA has also been reported as a risk factor for stroke in otherwise healthy children. We report a series of four young children aged 14 months to 48 months with significant IDA. Three children had venous sinus thrombosis and one had arterial ischaemic stroke, without other risk factors. We discuss the potential underlying mechanisms and review the relevant literature. This report further consolidates the evidence for a strong association between IDA and childhood stroke and highlights an easily treatable (and preventable) risk factor.     

Phagocyte metabolic functions in iron deficiency anaemia of Indian children

Nitroblue tetrazolium test (NBT) and bactericidal activity of polymorphonuclear leucocytes was studied in 40 patients with iron deficiency anaemia (aged 0-12 years). NBT test had a significant correlation with serum iron (P less than 0.001) in all cases of iron deficiency anemia. Haemoglobin levels less than 4 g/dl also correlated significantly with NBT score. Bactericidal activity with opsonin-coated Staphylococcus aureus was considerably decreased in severe anaemia, but no significant correlation was found with serum iron concentration (P less than 0.1). The phagocytic and bactericidal activity of polymorphonuclear leucocytes is dependent upon serum iron levels and is considerably reduced in iron deficient state in anaemic children.     

Milk versus medicine for the treatment of iron deficiency anaemia in hospitalised infants

Aims: To compare iron fortified follow-on milk (iron follow-on), iron fortified partially modified cows'' milk (iron milk), and iron medicine for the treatment of iron deficiency anaemia (IDA) in hospitalised infants. Methods: In a randomised controlled trial, infants aged 9–23 months with IDA and who were hospitalised with an acute illness received iron follow-on (12 mg/l ferrous iron), iron milk (12.9 mg/l ferrous iron), or iron medicine (ferrous gluconate at 3 mg/kg of elemental iron once daily). All interventions were given for three months. Changes in measures of iron status three months after hospital discharge were determined. Results: A total of 234 infants were randomised. Iron status was measured at follow up in 59 (70%) iron medicine, 49 (66%) iron follow-on, and 54 (70%) iron milk treated infants. There was a significant (mean, 95% CI) increase in haemoglobin (15 g/l, 13 to 16) and iron saturation (9%, 8 to 10) and decrease in ferritin (–53 µg/l, –74 to –31) in all three groups. Mean cell volume increased in iron follow-on (2 fl, 1 to 3) and iron milk (1 fl, 0.1 to 3) treated infants, but not in the iron medicine group (1 fl, –1 to 2). The proportion with IDA decreased in all three groups: iron medicine 93% to 7%, iron follow-on 83% to 8%, and iron milk 96% to 30%. Adverse effects, primarily gastrointestinal, occurred in 23% of the iron medicine, 14% of the iron follow-on, and 13% of the iron milk group. Conclusions: Iron fortified follow-on milk, iron fortified partially modified cows'' milk, and iron medicine all effectively treat IDA in infancy.     

Indices of iron deficiency and anaemia in Bedouin and Jewish toddlers in southern Israel

AIMS: To estimate the prevalence of iron deficiency and iron deficiency anaemia using haematological indices. METHODS: Prospective interventional study. Healthy toddlers from Bedouin and Jewish towns in southern Israel. Capillary blood was sampled to assess iron status and nutritional history recorded. Parents were given specific nutritional instructions. Anaemia was defined as haemoglobin level < or = 11 gr/dL. Iron deficiency without anaemia was defined as mean corpuscular volume (MCV) < 70 fL and/or red blood cell width (RDW) > or = 16, with haemoglobin level > 11 gr/dL. Toddlers with iron deficiency were treated with 5 mg/kg/day of elemental iron. Follow-up iron and nutritional status was performed 1 and 2 months after enrolment. RESULTS: At the time of enrolment 42% of the 107 Jewish and 93% of the 43 Bedouin toddlers were iron deficient (p < 0.001). Significantly higher proportions of Bedouin toddlers were breastfed, drank tea, did not eat meat, did not take supplementary iron in their first year of life and were previously diagnosed with anaemia. Rate of follow-up was 55% among Bedouins and 33% among Jews. The mean haemoglobin rise over two months was 0.91 gr/dL (95% CI: 0.63-1.18 gr/dL; p < 0.001) in Bedouins and 0.58 gr/dL (95% CI: 0.14-1.02 gr/dL; p = 0.014) in Jews. CONCLUSIONS: Higher rates of anaemia and iron deficiency, as well as most of the risk factors, found among the Bedouin toddlers, call for the design and implementation of innovative, culturally appropriate interventions in the Bedouin population.     

Helicobacter pylori infection with iron deficiency anaemia and subnormal growth at puberty

The purpose of this study was to determine whether Helicobacter pylori infection can contribute to growth deficit, especially in pubescent children who need large amounts of iron for growth. A structured questionnaire was sent to the parents of 532 healthy children aged 10 to 15 years (mean 12.9) to obtain demographic information on the parents and the environment. Of the 532 questionnaires sent out, 375 (70.5%; 170 girls and 205 boys) were returned. After collecting blood samples from participants, haemoglobin, serum iron, total iron binding capacity, serum ferritin, and serum IgG antibodies to H pylori were measured. The effects of risk factors such as H pylori infection, iron deficiency anaemia, sex, socioeconomic status, type of house, and crowding index on growth were analysed using multiple regression analysis. Of 63 H pylori positive children, 18 (28.6%) were below the 25th centile values for height, compared with 63 of 312 (20.2%) H pylori negative children. The prevalence rate of H pylori infection was 15.5% (53 of 343) in children without iron deficiency anaemia and 31.3% (10 of 32) in those affected. The relative risk of short stature was 2.2 (95% confidence interval (CI), 1.0 to 4.8) for iron deficiency anaemia, and 1.4 (95% CI, 0.8 to 2.4) for H pylori infection. The mean height was significantly lower in the group having both H pylori infection and iron deficiency anaemia. Therefore, H pylori infection accompanied by iron deficiency anaemia, rather than H pylori infection per se, might delay pubertal growth.     

Post-natal anaemia and iron deficiency in HIV-infected women and the health and survival of their children

Prenatal iron supplementation may improve pregnancy outcomes and decrease the risk of child mortality. However, little is known about the importance of post-natal maternal iron status for child health and survival, particularly in the context of HIV infection. We examined the association of maternal anaemia and hypochromic microcytosis, an erythrocyte morphology consistent with iron deficiency, with child health and survival in the first two to five years of life. Repeated measures of maternal anaemia and hypochromic microcytosis from 840 HIV-positive women enrolled in a clinical trial of vitamin supplementation were prospectively related to child mortality, HIV infection and CD4 T-cell count. Median duration of follow-up for the endpoints of child mortality, HIV infection and CD4 cell count was 58, 17 and 23 months, respectively. Maternal anaemia and hypochromic microcytosis were associated with greater risk of child mortality [hazard ratio (HR) for severe anaemia = 2.58, 95% confidence interval (CI): 1.66-4.01, P trend < 0.0001; HR for severe hypochromic microcytosis = 2.36, 95% CI: 1.27-4.38, P trend = 0.001]. Maternal anaemia was not significantly associated with greater risk of child HIV infection (HR for severe anaemia = 1.46, 95% CI: 0.91, 2.33, P trend = 0.08) but predicted lower CD4 T-cell counts among HIV-uninfected children (difference in CD4 T-cell count/μL for severe anaemia: -93, 95% CI: -204-17, P trend = 0.02). The potential child health risks associated with maternal anaemia and iron deficiency may not be limited to the prenatal period. Efforts to reduce maternal anaemia and iron deficiency during pregnancy may need to be expanded to include the post-partum period.