Zinc supplementation in infants with asymmetric intra uterine growth retardation; effect on growth, nutritional status and leptin secretion / Suplementación con zinc en niños con retraso de crecimiento intra-uterino asimétrico; efecto en el crecimiento, estado nutricional y secreción de leptina

Objetivos: Valorar el efecto de la suplementación con cinc en el crecimiento y estado nutricional de un grupo homogéneo de recién nacidos con retraso de crecimiento intra-uterino asimétrico. También se analizó el efecto delos cambios en el status del cinc en el crecimiento y las concentraciones séricas de leptina. Población y método: Se diseñó un ensayo clínico randomizado y doble ciego, con el fin de detectar diferencias en el crecimiento entre los grupos recibiendo cinc o placebo, durante los seis primeros meses de vida. 31 niños fueron incluidos en el grupo cinc (n = 14) (38,8 ± 1,4 semanas edad gestacional, 2.171 ± 253 g peso) o grupo placebo (n = 17) (38,9 ± 1.1 semanas edad gestacional, 2.249 ± 220 g peso). El grupo cinc recibió un suplemento de 3 mg de cinc elemental por día (en forma de sulfato de cinc).Resultados: No hubo diferencias significativas entre ambos grupos en cuanto a las medidas antropométricas a lo largo del período de estudio. Se observó un efecto significativo del grupo de estudio, en las concentraciones de cinc en el pelo, pero no en las concentraciones séricas de cinc; las comparaciones post-hoc para el cinc del pelo pusieron de manifiesto que había diferencias significativas entre los grupos, en los meses 1, 2 y 6 de edad. Los cambios en las concentraciones de cinc en el suero y en el pelo, desde el inicio del estudio hasta los 6 meses, mostraron correlaciones estadísticamente significativas con los cambios en peso/edad y longitud/edad (puntuación típica), en el grupo que recibió el suplemento de cinc. Los cambios en las concentraciones séricas de leptina durante el seguimiento, mostraron correlaciones estadísticamente significativas para la suma de 4 pliegues y para peso/edad (puntuación típica), en el grupo placebo. Los cambios en las concentraciones de cinc en el pelo mostraron correlaciones estadísticamente significativas con los cambios en las concentraciones séricas de leptina, desde el inicio del estudio hasta los 6 meses de seguimiento. Conclusiones: En un grupo homogéneo de niños con retraso de crecimiento intra-uterino asimétrico, el suplemento de cinc a una dosis de 3 mg/día, no origina mejora significativa en el crecimiento en peso y longitud. Los cambios en el status de cinc se relacionaron con los cambios en peso y longitud durante los 6 primeros meses de vida. Los cambios en las concentraciones séricas de leptina se relacionaron con los cambios en los índices antropométricos de acúmulo de grasa corporal

Objectives: To analyse the effect of zinc supplementation in growth and nutritional status of a homogeneous group of newborns with intra uterine growth retardation and asymmetric growth. The effect of changes of zinc status on growth and leptin serum concentrations was also analysed. Population and methods: A double blind, randomised clinical trial was designed in order to detect differences in growth between zinc and placebo groups during the first 6 months of life. 31 infants were included either to the zinc group (n = 14) (38.8 ± 1.4 weeks GA, 2,171 ± 253 g body weight) or the placebo group (n = 17) (38.9 ± 1.1 weeks GA, 2,249 ± 220 g body weight). The zinc group received a supplement of 3 mg elemental zinc per day (as zinc sulphate).Results: There were not significant differences between groups for anthropometric measurements through the study period. We found a significant effect of the study group, in hair zinc concentrations, but not in serum zinc concentrations; post-hoc comparisons for hair zinc revealed that there were significant differences between groups at 1, 2, and 6 months of age. Changes in serum and hair zinc concentrations from baseline to 6 months, showed significant correlations with changes in weight/age and length/age z-scores, in the supplement group. Changes in leptin serum concentrations during follow-up, showed significant correlations with changes in sum of 4 skinfolds and weight/age z-score, in the placebo group. Changes in hair zinc concentration through the study period showed significant correlations with changes in leptin serum concentrations from baseline to 6 months of follow-up. Conclusions: In a homogeneous group of intra uterine growth retardation infants with asymmetric growth, 3mg/day zinc supplementation do not show significant improvements in weight and length growth. Changes in zinc status were related with changes in weight and length during the first 6 months of life. Changes in leptin serum concentrations were related with changes in the anthropometric indices of body fat accretion

Iron status at 9 months of infants with low iron stores at birth.

OBJECTIVE: To determine the 9-month follow-up iron status of infants born with abnormally low serum ferritin concentrations. STUDY DESIGN: Ten infants of >34 weeks' gestation with cord serum ferritin concentrations <5th percentile at birth (<70 microg/L) and 12 control infants with cord serum ferritin concentrations >80 microg/L had follow-up serum ferritin concentrations measured at 9 +/- 1 month of age. The mean follow-up ferritins, incidences of iron deficiency and iron-deficiency anemia, and growth rates from 0 to 12 months were compared between the two groups. RESULTS: At follow-up, the low birth ferritin group had a lower mean ferritin than the control group (30 +/- 17 vs 57 +/- 33 microg/L; P =.03), but no infant in either group had iron deficiency (serum ferritin <10 microg/L) or iron-deficiency anemia. Both groups grew equally well, but more rapid growth rates were associated with lower follow-up ferritin concentrations only in the low birth ferritin group (r = -0.52; P =.05). Both groups were predominantly breast-fed without iron supplementation before 6 months. CONCLUSIONS: Infants born with serum ferritin concentrations <5th percentile continue to have significantly lower ferritin concentrations at 9 months of age compared with infants born with normal iron status, potentially conferring a greater risk of later onset iron deficiency in the second postnatal year.

Fetal growth restriction: adaptations and consequences.

A range of pathophysiological factors can result in a perturbation or restriction of fetal growth, and the cardiovascular, neuroendocrine and metabolic adaptations of the fetus to these stimuli will depend on their nature, timing and intensity. The critical importance of these physiological adaptations for both immediate survival and long-term health outcomes has provided an impetus for experimental studies of the nature and consequences of specific fetal adaptations to a poor intrauterine environment. This review summarizes data from recent studies that have focused on the responses of the fetal cardiovascular, sympathoadrenal, hypothalamo-pituitary-adrenal and renin-angiotensin systems to experimental restriction of placental function in the sheep and discusses the consequences of these adaptations for fetal, neonatal and adult health.

Efficacy and safety of intravenously administered iron sucrose with and without adjuvant recombinant human erythropoietin for the treatment of resistant iron-deficiency anemia during pregnancy.

OBJECTIVE: This study was undertaken to determine the efficacy and safety of intravenously administered iron sucrose with versus without adjuvant recombinant human erythropoietin in the treatment of gestational iron-deficiency anemia resistant to therapy with orally administered iron alone. STUDY DESIGN: Forty patients with gestational iron-deficiency anemia were randomly assigned to receive intravenously iron sucrose plus recombinant human erythropoietin or iron sucrose alone twice weekly. Target hemoglobin value was 11.0 g/dL. Efficacy measures were reticulocyte count, increase in hematocrit, and time to target hemoglobin level (treatment duration in weeks and need for continued therapy after 4 weeks). RESULTS: Both regimens were effective, but with adjuvant recombinant human erythropoietin the reticulocyte counts were higher from day 4 (P<.01), increases in hematocrit were greater from day 11 (P <.01), and the median duration of therapy was shorter (18 vs 25 days), with more patients reaching the target hemoglobin level by 4 weeks of treatment (n = 19 vs. n = 15). The groups did not differ with respect to maternal-fetal safety parameters. CONCLUSION: Adjuvant recombinant human erythropoietin safely enhanced the efficacy of iron sucrose in the treatment of gestational iron-deficiency anemia resistant to orally administered iron alone.

Primary, secondary, and tertiary prevention of pre-eclampsia.

Pre-eclampsia remains one of the major obstetrical problems in less-developed countries. The causes of this condition are still unknown, thus effective primary prevention is not possible at this stage. Research in the past decade has identified some major risk factors for pre-eclampsia, and manipulation of these factors might result in a decrease in its frequency. In the early 1990s aspirin was thought to be the wonder drug in secondary prevention of pre-eclampsia. Results of large trials have shown that this is not the case: if there is an indication for using aspirin it is in the patient at a very high risk of developing severe early-onset disease. The calcium story followed a more or less similar pattern, with the difference that existing evidence shows that women with a low dietary calcium intake are likely to benefit from calcium supplementation. Proper antenatal care and timed delivery are of utmost importance in tertiary prevention of pre-eclampsia. There is evidence to suggest that the intrinsic direct effect of moderate degrees of maternal hypertension is beneficial to the fetus. Severe hypertension needs treatment. If antihypertensive is indicated, there is no clear choice of a drug. Hydralazine should no longer be thought of as the primary drug, most studies show a preference for calcium channel blockers.

Sudden infant death syndrome: hypothalamic failure to sense elevated blood pyrogens.

Sudden infant death syndrome (SIDS) is frequently associated with a mild infection, the incidence peaking during the third month of life. We hypothesize that the neonatal immaturity of both the acute febrile response and hypothalamus promote neonatal protection from SIDS. Vagal afferents modify the febrile response. Vagotomized rodents displayed a loss of febrile responsiveness in a 'non-sensing' brain. The failure of a 'non-sensing' brain to react to elevated blood pyrogens leads to failure of the febrile response and to a shock-like state. SIDS infants may appear well yet, within hours of this observation, may be found dead. There is a mismatch between the acute febrile response and hypothalamic hypoactivation. The discrepancy increases with development. There is an elevated cytokine response in endothelial cells which induces nitric oxide (NO) production and retarded development of the hypothalamus. Cigarette smoke also induces NO production and retards hypothalamic development by augmented apoptosis. Zinc inhibits this effect in mouse thymocytes. Fetal haemoglobin (HbF) induces hypoxia, which is a stimulator of the immune response while vasodilator gases (carbon monoxide (CO), NO) reduce hypothalamic function. The hypothalamic failure to sense elevated blood pyrogens induces toxic shock - a feature of SIDS.

How should very low birthweight babies best be managed in Papua New Guinea?

Short-term outcome in very low birthweight babies has never been closely examined in Papua New Guinea. A cohort of neonates born over a year at Port Moresby General Hospital was followed from birth to death or discharge. Intrauterine growth retardation was an important contributor to low birthweight. Simple, inexpensive care resulted in respectable survival figures. Improving antenatal surveillance will have much more impact in reducing mortality in this group in the future than trying to emulate sophisticated and costly western neonatal care.

PIP: A cohort of 98 consecutive very-low-birth-weight infants (under 1500 g) born at Port Moresby General Hospital (Papua New Guinea) over a 12-month period was followed from birth until either death or discharge from the Special Care Nursery. The infants were managed with warming, "blind" antibiotic prophylaxis, intravenous fluids, nasopharyngeal oxygen for respiratory distress, and phototherapy and/or exchange transfusion for jaundice. The majority of these infants had intrauterine growth retardation. Mean weekly weight gain was 142 g, while the mean weekly increase in head circumference was 6.46 mm. Overall mortality was 54% and markedly inversely associated with birth weight. The major causes of death were intraventricular hemorrhage (31%), hyaline membrane disease (31%), and septicemia (10%). Since only 40% of discharged infants were returned for review beyond 6 weeks, late outcomes could not be assessed. One-third of infants who were examined after 6 weeks showed signs of subtle or isolated neurodevelopmental delay and there was one case of cerebral palsy. Prevention of very low birth weight depends on attention to intrauterine growth retardation--a result of poor maternal health and nutrition. Recommended are measures such as iron and chloroquine prophylaxis, tetanus toxoid vaccination, and improved nutrition during pregnancy.

A new syndrome of congenital hypoparathyroidism, severe growth failure, and dysmorphic features.

Twelve infants (six boys, six girls) with severe hypocalcaemic tetany or convulsions were seen over a three year period. Nine patients were symptomatic in the newborn period. Their hypocalcaemia was associated with hyperphosphataemia and very low concentrations of immunoreactive parathyroid hormone. None of the babies suffered from congenital cardiac disease. Cell mediated immunity, measured in five patients, was normal. There were no chromosomal abnormalities but all patients shared several dysmorphic features including deep set eyes, microcephaly, thin lips, beaked nose tip, external ear anomalies, micrognathia, and depressed nasal bridge. Mental retardation of varying degree was found in all patients. All had severe intrauterine and postnatal growth retardation. Four patients have died. The remaining eight patients are on treatments with vitamin D and calcium supplements with no change in their growth pattern. We believe that this association of congenital hypoparathyroidism with severe growth failure and dysmorphism represents a new syndrome.