Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0728731 (prematurity)
 7,134 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recombinant human erythropoietin (rHuEPO) was administered subcutaneously three times a week to 18 infants with the anaemia of prematurity at doses of 75, 150, 300, or 600 units/kg per week for 4 weeks, starting at 3-4 weeks of postnatal age. A significant and dose-dependent increase in reticulocyte count was observed from a mean baseline value of 71 x 10(9)/l to 200 x 10(9)/l after 3 weeks of therapy, compared with a change from 69 to 97 x 10(9)/l in 66 historical controls. The haematocrit value remained unchanged during rHuEPO treatment, whereas it steadily declined until 9 weeks of postnatal age in the controls. These effects were accompanied by a marked reduction in serum iron concentration and transferrin saturation in patients receiving standard-dose iron supplements, but not in those given larger doses. Only 3 of 18 patients required a red blood cell transfusion. These infants were among the most anaemic at entry into the study and 2 of them were unable to complete rHuEPO therapy, while the third developed iron deficiency anaemia. These data indicate that rHuEPO with appropriate iron supplementation may accelerate the recovery from anaemia of prematurity. Larger scale placebo-controlled studies are now needed to confirm these findings and verify their impact on transfusion requirements of premature infants.
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PMID:Recombinant human erythropoietin in the treatment of infants with anaemia of prematurity. 139 27

A prospective study was made which included 287 infants, 12 months of age and patients of two Vizcaya Health Centers, in order to determine the prevalence of anemia and/or depletion of iron stores. The study design included somatometry and a review of the clinical records, dietary habits and the socio-economic status of the family. Laboratory tests included: hematocrit, hemoglobin, mean corpuscular volume, number of erythrocytes, serum iron, transferrin, iron saturation percentage and serum ferritin. Anemia was present in 9.3% of these children and 6.9% had iron-deficiency anemia. Depletion of iron stores was found in 12.4%. Prematurity, socio-economic status, infants fed low-iron milk, early introduction of cow's milk and the weight at 12 months were all variables that correlated significantly with the anemic or iron deficient states. However, the number of infections during the first year of life did not show a significant correlation. A question about the necessity of routine screening is raised and recommendation is made for iron supplementation in the infants in the high risk group.
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PMID:[Anemia and depletion of iron reserves in healthy 12-month-old infants]. 141 18

In previous studies, transferrin C2 has been found to be associated with spontaneous abortion, prematurity, phototoxic eczema and rheumatoid arthritis. We have suggested that the mechanism behind these negative effects may be that transferrin C2 increases the risk for damage through hydroxyl radicals. This hypothesis predicts that the C2 frequency should decrease with age. Such an effect is demonstrated in this report. In a population from northern Sweden the C2 gene frequency was found to decrease from 0.173 in newborns to 0.099 in 70-year-old healthy individuals.
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PMID:Decrease of transferrin C2 frequency with age. 375

Ferritin concentrations in cord blood were determined in 22 normal term and 32 preterm infants (birth weights 600-2000 g). Eight of the preterms were SGA infants. AGA preterm infants had significantly lower concentrations than term infants, and the SGA preterm newborn had even lower levels. Plasma ferritin in cord blood of the term and AGA preterm infants correlated positively with plasma iron and transferrin saturations, but not with the transferrin level, while plasma iron and transferrin concentrations correlated positively. In a longitudinal study, 17 AGA preterm infants (birth weights 850-1500 g) were followed during the early anaemia of prematurity. Iron was supplemented from 4 weeks of age. Plasma ferritin rose rapidly during the first days after birth, peak levels being reached at 1-4 weeks. Thereafter linear falls (semilog) occurred with similar slopes in different infants. Transferrin concentrations showed a slow progressive increase from 0-8 weeks. Plasma ferritin, after reaching the peak value, correlated negatively with weight gain. No infant had low ferritin values indicating iron deficiency during the early anaemia.
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PMID:Plasma ferritin concentrations in preterm infants in cord blood and during the early anaemia of prematurity. 723 84

1. Non-protein-bound iron has been implicated in the aetiology of chronic lung disease of prematurity. 2. The modification of a method for the measurement of non-transferrin-bound iron in small volumes of plasma and bronchoalveolar lavage fluid from preterm babies is described. 3. The assay runs with a good degree of precision and a lower limit of detection of 0.02 mumol/l. 4. Non-transferrin-bound iron was detected in 50% of plasma samples and 11% of bronchoalveolar lavage fluid samples collected over the first week of life from babies born prematurely.
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PMID:Chromatographic method for the determination of non-transferrin-bound iron suitable for use on the plasma and bronchoalveolar lavage fluid of preterm babies. 894 3

Recombinant human erythropoietin is used in clinical practice mainly for treatment of anemia of renal failure. In the past years, however, its use has been approved for other indications, including prevention of anemia in surgical patients or in patients undergoing platinum-based chemotherapy, treatment of anemia of prematurity, of anemia induced by zidovudine therapy in HIV-infected patients, and of anemia induced by chemotherapy of nonmyeloid malignancies. Erythropoietin should routinely be given subcutaneously to maximize its effects. Most patients undergoing rHuEpo treatment develop functional iron deficiency, a situation in which iron supply to the erythroid marrow is inadequate for the erythrocyte precursor demand. Iron supplementation should, therefore, be given to all individuals receiving rHuEpo except for those patients with increased serum iron and transferrin saturation. Outside the setting of uremia, only a portion of patients can clearly benefit from erythropoietin therapy; therefore, the use of rHuEpo should be individualized in nonrenal applications.
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PMID:How and when to use erythropoietin. 957 Jul 2

The diagnosis and treatment of fetal and neonatal diseases requires knowledge of gestational age-dependent reference ranges for most laboratory values. It was the aim of the present study to establish reference values for serum iron, transferrin, ferritin and ceruloplasmin concentrations in premature neonates, thereby paying attention to the possible changes with gestational age. Blood samples were taken from 100 premature neonates within the first hour of life. Total serum iron, transferrin, ferritin and ceruloplasmin concentrations were determined, transferrin saturation was calculated. Newborns who developed a presumed oxygen radical disease of prematurity were excluded from the study (n = 37), because previous investigations could demonstrate significantly lower serum transferrin and ceruloplasmin concentrations in prematures suffering one of these disorders. Related to gestational age, only serum transferrin concentration showed a statistically significant increase and correlation (r = 0.47; p < 0.0001) with rising age. Although statistically not significant, even serum ferritin concentration increased with rising age of the neonates. None of the investigated laboratory values correlated with birth weight. Only ferritin showed a slight, but statistically not significant increase with higher body mass. We conclude that gestational age-dependent changes of serum transferrin levels must be considered in the judgement of fetal and neonatal diseases, whereas total serum iron and ceruloplasmin concentrations remain rather constant at least during the last weeks of gestation.
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PMID:Gestational age-dependent reference values for iron and selected proteins of iron metabolism in serum of premature human neonates. 969 Nov 61

In this report, we describe a brother and sister who presented at birth with short-limb skeletal dysplasia, polyhydramnios, prematurity, and generalized edema. Dysmorphic features included broad nose, thick ears, thin lips, micrognathia, inverted nipples, ulnar deviation at the wrists, spatulate fingers, fifth finger camptodactyly, nail hypoplasia, and talipes equinovarus. Other features included short stature, microcephaly, psychomotor retardation, B-cell lymphopenic hypogammaglobulinemia, sensorineural deafness, retinal detachment and blindness, intestinal malrotation with poor gastrointestinal motility, persistent hyponatremia, intermittent hypoglycemia, and thrombocytopenia. Cardiac anomalies included PDA, VSD, hypertrophic cardiomyopathy, and arrhythmias. The brother had a small penis with hypospadias, hypoplastic scrotum, and non-palpable testes. Skeletal findings included absent ossification of cervical vertebral bodies, pubic bones, knee epiphyses, and tali. Both sibs died before age 2 years, one of overwhelming sepsis and the other of cardiorespiratory failure associated with her cardiomyopathy. Metabolic studies showed a type 1 pattern of abnormal serum transferrin glycosylation. Fibroblasts synthesized truncated LLOs, primarily Man(7)GlcNAc(2), suggestive of CDG-Ig. Both sibs were compound heterozygotes for a novel 301 G > A (G101R) mutation and a previously described 437 G > A (R146Q) mutation in ALG12. Congenital disorders of glycosylation should be considered for children with undiagnosed multi-system disease including neurodevelopmental delay, skeletal dysplasia, immune deficiency, male genital hypoplasia, and cardiomyopathy.
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PMID:Expanding spectrum of congenital disorder of glycosylation Ig (CDG-Ig): sibs with a unique skeletal dysplasia, hypogammaglobulinemia, cardiomyopathy, genital malformations, and early lethality. 1750 7

Prematurity is a high risk factor threatening the well-being of newborns and their somatic and psychological development in the future. Preterm babies need special medical care in which proper nutrition and metabolic control play an evident role. Our review presents the current knowledge concerning the clinical value of different methods investigated in the neonatal unit setting, including: protein markers of nutritional status (albumin,prealbumin, transferrin, and Retinol Binding Protein (RBP) and hormonal markers of nutritional status (somatomedin C, visfatin and ghrelin). Moreover, there is a discussion of the methods used for evaluating body composition. A variety of different techniques based on the physical properties of organisms was tested on neonates, e.g. the Dual Energy X-ray Absorptiometry (DEXA) method and Bioelectrical Impedance Analysis (BIA). Based on the review of the literature, we can speculate that none of the above methods represents a good single marker of the babies' nutritional status, or a prognostic factor for the future development of premature infants and infants born with IUGR. A combination of several methods from different groups seems to be a promising possibility. It is critical to continue looking for markers that will in a simple and efficient way help to optimize the correct nutritional therapy in infants with IUGR and those who were born prematurely.
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PMID:HOW TO DETERMINE THE NUTRITIONAL STATUS OF PRETERM BABIES?--REVIEW OF THE LITERATURE. 2695 97

The consequences of neonatal white matter injury are devastating and represent a major societal problem as currently there is no cure. Prematurity, low weight birth and maternal pre-natal infection are the most frequent causes of acquired myelin deficiency in the human neonate leading to cerebral palsy and cognitive impairment. In the developing brain, oligodendrocyte (OL) maturation occurs perinatally, and immature OLs are particularly vulnerable. Cell replacement therapy is often considered a viable option to replace progenitors that die due to glutamate excitotoxicity. We previously reported directed specification and mobilization of endogenous committed and uncommitted neural progenitors by the combination of transferrin and insulin growth factor 1 (TSC1). Here, considering cell replacement and integration as therapeutic goals, we examined if OL progenitors (OLPs) grafted into the brain parenchyma of mice that were subjected to an excitotoxic insult could rescue white matter injury. For that purpose, we used a well-established model of glutamate excitotoxic injury. Four-day-old mice received a single intraparenchymal injection of the glutamate receptor agonist N-methyl-D-aspartate alone or in conjunction with TSC1 in the presence or absence of OLPs grafted into the brain parenchyma. Energetics and expression of stress proteins and OL developmental specific markers were examined. A comparison of the proteomic profile per treatment was also ascertained. We found that OLPs did not survive in the excitotoxic environment when grafted alone. In contrast, when combined with TSC1, survival and integration of grafted OLPs was observed. Further, energy metabolism in OLPs was significantly increased by N-methyl-D-aspartate and modulated by TSC1. The proteomic profile after the various treatments showed elevated ubiquitination and stress/heat shock protein 90 in response to N-methyl-D-aspartate. These changes were reversed in the presence of TSC1 and ubiquitination was decreased. The results obtained in this pre-clinical study indicate that the use of a combinatorial intervention including both trophic support and healthy OLPs constitutes a promising approach for long-term survival and successful graft integration. We established optimal conditioning of the host brain environment to promote long-term survival and integration of grafted OLPs into an inflamed neonate host brain. Experimental procedures were performed under the United States Public Health Service Guide for the Care and Use of Laboratory Animals and were approved by the Institutional Animal Care Committee at (UCLA) (ARC #1992-034-61) on July 1, 2010.
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PMID:Trophic factors are essential for the survival of grafted oligodendrocyte progenitors and for neuroprotection after perinatal excitotoxicity. 3157 68


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