Short-term developmental outcome of iron prophylaxis in infants

BACKGROUND: Previous studies on the cognitive effects of iron treatment have focused on anemic or non-anemic iron-deficient infants. The effect of iron supplementation on cognitive development among iron-sufficient infants has not been studied. The aim of the present study was to examine the effect of iron supplementation on performance in the Bayley Scales of Infant Development (BSID) and anthropometric measurement in 6-month-old iron-sufficient healthy infants. METHODS: Healthy, iron-sufficient infants who were 6 months of age and were attending the Well Baby Clinic were considered for enrollment. Infants were randomly assigned to take ferrous sulfate supplementation (1 mg/kg per day) or no supplementation and were followed for 3 months. Anthropometric measurement, hematologic status and BSID were evaluated on admission and after 3 months. RESULTS: Seven infants in the intervention group and nine in the control group completed the study. No significant differences were observed in anthropometric measurements and complete blood counts between the two groups after the 3 month study period. The mean transferrin saturation (TS) level decreased significantly in the control group during the study period (from 15.3+/-2.6 to 7.8+/-5.1%; P = 0.0117), but no such reduction was seen in the intervention group. At the end of the study, the TS of the control group was found to be significantly lower than that of the intervention group (7.8+/-5.1 vs. 19.9+/-7.9%, respectively; P = 0.0033). The BSID scores of infants in both groups were within the normal range on admission and at the end of the study period. CONCLUSIONS: Short-term iron supplementation did not change developmental test scores despite the hematologic response in iron-sufficient healthy infants. The high prevelance of iron-deficiency anemia and its relationship with adverse developmental outcome suggests that prevention of iron-deficiency anemia with prophylaxis needs to be emphasized, rather than treatment.     

Oral iron supplementation in preterm infants treated with erythropoietin

BACKGROUND: It is not known whether a moderate dose of oral iron supplementation would further enhance erythropoiesis in recombinant human erythropoietin (EPO)-treated very low-birthweight (VLBW) infants. METHODS: In total, 24 preterm infants with birthweights 750-1499 g were enrolled at the age of 14-28 days to receive 400 IU/kg per week EPO subcutaneously for 8 weeks. The infants were randomly allocated either to receive oral iron supplementation 4 mg/kg per day or to serve as controls. RESULTS: Hemoglobin and the absolute reticulocyte count in the iron supplementation and the control groups remained identical throughout the study period, whereas serum ferritin was significantly lower in the control group at study exit and follow up. Rates of treatment success (no need for transfusion and hemoglobin never below 8 g/dL) also did not differ between the groups. CONCLUSIONS: In this study we did not find a clear advantage in a moderate dose of oral iron supplementation on erythropoiesis in EPO-treated VLBW infants. Whether a higher dose would lead to enhanced erythropoiesis remains to be answered.     

Developmental screening and detection of developmental delays in infants and toddlers with fragile X syndrome

Three developmental screening tests (the Denver-II, Battelle Developmental Inventory Screening Test, and Early Language Milestone Scale-2) were administered to 18 infants and toddlers (13 boys and 5 girls) with confirmed diagnoses of fragile X syndrome as part of a comprehensive developmental assessment at 9, 12, and 18 months of age. The Denver-II identified delays for 10 of 11 boys at 9 months of age and the Denver-II and the Early Language Milestone Scale-2 identified delays in 100% of the boys at 12 and 18 months. The Battelle Developmental Inventory Screening Test identified delays in 75% of the children at 12 and 18 months. When compared with more comprehensive developmental tests (Mullen Scales of Early Learning and Receptive-Expressive Emergent Language Scale-2), the screening tests concurred at least 76% of the time at the 12- and 18-month assessments. These results indicate that developmental delays could be detected in most children with fragile X syndrome through routine developmental screening by the age of 9 to 12 months.     

Predicting IQ change in preschoolers with developmental delays.

This study examined IQ change over a 2-year period in 291 young children (mean age 39 months) referred to a pediatric developmental clinic for evaluation of developmental problems. Although correlation between initial and follow-up IQ was very high (0.78), there was also a significant increase in mean IQ score, from 67.12 to 74.06. Moreover, 26% of the subjects showed IQ increase of 16 points or more. Variables making some contribution to IQ change were initial clinical diagnosis, etiology, and intervention. Children diagnosed with a developmental language disorder made significantly greater gains than those diagnosed as mentally retarded. Sex, family status, initial age, and test interval were not significantly correlated with IQ change. We concluded that prediction for individual children is difficult, but that initial diagnosis may be useful in differentially predicting IQ change in young children with developmental delays.     

Reversal of iron deficiency anemia-induced peripheral neuropathy by iron treatment in children with iron deficiency anemia

The effects of iron deficiency anemia (IDA) on nerve conduction and efficiency of iron therapy were investigated by peripheral nerve-electrophysiological measurements. Eighteen children (10 boys, eight girls; mean age 31 +/- 1.3 months) with IDA and 12 healthy children (six boys, six girls; mean age 29 +/- 1.3 months) were enrolled into the study. Nerve conduction velocity was measured in the median and posterior tibial nerve. After nerve conduction values were determined in the patients and controls, 6 mg/kg/24 h ferrous sulphate was given orally to the patients for 3 months and nerve conduction velocity tests were performed again. Median/motor and sensory nerve conduction velocity and tibial/motor nerve distal-amplitute values of children with IDA were lower than for the control group (p < 0.05, p < 0.01 and p < 0.001 respectively). With iron supplementation these values increased to the normal levels and even higher than control levels for some parameters. In correlation studies between whole blood parameters and nerve conduction velocity results, there was a correlation between median/sensory nerve conduction velocity values and serum iron levels. Additionally there was a correlation between some nerve conduction velocity values and age. In conclusion, the evidence from this preliminary study suggests that peripheral neuropathy may develop in children with IDA. Peripheral neuropathy symptoms in these patients may be improved by iron therapy.     

The effects of short-term oral iron therapy on developmental deficits in iron-deficient anemic infants

To assess the effects of iron therapy on developmental test scores in infants with iron deficiency anemia, 68 Guatemalan babies 6 to 24 months of age, with and without mild iron deficiency anemia, were tested with the Bayley Scales of Infant Development before and after one week of oral iron treatment. The two major findings of the study were developmental deficits in the anemic group prior to treatment, and lack of rapid improvement with short-term oral iron therapy. The mean pretreatment Mental Development Index of the anemic group was significantly lower than that of nonanemic infants. The anemic group's pretreatment Psychomotor Development Index was also lower than that of the nonanemic control group. In a double-blind randomized study, six to eight days of oral iron therapy did not reverse these deficits. Consequently, the deficits of the anemic group cannot be unequivocably attributed to iron lack. However, no significant differences were found between anemic and nonanemic groups in birth histories, socioeconomic level, or general nutritional status which might otherwise explain the lower developmental test scores of the anemic babies.     

Serial developmental assessments in infants with deformational plagiocephaly

Aim: An association between positional plagiocephaly and developmental problems has previously been noted, but whether delays persist over time has not been established. This study aimed to determine developmental outcomes for children with deformational plagiocephaly over 1 year of follow up. Methods: This was a longitudinal cohort study of 126 infants with deformational plagiocephaly recruited at an outpatient clinic. Development was assessed with the parent‐completed Ages and Stages Questionnaires at recruitment and repeated at follow‐up assessments in the home 3, 6 and 12 months later. Questionnaires were scored according to cut‐off scores from the Ages and Stages Questionnaires, Third Edition. Results: Ninety‐six percent of children were followed up for the full 12 months. The existence of one or more delays initially was 30%; this rose to 42% at the 3‐month follow up then dropped back to 23% by the 12‐month follow up. Delays were predominantly in the gross motor domain. Ten percent had >4 delays in total over the four assessments. Mothers with tertiary education were more likely to have infants showing delays that persisted over time. Conclusions: Infants with deformational plagiocephaly exhibited marked delays especially in early infancy. These delays were largely gross motor in type but had reduced to approach the expected level by the time of the 12‐month follow up, at a mean age of 17 months.     

Hyperglycinuria and hyperglycinemia in two siblings with mild developmental delays.

Two preschool-age siblings with similar histories of encephalopathy were examined for developmental retardation and found to have elevated levels of urinary and blood glycine. Their inability to convert glycine into serine in the absence of elevated blood and urinary ketone levels was suggestive of a defect in the glycine-cleavage enzyme system (or serine hydroxymethyl transferase). These patients differ significantly from the majority of reported cases of nonketotic hyperglycinemia in that they did not manifest life-threatening neonatal illness, severe mental retardation, or neurological deficits. However, during an oral glycine load, alterations in the electroencephalographic pattern occurred that suggested a relationship between elevated blood glycine levels and pathological involvement of the central nervous system. The ratio of CSF-blood glycine was found to be in the range expected for nonketotic hyperglycinemia.     

A randomized trial of two levels of iron supplementation and developmental outcome in low birth weight infants

OBJECTIVES: To investigate the effect of increased iron intakes on hematologic status and cognition in low birth weight infants. STUDY DESIGN: We randomly assigned 58 infants to receive formula with 13.4 mg iron/L (normal iron) or 20.7 mg iron/L (high iron). At baseline, discharge, and at 3, 6, 9, and 12 months' corrected age, we assessed anthropometry; infections; red blood cell hemoglobin, catalase, glutathione peroxidase, red blood cell fragility (hydrogen peroxide test), and superoxide dismutase values; plasma malondialdehyde, ferritin, iron, transferrin, zinc and copper levels; and diet intake. Griffiths' Development Assessment was done at 3, 6, 9, and 12 months only. RESULTS: No statistical differences (P <.05) were noted for weight, catalase or malondialdehyde levels, red blood cell fragility, or Griffith's Development Assessment. Iron intakes were greater in the high iron group except at 12 months. Hemoglobin (high iron, 123 +/- 9; normal iron, 118 +/- 8) was not different at 3 months (P =.07). Plasma zinc levels (high iron, 70 +/- 14; normal iron, 89 +/- 27) and copper levels (high iron, 115 +/- 26; normal iron, 132 +/- 27; P =.06) at 12 months suggested inhibition of absorption by high iron formula. Glutathione peroxidase levels were higher in the high iron group. The total number of respiratory tract infections was greater in the high iron group (3.3 +/- 0.9) than in the normal iron group (2.5 +/- 0.9). CONCLUSION: In terms of cognitive outcome, there is no advantage associated with elevated iron intake for low birth weight infants.     

III health and developmental delays in Adelaide four-year-old children

Standardized medical, visual, audiometric screening and two developmental tests were carried out on 982 four-year-old children. The aims of the study were to determine the prevalence of functionally important health problems, to compare a comprehensive developmental screening test with a simpler one, to assess observer bias in visual screening, and to measure effects of socio-economic status on health and development. Eighteen per cent had minor problems commonly related to development, nutrition, vision and hearing, requiring counselling and / or observation, 16% had new problems requiring assessment and/or treatment, and 0.9% had a severe handicap. Twenty-five per cent had multiple problems of varying severity. The commonest problems of moderate severity were visual 5.4%, secretory otitis media 6.6%, hearing toss 6.1%, wheezing bronchitis 3%, obesity 5.3%, male urogenital delects 4%, minor heart disease 1.1%, and 4.9% had generalized developmental delay confirmd by psychological assessment (I.Q. 50–90). The shorter test failed to detect delay in many of these. Developmental language disorders were confirmed in 4.6% of the total. Many of the 4.2% with behavioural problems, which were significantly more common in one parent families, also showed developmental delays Orthoptists were more accurate at vision screening than nurses. The increased prevalence of developmental delays and benaviour problems in lower socio-economic groups is significant but, with the exception of obesity, the variations in physical problems are not.     

Clinical genetic evaluation of the child with mental retardation or developmental delays

This clinical report describes the clinical genetic evaluation of the child with developmental delays or mental retardation. The purpose of this report is to describe the optimal clinical genetics diagnostic evaluation to assist pediatricians in providing a medical home for children with developmental delays or mental retardation and their families. The literature supports the benefit of expert clinical judgment by a consulting clinical geneticist in the diagnostic evaluation. However, it is recognized that local factors may preclude this particular option. No single approach to the diagnostic process is supported by the literature. This report addresses the diagnostic importance of clinical history, 3-generation family history, dysmorphologic examination, neurologic examination, chromosome analysis (> or =650 bands), fragile X molecular genetic testing, fluorescence in situ hybridization studies for subtelomere chromosome rearrangements, molecular genetic testing for typical and atypical presentations of known syndromes, computed tomography and/or magnetic resonance brain imaging, and targeted studies for metabolic disorders.