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Systolic and diastolic blood pressures were evaluated in a cohort of 61 non-hypertensive premature [very low birth weight (VLBW), n = 16; low birth weight (LBW), n = 22] and full-term [normal birth weight (NBW), n = 23] newborn infants admitted to a neonatal intensive care unit (NICU) and followed to their 4-month age-adjusted outpatient examination. All were receiving routine postnatal care by 7 days of age. Blood pressure was measured at 7 days of age, at discharge from the NICU, and at the outpatient examination. Simple linear regression of blood pressure on weight was used to fit a straight line to the three measurements for each infant and the average regression line for each birth weight group was then obtained. There was a significant correlation between systolic blood pressure and both weight and length at each of the measurement points and also between the change in systolic blood pressure and change in weight from the discharge to the 4-month examination. Diastolic blood pressure tended to follow this same pattern. Gestational age was correlated significantly with the 7-day blood pressure, but postnatal age at the outpatient examination was not correlated with either systolic or diastolic blood pressure. The average slopes of systolic and diastolic blood pressure on weight (mmHg/kg body weight) were virtually identical for the LBW and NBW groups; in contrast, the average slope of the VLBW group was greater than the other two groups, and the difference was statistically significant for diastolic blood pressure. These results show significant group differences in mean blood pressure prior to 4 months of age between VLBW, LBW, and NBW groups and, for the VLBW infants, a steeper slope of the estimated regression line of blood pressure on weight between birth and 4 months.

Erythropoietin, the primary stimulator of erythropoiesis, represents an important potential therapy for the anemia of prematurity. Enhancement of the therapeutic benefit of recombinant human erythropoietin (rhEp) in very-low-birth-weight infants will require a better understanding of rhEp's pharmacodynamic effects including its interaction with iron in stimulating erythropoiesis. The purpose of this study was to determine the effects of chronic rhEp administration on plasma iron levels and hematopoiesis using a twin lamb model. Nine pairs of twin lambs in which one twin was randomized to receive rhEp, and the other saline, were studied during a 1-week baseline and a subsequent 4- to 5-week treatment period. The effects of therapy on plasma iron levels and erythropoiesis were measured by integrating the areas under the concentration-time curves (AUC) of the study variables. During the rhEp treatment period, significantly greater negative daily AUCs were observed in the rhEp-treated lambs for plasma iron concentration (p = 0.0008), while significantly greater positive daily AUCs were observed for hemoglobin concentration (p = 0.04) and reticulocyte count (p = 0.02). In the rhEp-treated group, pretreatment iron concentrations were directly associated with the magnitude of the iron response during treatment such that the greater the pretreatment iron, the greater the daily AUC below the plasma iron concentration-time plot (r = -0.66, p = 0.05). For the placebo-treated group, this association tended toward, but did not achieve, statistical significance (r = -0.52, p = n.s.). These observations suggest that treatment of rapidly growing newborn lambs with rhEp results in increased iron utilization due to increased erythropoiesis and depends on iron status at the initiation of rhEp treatment. Use of the term neonatal lamb model offers advantages over studies in human infants for more detailed or invasive examinations of the interaction of iron and rhEp treatment.

Abnormal fetal growth patterns are associated with higher rates of neonatal morbidity. Measurement of anthropometric parameters immediately after birth, prior to the onset of potential neonatal symptoms, allows the physician to make an assessment as to which infants are at high risk. In general, a two-tiered approach will allow the physician to make the distinction between high- and low-risk infants. First, the standard one-factor anthropometrics--weight, length, and occipitofrontal head circumference--are plotted on curves that are appropriate for the population. In the vast majority of cases, these measurements give enough information regarding neonatal risk. When the standard measurements conflict with the clinical history or are disproportionate, the use of specialty one-factor anthropometrics, and especially two-factor body proportion assessments represent the second tier of assessment that can give greater insights into the etiology of abnormal fetal growth and can further define the groups at risk for neonatal sequelae.

Neonatal liver (storage) but not heart (nonstorage) tissue iron concentrations were reduced by 60% at autopsy in 15 newborn infants who had gestations complicated by uteroplacental insufficiency because of maternal hypertension or Potter syndrome. The hepatic iron reductions in term and preterm infants, and with either antecedent condition, were similar.

In summary, careful attention to nutrient delivery in the IUGR infant is important to prevent and treat neonatal metabolic derangements and to improve postnatal growth. Carbohydrates are the essential fuel in the first days of life, to prevent hypoglycemia. Subsequent delivery of protein and fat helps rectify reduced muscle and fat stores and promotes weight gain. Calcium supplementation to prevent further bone demineralization and iron supplementation to replete iron stores may be necessary. Of special interest is that the neurologic outcome of these infants appears linked to the rate of catch-up growth. The rate of postnatal head growth depends on many perinatal and neonatal risk factors, and is a strong predictor of early developmental outcome in low-birthweight infants. Insufficient energy delivery beyond 2 weeks postnatal age in SGA premature infants results in failure to initiate subsequent catch-up head growth, with consequently smaller head circumferences at 1-year follow-up.

The use of dietary fat in preference to carbohydrate offers the theoretic advantage of diminishing carbon dioxide production and thus the respiratory quotient, which may be beneficial for babies with chronic lung disease. Ten premature infants (birth weight (mean +/- SEM), 1.13 +/- 0.12 kg; postnatal age, 9 +/- 1 weeks) with bronchopulmonary dysplasia were alternately fed a high-fat and a high-carbohydrate formula each for 1 week, in randomized order. Lower rates of carbon dioxide production (6.6 +/- 0.3 versus 7.4 +/- 0.4 ml/kg per minute; p < 0.05), and consequently lower respiratory quotients (0.80 +/- 0.02 versus 0.94 +/- 0.01 ml/kg per minute; p < 0.005), were observed during the administration of the high-fat formula. There were no significant differences in results of pulmonary function tests with the use of either formula. Both formulas were equally well tolerated and able to promote adequate growth and normal biochemical profiles. However, weight gain was significantly greater with the administration of the high-carbohydrate formula, possibly because of an increase in the accretion of body fat. We conclude that the short-term use of high-fat formula for infants with bronchopulmonary dysplasia decreases carbon dioxide production while maintaining adequate growth and nutritional status.

In older children and adults, physiologic instability associated with severe illness causes increased cellular oxygen consumption (VO2), increased serum lactate and cortisol levels, and more negative nitrogen balance. To determine the metabolic response of preterm infants to severity of respiratory illness, we analyzed VO2, nitrogen balance, urinary 3-methyl-histidine and norepinephrine concentrations, and serum levels of lactate and cortisol as a function of ventilatory index (VI). Twelve 2-day-old premature infants who were appropriate in size for gestational age (mean +/- SEM birth weight: 1460 +/- 251 gm) and who required mechanical ventilation for respiratory distress syndrome had VO2 and carbon dioxide production measured by indirect calorimetry and blood and urine samples obtained concurrently. All infants received amino acids, 1.0 gm/kg per day, and a mean energy intake of 27 +/- 3 kcal/kg per day, provided as a parenteral dextrose solution. The resting energy expenditure exceeded energy intake in all infants. The VO2 value ranged from 5.5 to 9.2 ml/kg per minute and was directly correlated with VI (r = 0.79; p = 0.002). Nitrogen balance ranged from -160 to 53 mg/kg per day (mean: -33 +/- 21 mg/kg per day) but was not dependent on VI (r = 0.04) or VO2 (r = 0.01). The serum lactate level correlated directly with VI (r = 0.82; p = 0.002) and VO2 (r = 0.60; p = 0.05), but cortisol and urinary norepinephrine levels did not. We conclude that preterm infants with respiratory distress syndrome have increased VO2 rates and serum lactate concentrations directly related to the degree of respiratory illness. They are generally in a state of mildly negative nitrogen balance, the degree of which is not related to severity of illness. Although these infants may require increased energy delivery during illness, they do not appear to require excessive amounts of amino acids.

At present, nearly all infants with birth weights of < 1 kg receive blood transfusions for treatment of clinical signs of tissue hypoxia resulting from anemia of prematurity. In contrast to the successful use of recombinant human erythropoietin (rhEp) in adults, treatment of anemic neonates with rhEp to stimulate red cell production and reduce the need for transfusions that pose serious infectious and immunologic risk has not been effective. The present study investigates the pharmacodynamics (PD) of endogenous erythropoietin (Ep) in sheep fetuses to determine possible causes for the poor rhEp response in early development. The dynamic relationship between plasma Ep and plasma iron resulting from spontaneous hypoxemic episodes is investigated by PD system analysis. The erythropoietic effect of Ep is measured in terms of the mobilization of plasma iron needed in the production on new erythrocytes. A hysteresis minimization approach is employed to determine the intrinsic PD dose-response relationship (transduction) of Ep. The dose-response relationship shows a well-defined threshold level that has to be exceeded before Ep begins to show a significant effect on plasma iron. It is postulated that the threshold mechanism may serve a useful purpose during early development by reducing the risk of the fetus developing a pathological degree of polycythemia and hyperviscosity in the relatively hypoxemic fetal environment. At the same time, the threshold serves the purpose of providing a needed response to more severe pathologic hypoxemic episodes. The occurrence of anemia during subsequent postnatal life when PaO2 levels increase markedly may be the inevitable, but unfortunate corollary of a continuation of this mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Myoglobin, a hemoprotein found in abundance in the muscle of postnatal animals, increases in concentration in response to hypoxia, thereby protecting tissue from damage. Fetuses exposed to intrauterine hypoxemia are also susceptible to organ damage, but the response of fetal muscle myoglobin to hypoxemia is unknown. To study whether fetal muscle myoglobin concentrations are elevated following intrauterine hypoxemia, we exposed eight chronically catheterized late gestation sheep to a wide range of fetal oxygen levels over 15 to 30 days and correlated the level of fetal oxygenation with heart and skeletal muscle myoglobin concentrations measured at sacrifice. A lower level of fetal oxygenation, expressed as the integrated area under the arterial saturation (SaO2)-time curve, was associated with greater myocardial myoglobin concentration (r = 0.90; P < 0.01). This relationship was not observed for skeletal muscle (r = 0.43; P = ns). A lower level of fetal oxygenation was associated with lower myoglobin:iron (w/w) ratio in skeletal muscle (r = 0.71; P < 0.03), implying less incorporation of iron into myoglobin. A similar relationship was not apparent for cardiac tissue. The higher myocardial myoglobin concentrations found in the more hypoxic fetuses were consistent with previous observations in postnatal animals. This likely represents an intracellular compensatory mechanism for sustaining short-term mitochondrial oxygen delivery in a critical organ with a high rate of oxygen consumption. The lack of myoglobin responsiveness to hypoxia in fetal skeletal muscle may be due to its much lower oxygen consumption rate and activity level.

Objective: To determine the medical condition of Romanian adoptees and the effects of the Romanian orphanage system on their health., Design: Case series., Setting: The international adoption clinics at the University of Minnesota, Minneapolis, and the New England Medical Center, Tufts University, Boston, Mass., Participants: Sixty-five Romanian adoptees who were brought to the United States during a 12-month period beginning in October 1990., Main Outcome Measures: Incidence of hepatitis B, intestinal parasites, tuberculosis, syphilis, human immunodeficiency virus type 1, growth failure, and developmental delay., Results: Although the adopted children were presumably chosen from the most vital and attractive adoptees, only 15% were judged to be physically healthy and developmentally normal. Fifty-three percent had serological evidence of past or present hepatitis B infection, and 20% of screened children tested positive for hepatitis B surface antigen. In children aged 7 months or older, the overall prevalence of chronic hepatitis B was 23%. Intestinal parasites were found in 33% of subjects, and 45% of infected children had two or more pathogens identified. All the children tested for human immunodeficiency virus type 1 were negative. Two patterns of growth failure were observed that resembled the two subtypes of psychosocial short stature that occur in association with prolonged psychological harassment or emotional deprivation. Infants' length, weight, head circumference, and weight-for-height were adversely affected by institutionalization. Older children's height was reduced. Only 10% of children older than 12 months were developmentally normal., Conclusion: Romanian adoptees are an extraordinarily high-risk pediatric group as a consequences of decades of government-sanctioned child neglect and abuse.

Transient hyperammonemia of the newborn is an overwhelming disease manifested by hyperammonemic coma in ill premature infants. A summary of evidence is presented supporting the hypothesis that this syndrome is a vascular complication caused by shunting of blood away from the portal circulation of the liver into the systemic circulation with subsequent lack of ammonia removal. Alternative, nontraditional approaches of investigation and therapy targeting the hepatic portal circulation should be explored in patients with transient hyperammonemia of the newborn.

Infants of diabetic mothers frequently have polycythemia, elevated serum erythropoietin concentrations, and decreased serum iron and ferritin concentrations, likely representing a redistribution of fetal iron into erythrocytes to support augmented fetal hemoglobin synthesis. We hypothesized that fetal liver, heart, and brain iron concentrations are also reduced in these infants. After obtaining autopsy tissue from infants who had died before 7 days of age, we measured liver, heart, and brain iron concentrations using atomic absorption spectrophotometry. Seven infants of diabetic mothers and seven gestational age-matched control infants were studied. All infants of diabetic mothers had pancreatic islet cell hyperplasia, indicating fetal hyperglycemia and hyperinsulinemia. Liver iron concentrations in the infants of diabetic mothers were 6.6% of control values (489.0 +/- 154.4 vs 7379.7 +/- 1473.8 micrograms/gm dry tissue weight (mean +/- SEM); p less than 0.001), heart iron concentrations were 43.9% of control values (124.7 +/- 20.5 vs 284.1 +/- 34.8 micrograms/gm dry tissue weight; p less than 0.002), and brain iron concentrations were 60.6% of control values (106.1 +/- 13.7 vs 175.2 +/- 10.7 micrograms/gm dry tissue weight; p less than 0.003). Heart and brain iron concentrations were directly correlated with liver iron concentrations (r = 0.80 for both; p less than 0.001) and indicated that hepatic iron was greater than 75% depleted before heart and brain iron reduction. We conclude that severely affected infants of diabetic mothers have reduced liver, heart, and brain iron concentrations. The role of tissue iron deficiency in the genesis of the abnormal clinical findings in these infants deserves further consideration.

Newborn infants of diabetic mothers have serum biochemical signs of iron deficiency in cord blood directly related to elevations of cord erythropoietin and Hb concentrations. In sheep, chronic fetal hyperinsulinemia results in fetal hypoxemia, expansion of the red cell mass, and decreased iron concentrations, most likely due to increased iron utilization for Hb synthesis. To determine whether fetal insulin exposure also results in reduced tissue iron concentrations, we measured liver, skeletal muscle, small intestine, heart, and brain iron concentrations in newborn rat pups after s.c. fetal injection of insulin or diluent alone on d 19 of gestation. The fetuses of 11 pregnant rats were exteriorized, injected with 2 U neutral protamine Hagedorn insulin or diluent, replaced in utero, and delivered on d 22. To determine dose dependency, the fetuses of six pregnant rats were injected with 3 U of longer-acting protamine zinc insulin and delivered on d 21. At delivery, the insulin-treated groups had higher birth weights than the placebo-treated group, although plasma insulin concentrations were not different. The 2 U neutral protamine Hagedorn insulin-treated fetuses had significantly lower mean +/- SEM liver iron concentrations than the control fetuses (910 +/- 34 versus 1014 +/- 43 micrograms/g dry tissue weight; p less than 0.05), but had similar skeletal muscle iron concentrations. The 3 U protamine zinc insulin-treated fetuses had significantly lower liver and skeletal muscle iron concentrations compared to control and to 2 U neutral protamine Hagedorn insulin-treated fetuses (p less than 0.05). No differences in small intestine, heart, or brain iron concentrations were seen among groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Because chronic hypoxemia causes a redistribution of iron from serum and storage pools into an expanding erythrocyte mass, and because infants of diabetic mothers are often hypoxemic in utero and have a high prevalence of polycythemia at birth, we studied iron distribution in 43 term infants of diabetic mothers. Twenty-four infants were at an appropriate size for gestational age; 19 were large for gestational age. At birth, 28 infants (65%) had abnormal serum iron profiles; eight had decreased ferritin concentrations only (stage 1), nine had decreased ferritin and increased total iron-binding capacity values (stage 2), and 11 had these serum findings plus elevated free erythrocyte protoporphyrin concentrations (stage 3). The hypoglycemic infants who were large for gestational age (n = 14) had a higher prevalence of abnormal iron profiles than euglycemic infants who were appropriate in size for gestational age (n = 20; 93% vs 50%; p = 0.009). Progressively abnormal iron profiles were associated with higher glycosylated fetal hemoglobin values, greater degrees of macrosomia, increased hemoglobin and erythropoietin concentrations, and increased erythrocyte/storage iron ratios. Erythropoietin concentrations were inversely linearly correlated with serum iron values (n = 32, r = -0.54; p = 0.003). The combined erythrocyte and storage iron pools were significantly lower in infants with abnormal iron values whose mothers were diabetic, particularly in infants of women with confirmed diabetic vasculopathy. We speculate that these findings are likely due to (1) increased fetal iron utilization during compensatory hemoglobin synthesis in response to chronic hypoxemia and (2) reduced iron transfer during late gestation complicated by diabetes.

We studied catch-up growth, muscle and fat accretion, and body proportionality at 4 and 12 months of age corrected for prematurity in 30 very low birth weight (VLBW) (less than 1500 gm), 30 low birth weight (LBW) (1500 to 2499 gm) and 30 normal birth weight (greater than or equal to 2500 gm) infants who required newborn intensive care. At 4 and 12 months, the VLBW infants had significantly lower mean weight and length (p less than 0.01), but not lower occipitofrontal circumference percentiles, than the LBW and normal birth weight groups, and showed no catch-up weight or length growth between 4 and 12 months. All three groups had significant increases in mean upper mid-arm circumferences, mid-arm muscle circumferences, and arm muscle areas between 4 and 12 months. Mean mid-arm muscle circumferences and arm muscle areas were similar among the three groups at 4 months but became significantly stratified by birth weight groups by 12 months, with VLBW infants having the lowest mean value. In contrast, analysis of fat stores by triceps skin-fold thickness and arm fat area demonstrated no significant increases in any group between 4 and 12 months, except for arm fat area in the LBW group. The VLBW infants had significantly less fat than normal birth weight infants at 4 and 12 months. All three groups had proportional growth at both visits, as assessed by mid-arm circumference/head circumference ratio and weight-length percentile for age. The VLBW infants were significantly lighter for their length than normal birth weight infants. We conclude that VLBW infants have no first-year catch-up growth, remaining smaller than higher birth weight infants, although appropriately proportional. Somatic growth during the first year is due more to muscle than to fat accretion, especially in VLBW infants.

Thirty-four outborn premature infants of appropriate gestational ages with birth weights less than 1,750 g were seen in follow-up at 3, 6, 12, and 18 months, corrected age to assess the incidence of abnormalities of muscle tone and the relationship of the site of early abnormalities to 18-month developmental status. The incidence of abnormal tone was most common at 3 months and declined with increasing age. The percentages of infants with abnormal tone at 3, 6, 12, and 18 months, respectively, were: increased lower extremity tone--62%, 71%, 38%, 9%; decreased lower extremity tone--3%, 3%, 6%, 9%; increased truncal tone--41%, 15%, 6%, 0%; decreased truncal tone--21%, 18%, 15%, 6%. Infants with truncal hypertonicity at 3 months had significantly lower Bayley motor and mental scores at 18 months when compared with infants with normal truncal tone (P less than .05). However, infants with lower extremity hypertonicity at 3 months were no different developmentally at 18 months from infants with normal tone. Infants with truncal or lower extremity hypotonicity fared the worst developmentally (P less than .05). We conclude that there is a high incidence of abnormal muscle tone in premature infants up to 18 months of age and that early truncal tone abnormalities are associated with a worse developmental outcome.

Two hundred four neonates, 25 to 42 weeks estimated gestational age (EGA), were measured on day 2 or 3 of life for upper mid-arm circumference (MAC) and head circumference. Regression analysis was used to construct standard curves for MAC versus EGA and mid-arm circumference/head circumference ratio (MAC/HC) versus EGA. Correlation coefficients were 0.93 for MAC versus EGA, and 0.84 for MAC/HC versus EGA. MAC, MAC/HC, and head circumference were also highly correlated with birth weight. These measurements may more accurately assess intrauterine growth and body proportionality at birth than weight, length, and head circumference.

To document the incidence of and neonatal factors associated with abnormal shoulder girdle muscle tone in premature infants at follow-up, we studied 125 consecutively admitted infants weighing less than 1,750 g treated in The Children's Hospital of Philadelphia intensive care nursery and subsequently seen in the Neonatal Follow-up Program up to 18 months of age. Fifty-seven infants (46%) displayed abnormal shoulder girdle muscle tone which presented clinically as scapular retractions. These infants had significantly lower birth weights (P less than .001) and gestational age (P less than .001) as well as a higher incidence of acute and chronic pulmonary disease (P less than 0.01) and CNS insults (P less than .05) when compared with infants without scapular retractions. The 57 infants with scapular retractions were further divided into two groups: 42 infants (74%) in whom scapular retractions were associated with generalized mild hypertonicity and 15 infants (26%) in whom scapular retractions compensated for trunk and neck hypotonicity. The infants with scapular retractions and hypotonicity had a significantly higher incidence of neonatal neurologic morbidity including seizures, major resuscitations, and birth asphyxia (P less than .01) when compared with the infants with scapular retractions and hypertonicity. Shoulder girdle tone abnormalities in the first year of life inhibit crawling, sitting, and object manipulation and, therefore, may manifest as delays in motor development. Identification of infants with significant neonatal risk factors for tone abnormalities is important to allow for earlier therapeutic intervention.

We evaluated the routine use of dexamethasone for the prevention of postextubation respiratory distress by entering 60 ventilated infants into a prospective, randomized, blinded study. Thirty minutes before extubation, 30 infants were given a single dose of intravenous dexamethasone (0.25 mg/kg), and 30 infants received saline placebo. Infants were intubated orotracheally for at least 48 hours following a single intubation and were maintained on low ventilator settings (F10(2) less than 0.35, intermittent mandatory ventilation [IMV] less than 6, positive end-expiratory pressure [PEEP] less than 4) at least 12 hours before extubation. Following extubation, all infants weighing less than 1500 g were routinely placed on nasal continuous positive airway pressure (NCPAP). There was no difference between the two groups in postextubation Downes' score, serum pH, PCO2, or oxygen requirement at 30 minutes, 6 hours, and 24 hours. Respiratory acidosis occurred in one steroid-treated patient and in two placebo-treated infants. Stridor occurred in four infants in each group. No infant developed postextubation lobar atelectasis or required reintubation. We conclude that prophylactic administration of dexamethasone does not improve the immediate postextubation course of infants following a single intubation and that its routine use at the time of extubation is not indicated.

Pulmonary neuroendocrine cells (PNEC) are granulated epithelial cells distributed throughout conducting airways. Among the bioactive products identified within the secretory granules of these cells are potent mitogens and bronchoactive and vasoactive agents. The secretory status of these cells, which are in greatest number in the fetus and newborn, is modulated by neural reflexes and by changes in airway gas composition. The aggregate data suggest roles for PNEC in airway "chemoception" and/or regulation of airway epithelial differentiation. Marked increases in PNEC are observed in bronchopulmonary dysplasia, where airway and alveolar fibrosis, epithelial metaplasia, and airway and vascular smooth muscle hypertrophy contribute to marked pathophysiologic changes in lung function. Considering the biologic effects of PNEC secretory products, particularly gastrin-releasing peptide on airway epithelial cell and fibroblast proliferation, we propose that an increase in PNEC secretory products in the regenerating airway epithelium may contribute to the development of the pathologic alterations in lung structure seen in bronchopulmonary dysplasia. In this proposed scheme, secretion of abnormally large amounts of bronchoactive and vasoactive agents from PNEC (e.g., serotonin, gastrin-releasing peptide) in response to airway hypoxia and hypercapnia may be partially responsible in the genesis of reactive airway disease and pulmonary hypertension seen in this disease.

We assessed the relationship between neonatal hypoglycemia and newborn iron status in 15 hypoglycemic, large-for-date newborn infants, 12 of whom were infants of diabetic mothers. These infants had significantly lower mean serum iron concentrations, ferritin concentrations, percent iron-binding saturation and calculated iron stores, and significantly higher mean transferrin concentrations, total iron-binding capacity concentrations and mid-arm circumference:head circumference ratios when compared with either 15 euglycemic large-for-date or 15 euglycemic appropriate-for-date control infants (p less than 0.001 for all comparisons). All hypoglycemic infants had ferritin concentrations below the 5th percentile as compared to 3% of controls (p less than 0.001), and 67% had transferrin concentrations above the 95th percentile (controls: 0%; p less than 0.001). Only the hypoglycemic infants demonstrated a significant negative linear correlation between ferritin and transferrin concentrations (r = -0.83; p less than 0.001). Decreased serum iron concentrations were associated with size at birth (r = -0.60; p = 0.01) and with increased red cell iron (r = -0.60; p = 0.01), implying a redistribution of iron dependent on the degree of fetal hyperglycemia and hyperinsulinemia. Infants with increased red cell iron had more profound neonatal hypoglycemia. These results show a significant association between decreased iron stores and neonatal hypoglycemia in macrosomic newborn infants associated with a significant shift of iron into red blood cells.

We compared the in-hospital and postdischarge growth of 47 preterm very-low-birth-weight infants born in 1982 with that of 29 born in 1986. Infants in the two groups were of comparable gestational age, size, and illness at birth. During hospitalization, the 1986 infants began parenteral and enteral nutrition earlier, had fewer days when they received less than 252 kJ/kg, were treated earlier for patent ductus arteriosus (6.1 +/- 4.5 days vs 14.5 +/- 7.7 days), and had a lower prevalence of severe medical complications. By hospital discharge, these infants had significantly higher mean growth percentiles and fewer of them had weights and occipitofrontal circumferences below the fifth percentile. Follow-up at 4 and 12 months corrected age showed that these infants continued to have significantly higher growth percentiles, and fewer of them had weights below the fifth percentile (49% vs 24%) or major neurologic abnormalities. Infants whose weights were below the fifth percentile had significantly poorer 12-month developmental outcomes. We speculate that more aggressive early neonatal nutritional management, changes in cardiopulmonary management, and lower incidences of chronic disease promote earlier onset of and more rapid rates of postnatal growth, which extend through the first year of follow-up.

We assessed cord prealbumin concentrations in 214 appropriate for gestational age newborn infants, 21 small for gestational age infants, and 27 large for gestational age infants to establish normal values and to assess the effect of intrauterine growth, prenatal steroids, and pulmonary maturity on prealbumin levels. Cord prealbumin values were significantly correlated with increasing gestational age (r = 0.33; P less than 0.001) and birth weight (r = 0.40, P less than 0.001) in the AGA neonates. Neonates born before 37 weeks gestation had significantly lower prealbumin levels than those born at term (P less than 0.001). The SGA infants had significantly lower levels than age-matched AGA controls (P less than 0.01), and LGA infants had significantly higher levels than age-matched AGA controls (P less than 0.001). In preterm infants, those with exposure to prenatal steroids (betamethasone or premature rupture of membranes) had significantly higher prealbumin values than control infants of comparable age and weight (P less than 0.001). Infants without respiratory distress syndrome had higher levels than those of comparable age and weight with hyaline membrane disease (P less than 0.05). This study demonstrates that a correlation of gestational age and birth weight exists with cord prealbumin levels, and that the large variability at each gestational age may be accounted for in part by appropriateness of size for dates, prenatal steroid exposure, and pulmonary maturity.

We measured cord transferrin and ferritin levels in 50 newborn infants with fetal conditions associated with either uteroplacental vascular insufficiency or chronic hypoxia. Sixteen small for gestational age infants, 21 infants of mothers with preeclampsia, and 13 symptomatic infants of diabetic mothers had significantly higher transferrin levels and lower ferritin levels and calculated iron stores than did asymptomatic gestational age-matched control infants without these conditions. Cord ferritin levels and calculated iron stores were significantly lower in the infants of diabetic mothers than in any other group of infants. Cord transferrin levels were inversely correlated with ferritin levels (r = -0.59, P less than 0.001) and were unrelated to transthyretin levels and birth weight in the high-risk infants, but were positively correlated with ferritin levels (r = 0.50, P less than 0.001), transthyretin levels (r = 0.65, P less than 0.001), and birth weight (r = 0.75, P less than 0.001) in the control infants. We conclude that cord transferrin levels do not reflect protein-energy status in newborn infants with prenatal histories suggesting uteroplacental insufficiency or chronic hypoxia, and that when associated with decreased cord ferritin levels, indicate possible impaired iron stores in these infants.

Application of nutritional assessment techniques during the neonatal period provides the clinician with a strategy for evaluating the adequacy of macronutrient intake. To this end, the MAC:HC ratio and ponderal index appear to be more sensitive than birth weight in identifying newborns at risk for morbidity from fetal growth aberrations. In longitudinal assessment of postnatal growth the clinician is faced with several choices of anthropometric and/or biochemical techniques, either singly or in combination, to identify specific problems concerning protein energy nutritional status. Measurements of weight, length, and head and mid arm circumferences may be used both as static and dynamic assessments, but are more valid indicators when considered in relation to each other. Short-term biochemical markers, such as prealbumin, are more useful than albumin in assessing the effect of recent changes in protein intake. At the present time other biochemical tests are not helpful in the daily management of protein energy nutrition in infancy.

The effects of neonatal illness and caloric intake on head growth velocity and on 1-year developmental outcome were studied in 73 appropriate (AGA) and small for gestational age (SGA) premature infants of (mean +/- SD) 30 +/- 2 weeks gestation who received intensive care during the neonatal period. Head growth from birth to 1 year of corrected age was characterized by a triphasic curve initiated by a period of growth arrest or suboptimal growth followed by a period of catch-up growth and terminated by a period of growth along standard curves. Head growth arrest or suboptimal head growth were directly related to the duration of the initial period of caloric deprivation (less than 85 kcal/kg/day) and to the duration of mechanical ventilation. Catch-up head growth was influenced by the duration of the preceding period of caloric deprivation in all infants and by the caloric intake during that phase only in SGA infants; catch-up growth was unrelated to the duration of mechanical ventilation. Head growth along standard curves occurred in all infants by 3 months of corrected age and persisted up to 1 year of corrected age. Infants calorically deprived the longest (AGA 4 to 6 weeks, SGA 2 to 3 weeks) had head growth along standards at curves below -1 SD on the growth chart; all other groups had this phase of head growth at curves between the mean and -1 SD. Infants calorically deprived for more than 4 weeks had developmental scores below normal ranges by 1 year of corrected age.

Newborn infants of poorly controlled insulin-dependent diabetic mothers demonstrate a redistribution of iron from serum and tissue stores into red blood cells. These changes may be due to increases in iron utilization during augmented Hb synthesis, which compensates for chronic intrauterine hypoxemia induced by prolonged fetal hyperinsulinemia. We tested this hypothesis by measuring plasma iron, total iron-binding capacity, percent iron-binding capacity saturation (total iron-binding capacity saturation), Hb concentration, total red cell Hb, and total red cell iron in the arterial blood of 11 chronically instrumented fetal sheep after 7-12 d of infusion with 15 U/day of insulin (n = 5) or placebo (n = 6). The insulin-infused fetal sheep had higher mean +/- SD plasma insulin concentrations (448 +/- 507 versus 11 +/- 8 mU/L; p less than 0.001) and lower arterial oxygen saturations (38 +/- 7 versus 54 +/- 9%; p less than 0.02). The insulin-infused group had a lower mean plasma iron concentration (20.8 +/- 10.9 versus 42.1 +/- 14.7 microM/L; p less than 0.02) and total iron-binding capacity saturation (36 +/- 20 versus 64 +/- 22%; p less than 0.02) and a higher total red cell Hb (45.4 +/- 8.7 versus 32.6 +/- 8.8 g; p less than 0.02) and total red cell iron content (154 +/- 29 versus 111 +/- 29 mg; p less than 0.02) when compared with the placebo group. Seven to 12 d of intrauterine hyperinsulinemia decreases serum iron and increases total red cell iron, most likely by stimulating increased Hb synthesis in response to low arterial oxygen saturation.(ABSTRACT TRUNCATED AT 250 WORDS)

Mid-arm circumference/head circumference ratios (MAC/HC) and birth weights obtained in 73 neonates were studied to compare which of these growth measurements could more accurately predict risk of metabolic complications resulting from either acceleration or retardation of fetal growth. The MAC/HC ratio was more sensitive than birth weight in distinguishing symptomatic large for gestational age (LGA) infants who were born to diabetic mothers from other LGA infants who were asymptomatic, and symptomatic from asymptomatic small for gestational age infants. In addition, the MAC/HC ratio identified symptomatic appropriate for gestational age (AGA) infants born to diabetic mothers and AGA infants with signs and symptoms of growth retardation. The MAC/HC is more useful than birth weight in assessing newborn infants at risk for the metabolic complications associated with fetal growth disorders.