Insufficiency In Preterm Infants Research Articles

The effect of iron supplementation in preterm infants at different gestational ages

BackgroundIron deficiency (ID) is the most prevalent nutritional deficiency disease in preterm infants, significantly affecting their growth and development. For preterm infants to flourish physically and neurologically, timely iron supplementation is essential. The main goals of this study were to determine whether the present iron supplementation regimen results in iron overload in late preterm infants and whether it can meet the growth requirements of early preterm infants for catch-up.MethodsWe conducted a prospective follow-up study on preterm infants at the Department of Child Health, West China Second University Hospital, Sichuan University, from January 1, 2020, to August 31, 2020. In this study, 177 preterm infants were divided into two groups based on gestational age—early preterm infants (gestational age < 34 weeks) and late preterm infants (gestational age ≥ 34 weeks and < 37 weeks)—to compare the incidence of iron deficiency, iron status, and physical growth of preterm infants receiving iron supplements (2–4 mg/kg/d).ResultsIron supplementation considerably reduced the incidence of iron deficiency in preterm infants. The prevalence of iron deficiency in early preterm infants and late preterm infants was 11.3% and 5.1%, respectively, at the corrected gestational age of 3 months; at the corrected gestational age of 6 months, the prevalence was 5.3% and 6.3%, respectively. No preterm infants with iron deficiency were detected in either group at the corrected gestational age of 12 months. Ferritin was substantially lower in early preterm infants (36.87 ± 31.57 ng/ml) than in late preterm infants (65.78 ± 75.76 ng/ml) at the corrected gestational age of 3 months (p < 0.05). A multifactorial regression analysis of factors influencing iron metabolism levels in preterm infants revealed a positive relationship between log10hepcidin, birth weight, and ferritin, with higher birth weights resulting in higher ferritin levels.ConclusionsPostnatal iron supplementation at 2–4 mg/kg/d in preterm infants significantly decreases the incidence of ID. There were substantial differences in iron levels across preterm infants of varying gestational ages. A tailored iron supplementation plan based on growth, birth weight, and gestational age may be a more suitable route for iron supplementation. Although the current study found that the postnatal iron status of early preterm infants differed from that of late preterm infants, the actual mechanism of action remains unknown, and large-sample, multicenter clinical studies are required to investigate this further.

Comparison of two dosage regimens of iron in preterm infants for the prevention of iron deficiency: A prospective interventional study

Abstract BACKGROUND: The majority of infants born &lt;32 weeks of gestation develop anemia. The cause depends on multiple factors, most common being iron deficiency. Iron being a major nutrient, its deficiency may lead to irreversible neurodevelopment and cognitive impairment and overdose lead to neurodegeneration and gastrointestinal intolerance. Although the need for iron and outcome of iron deficiencies has been studied much, valid studies pertaining dosage for prevention of iron deficiency in preterm infants are insufficient. OBJECTIVE: To compare two dosage regimens of iron for the prevention of iron deficiency among preterm infants born &lt;32 weeks at 6 weeks of chronological age. MATERIALS AND METHODS: A prospective interventional study performed in a level III neonatal intensive care unit. A total of 64 infants with &lt;32 weeks of gestation were studied, were classified into two grouped, and initiated with iron at two different doses (2 and 4 mg/kg/day). The preintervention and postintervention hemoglobin and serum ferritin were compared at 6 weeks of chronological age. RESULTS: Of the 32 babies with iron initiated at 2 mg/kg/day, 21 babies had low hemoglobin level and 11 babies had normal hemoglobin level, and 10 babies had low ferritin level and 22 babies had normal ferritin level. Of the 32 babies with iron at 4 mg/kg/day, all babies had normal hemoglobin and ferritin levels. Conclusion: The incidence of anemia is lower in the infants receiving iron at 4 mg/kg/day compared with infants receiving iron at 2 mg/kg/day.

Exclusively breastmilk‐fed preterm infants are at high risk of developing subclinical vitamin K deficiency despite intramuscular prophylaxis at birth

BackgroundThere is near‐global consensus that all newborns be given parenteral vitamin K1 (VK1) at birth as prophylaxis against VK deficiency bleeding (VKDB). Breastmilk has a low VK content and cases of late VKDB are reported in exclusively breastmilk‐fed preterm infants despite VK prophylaxis at birth. ObjectivesTo assess the prevalence of functional VK insufficiency in preterm infants based on elevated under‐γ‐carboxylated (Glu) species of Gla proteins, factor II (PIVKA‐II), and osteocalcin (GluOC), synthesized by liver and bone, respectively. Patients/MethodsProspective, multicenter, observational study in preterm infants born <33 weeks' gestation. Blood samples and dietary history were collected before hospital discharge, and after discharge at 2–3 months’ corrected age. Outcome measures were serum VK1, PIVKA‐II, and %GluOC (GluOC as a percentage of the sum of GluOC plus GlaOC) compared between exclusively breastmilk‐fed and formula/mixed‐fed infants after discharge. ResultsAfter discharge, breastmilk‐fed babies had significantly lower serum VK1 (0.15 vs. 1.81 μg/L), higher PIVKA‐II (0.10 vs. 0.02 AU/ml) and higher %GluOC (63.6% vs. 8.1%) than those receiving a formula/mixed‐feed diet. Pre‐discharge (based on elevated PIVKA‐II), only one (2%) of 45 breastmilk‐fed infants was VK insufficient. After discharge, eight (67%) of 12 exclusively breastmilk‐fed babies were VK insufficient versus only one (4%) of 25 formula/mixed‐fed babies. ConclusionsPreterm infants who remain exclusively or predominantly human breastmilk‐fed after neonatal unit discharge are at high risk of developing subclinical VK deficiency in early infancy. Routine postdischarge VK1 supplementation of breastfed infants to provide intakes comparable to those from formula milks should prevent this deficiency.

Single Nucleotide Polymorphisms Interactions of the Surfactant Protein Genes Associated With Respiratory Distress Syndrome Susceptibility in Preterm Infants.

Background: Neonatal respiratory distress syndrome (RDS), due to surfactant deficiency in preterm infants, is the most common cause of respiratory morbidity. The surfactant proteins (SFTP) genetic variants have been well-studied in association with RDS; however, the impact of SNP-SNP (single nucleotide polymorphism) interactions on RDS has not been addressed. Therefore, this study utilizes a newer statistical model to determine the association of SFTP single SNP model and SNP-SNP interactions in a two and a three SNP interaction model with RDS susceptibility.Methods: This study used available genotype and clinical data in the Floros biobank at Penn State University. The patients consisted of 848 preterm infants, born <36 weeks of gestation, with 477 infants with RDS and 458 infants without RDS. Seventeen well-studied SFTPA1, SFTPA2, SFTPB, SFTPC, and SFTPD SNPs were investigated. Wang's statistical model was employed to test and identify significant associations in a case-control study.Results: Only the rs17886395 (C allele) of the SFTPA2 was associated with protection for RDS in a single-SNP model (Odd's Ratio 0.16, 95% CI 0.06–0.43, adjusted p = 0.03). The highest number of interactions (n = 27) in the three SNP interactions were among SFTPA1 and SFTPA2. The three SNP models showed intergenic and intragenic interactions among all SFTP SNPs except SFTPC.Conclusion: The single SNP model and SNP interactions using the two and three SNP interactions models identified SFTP-SNP associations with RDS. However, the large number of significant associations containing SFTPA1 and/or SFTPA2 SNPs point to the importance of SFTPA1 and SFTPA2 in RDS susceptibility.

Severe vitamin D deficiency in preterm infants: possibly no association with clinical outcomes?

Purpose The primary objective of this study was to compare clinical outcomes of very low birth weight (VLBW) infants with 25-hydroxy vitamin D [25(OH)D] levels <25 nmol/l in umbilical cord blood versus VLBW infants with 25(OH)D levels in cord blood >25 nmol/l. The secondary objective was to evaluate umbilical cord vitamin D as a risk factor for respiratory distress syndrome (RDS) in preterm infants. Methods We examined 25(OH)D levels in umbilical cord blood and in infants’ serum at discharge from the neonatal intensive care unit. We evaluated the associations between severe vitamin D deficiency and various laboratory findings and clinical outcomes. Results Eighty one infants with birth weight less than 1500 g met the entry criteria for this study and were divided to groups according to umbilical cord blood vitamin D [Group A: 25(OH)D < 25 nmol/l; 10 ng/ml and Group B: 25(OH)D > 25 nmol/l; 10 ng/ml]. Overall, 81.5% of the infants had a 25(OH)D level <50 nmol/L and 44.4% had a level <25 nmol/L. The laboratory findings and the subsequent clinical outcomes were comparable in infants in both groups (non-significant difference). Only the infants in the 25(OH)D 25 nmol/L group had a lower calcium in urine at age 28 d (p=.0272). In addition, we found in this study that umbilical cord vitamin D level does not lead to a higher or lower risk of RDS (odds ratio 1.044; 95% confidence interval 0.349–0.88; p=.0771). Conclusions In our prospective cohort study, we found no significant association between vitamin D status and selected clinical outcomes when using a cut-off of 25 nmol/l (severe vitamin D deficiency) in preterm infants.

Retrospective Assessment of Selenium Status in High Risk Infants

Abstract Objectives Selenium (Se) is an essential trace mineral important in neonatal development that contributes to oxidative stress and the inflammatory response. Se deficiency in preterm infants is associated with late onset sepsis, bronchopulmonary dysplasia, poor neurodevelopmental outcomes, and retinopathy of prematurity. Current Se dosing in many US Neonatal Intensive Care Units is based on the amount of Se in term breastmilk. However, it is unclear if this is sufficient and higher levels may be needed to prevent or treat Se deficiency. Our goal was to evaluate if the current practice supplementing total parenteral nutrition (TPN) with sodium selenite 2 mcg/kg/d is sufficient at preventing Se deficiency in high risk infants. Methods This is a retrospective chart review of Se status at a level IV Children's Hospital NICU from January 1, 2017 to August 30, 2019. Infants were included if born from 22–42 weeks gestation and received TPN for &amp;gt;4 weeks. They were excluded if there was concern for active sepsis or bacterial illness at time of Se draw. Normal Se status was defined as 45–90 ng/mL for infants 0–2 months. Birth weight, IUGR status, gestational age, and % enteral feeds were evaluated. Se deficient infants received higher Se dosing at 5–7 mcg/kg/d. Repeat levels were evaluated after 4 weeks. Results are reported as mean ± SD. Results Se status was assessed for 39 infants. Average gestational age was 29.8 ± 5.36 weeks. Average birth weight was 1499 ± 837 g. At the time of first Se assessment, 78% of infants were Se deficient, with a mean Se level of 40.95 ± 12 ng/mL. Repeat Se levels on higher dosing was assessed in 23 infants. After &amp;gt;4 weeks of higher Se dosing, 35% of infants remained Se deficient, with a mean Se level of 54.04 ± 14 ng/mL. By t-test, statistically fewer infants were Se deficient on higher Se dosing (P &amp;lt; 0.0003). Conclusions Infants on prolonged TPN &amp;gt;4 weeks are at high risk for Se deficiency. Se dosing at 2 mcg/kg/day is insufficient in preventing deficiency for a majority of these babies. Higher Se dosing improved the percentage of Se sufficient infants, but a third remained deficient. Future studies are needed to prospectively determine if higher Se in TPN prevents Se deficiency. Funding Sources University of Colorado, Section of Neonatal-Perinatal Medicine.

Persistent Respiratory Distress in the Term Neonate: Genetic Surfactant Deficiency Diseases.

Respiratory distress is one of the most common clinical presentations in newborns requiring admission to a Neonatal Intensive Care Unit (NICU). Many of these infants develop respiratory distress secondary to surfactant deficiency, which causes an interstitial lung disease that can occur in both preterm and term infants. Pulmonary surfactant is a protein and lipid mixture made by type II alveolar cells, which reduces alveolar surface tension and prevents atelectasis. The etiology of surfactant deficiency in preterm infants is pulmonary immaturity and inadequate production. Term infants may develop respiratory insufficiency secondary to inadequate surfactant, either from exposure to factors that delay surfactant synthesis (such as maternal diabetes) or from dysfunctional surfactant arising from a genetic mutation. The genetics of surfactant deficiencies are very complex. Some mutations are lethal in the neonatal period, while others cause a wide range of illness severity from infancy to adulthood. Genes that have been implicated in surfactant deficiency include SFTPA1, SFTPA2, SFTPB, SFTPC, and SFTPD (which encode for surfactant proteins A, B, C, and D, respectively); ABCA3 (crucial for surfactant packaging and secretion); and NKX2 (a transcription factor that regulates the expression of the surfactant proteins in lung tissue). This article discusses the interplay between the genotypes and phenotypes of newborns with surfactant deficiency to assist clinicians in determining which patients warrant a genetic evaluation.

Origins of neonatal leptin deficiency in preterm infants.

Background:Cord blood leptin increases with advancing gestation. Preterm delivery leads to premature separation from the maternal and placental leptin source predisposing infants to postnatal leptin deficiency, but this has not been fully described.Method:Blood leptin levels were measured for infants born before 33 weeks gestation daily for the first 2 days, then weekly until 36 weeks postmenstrual age (PMA). Cord blood was obtained to provide gestational age (GA)-specific standards.Results:Cord blood leptin levels were positively associated with GA at birth, maternal body mass index (BMI) and pregnancy weight gain (all P<0.05). Following birth, infant leptin levels decreased rapidly (74% decrease within 48 hours). The extent of this decline correlated with GA (P<0.05). Postnatal leptin began to increase by 33-36 weeks PMA, but remained below cord blood leptin levels (P<0.01). At 36 weeks PMA, leptin levels were influenced by infant’s weight and sex (P<0.01), with females having higher leptin levels (1213 pg/ml vs. 984, P<0.05).Conclusion:Cord blood leptin is influenced by maternal weight gain and BMI, suggesting an important role for trans-placental leptin delivery. Preterm delivery leads to sustained leptin deficiency through 36 weeks PMA, with the most premature male infants facing the longest and harshest deficiency.

A Study of the Relationship Between Cystatin C and Metabolic Bone Disease in Preterm Infants

Objective:Cystatin C (CysC) is commonly used as a marker of renal failure in premature infants. The aim of this study was to investigate serum CysC levels in osteopenia of prematurity (OP) and determine whether CysC could be safely used as a marker of renal insufficiency in infants with OP.Methods:Subjects were 50 preterm infants (≤32 gestational weeks). Calcium (Ca), phosphorus (P) and alkaline phosphatase (ALP) serum levels were measured in postnatal week nine, and bone density was measured concurrently by quantitative ultrasonography. Patients with a Z score of <-2 were considered to have OP.Results:The mean serum CysC levels in preterm infants in postnatal week nine were 1.50±0.19 mg/L. Serum CysC levels were not correlated with speed of sound values, Z scores, serum Ca, P or ALP levels. Serum CysC levels were not significantly different between infants with OP [1.50 (1.35-1.61) mg/L] and in infants without OP [1.58 (1.28-1.70) mg/L].Conclusion:The presence of OP does not affect the safety of CysC as a marker of renal insufficiency in preterm infants.

Carnitine deficiency in preterm infants: A national survey of knowledge and practices.

Lipid supplementation improves developmental outcomes in preterm infants. Carnitine is essential for lipid metabolism; however, despite high risk for carnitine deficiency, there are no standards for carnitine supplementation in preterm infants receiving total parenteral nutrition (TPN). Our objective was to assess knowledge, beliefs and practices regarding preterm carnitine deficiency and supplementation among neonatal practitioners. Cross-sectional electronic survey administered via a nationally representative listserv of neonatal practitioners. 492 respondents participated in the survey. Only 21% of respondents were aware that carnitine is secreted by the placenta. 72% believed that carnitine deficiency was common, and 60% believed deficiency could have serious consequences. Five percent routinely screened for deficiency, and 40% routinely provided carnitine supplementation. Respondents with >5 years' experience were more likely to report using carnitine supplementation (50% vs. 38%). Although most respondents believed that carnitine deficiency is common and could have serious consequences, few screened for deficiency and fewer than half routinely supplemented. Thus, many preterm infants remain at risk for carnitine deficiency. Further research is needed to elucidate the risks of carnitine deficiency in these vulnerable infants.

Nutritional status of vitamin D and its influencing factors in preterm infants at the early stage after birth

Objective To investigate the nutritional status of vitamin D in preterm infants after birth and further explore its possible influencing factors, so as to guide clinical vitamin D therapy and to screen the preterm infants who are at high risk of vitamin D deficiency. Methods Retrospective analysis was conducted in the neonatal department of our hospital from April 21st, 2014 to February 5th, 2016. The serum 25(OH)D level in preterm infants were measured 2 weeks after birth. Data including gender, season of birth, time to initiation of breastfeeding were collected. According to the 25(OH)D levels[25(OH)D≤37.5 nmol/L, 37.5 nmol/L≤50.0 nmol/L, and 25(OH)D>50.0 nmol/L], all the preterm infants were divided into three groups: vitamin D deficiency, insufficiency, and sufficiency groups. The influencing factors of vitamin D in preterm infants were screened by using statistical method. Results The mean 25(OH)D level of 172 preterm infants was (43.1±16.7)nmol/L. In vitamin D deficient, insufficient, and sufficient groups, there were 68 (40%), 50 (29%) and 54(31%) cases of preterm babies, respectively. The mean values of 25(OH)D in these three groups were (27.8±16.7)nmol/L, (42.4±3.4)nmol/L, and (63.0±11.7)nmol/L, respectively. Only the season of birth had significant difference among three groups (P=0.013): 44.2% of the preterm infants born in winter had vitamin D deficiency, which was higher than those in spring (41.7%), summer(33.3%), and autumn (38.1%); 44.2% of the preterm infants born in winter had vitamin D insufficiency, which was much higher than those in spring (30.6%), summer (25.1%), and autumn (19.0%); furthermore, only 11.6% of the preterm infants born in the winter had vitamin D sufficiency, which was much lower than those in spring (27.8%), summer (41.2%), and autumn (42.9%) (OR=4.655, 95% CI=1.716-12.627, P=0.003). Conclusion Vitamin D deficiency in preterm infants 2 weeks after birth is prevalent, and winter birth is a risk factor of vitamin D deficiency and insufficiency in preterm infants. Key words: Vitamin D; Preterm infants; Vitamin D deficiency

Importance of neonatal immunoglobulin transfer for hippocampal development and behaviour in the newborn pig.

Neurological disorders are among the main clinical problems affecting preterm children and often result in the development of communication and learning disabilities later in life. Several factors are of importance for brain development, however the role of immunoglobulins (passive immunity transfer) has not yet been investigated. Piglets are born agammaglobulinemic, as a result of the lack of transfer of maternal immunoglobulins in utero, thus, they serve as an ideal model to mimic the condition of immunoglobulin deficiency in preterm infants. Thirty six, unsuckled newborn piglets were fed an infant formula or colostrum and supplemented orally or intravenously with either species-specific or foreign immunoglobulin and then compared to both newborn and sow-reared piglets. Two days after the piglets were born behavioural tests (novel recognition and olfactory discrimination of conspecifics scent) were performed, after which the piglets were sacrificed and blood, cerebrospinal fluid and hippocampi samples were collected for analyses. Both parameters of neuronal plasticity (neuronal maturation and synapse-associated proteins) and behavioural test parameters appeared to be improved by the appearance of species-specific porcine immunoglulin in the circulation and cerebrospinal fluid of the piglets. In conclusion, we postulate possible positive clinical effects following intravenous infusion of human immunoglobulin in terms of neuronal plasticity and cognitive function in preterm infants born with low blood immunoglobulin levels.

Assessment of Iron Status and the Effect of Red Blood Cell Transfusion in Premature Infants.

Objective The objective of this study was to evaluate iron deficiency in preterm infants and determine impact of blood transfusions on serum iron (SI) and ferritin (FTN). Study Design A prospective evaluation of baseline and weekly hemoglobin (Hgb), hematocrit (Hct), SI, FTN levels in premature infants with birth weights (BWs) &lt; 2,500 g or gestational age (GA) &lt; 34 weeks was performed to determine the impact of GA, BW, and blood transfusion on iron status. Comparisons of the baseline and 1 month values of these measures were performed as well as pre- and posttransfusion. Results In 125 preterm infants, the mean Hgb, Hct, and SI levels at birth were lower for infants &lt; 28 weeks GA. Post hoc analysis revealed statistically significant lower iron values in infants ≤ 28 weeks GA compared with infants at 28 to 34 weeks GA (p = 0.013) and infants ≥ 34 weeks GA (p = 0.007). FTN and SI values at 1 month were not significantly impacted by blood transfusions. Conclusion Infants &lt; 28 weeks have lower SI levels at birth. The SI and FTN at 1 month of age were not significantly influenced by blood transfusions.

Brain ultrasonographic findings of late-onset circulatory dysfunction due to adrenal insufficiency in preterm infants.

Purpose:The aim of this study was to characterize the brain ultrasonographic findings of late-onset circulatory dysfunction (LCD) due to adrenal insufficiency (AI) in preterm infants.Methods:Among the 257 preterm infants born at <33 weeks of gestation between December 2009 and February 2014 at our institution, 35 preterm infants were diagnosed with AI. Brain ultrasonographic findings were retrospectively analyzed before and after LCD in 14 preterm infants, after exclusion of the other 21 infants with AI due to the following causes: death (n=2), early AI (n=5), sepsis (n=1), and patent ductus arteriosus (n=13). Results:Fourteen of 257 infants (5.4%) were diagnosed with LCD due to AI. The age at LCD was a median of 18.5 days (range, 9 to 32 days). The last ultrasonographic findings before LCD occurred showed grade 1 periventricular echogenicity (PVE) in all 14 patients and germinal matrix hemorrhage (GMH) with focal cystic change in one patient. Ultrasonographic findings after LCD demonstrated no significant change in grade 1 PVE and no new lesions in eight (57%), grade 1 PVE with newly appearing GMH in three (21%), and increased PVE in three (21%) infants. Five infants (36%) showed new development (n=4) or increased size (n=1) of GMH. Two of three infants (14%) with increased PVE developed cystic periventricular leukomalacia (PVL) and rapid progression to macrocystic encephalomalacia. Conclusion:LCD due to AI may be associated with the late development of GMH, increased PVE after LCD, and cystic PVL with rapid progression to macrocystic encephalomalacia.

Severe vitamin D deficiency in preterm infants: maternal and neonatal clinical features.

PurposeWe investigated the vitamin D status of preterm infants to determine the incidence of vitamin D deficiency.MethodsA total of 278 preterm infants delivered at Kyungpook National University Hospital between January 2013 and May 2015 were enrolled. The serum concentrations of calcium, phosphorous, alkaline phosphatase, and 25-hydroxyvitamin D (25-OHD) were measured at birth. We collected maternal and neonatal data such as maternal gestational diabetes, premature rupture of membranes, maternal preeclampsia, birth date, gestational age, and birth weight.ResultsMean gestational age was 33+5±2+2 weeks of gestation and mean 25-OHD concentrations were 10.7±6.4 ng/mL. The incidence of vitamin D deficiency was 91.7%, and 51.1% of preterm infants were classified as having severe vitamin D deficiency (25-OHD<10 ng/mL). The serum 25-OHD concentrations did not correlate with gestational age. There were no significant differences in serum 25-OHD concentrations or incidence of severe vitamin D deficiency among early, moderate, and late preterm infants. The risk of severe vitamin D deficiency in twin preterm infants was significantly higher than that in singletons (odds ratio, 1.993; 95% confidence interval [CI], 1.137-3.494, P=0.016). In the fall, the incidence of severe vitamin D deficiency decreased 0.46 times compared to that in winter (95% CI, 0.227-0.901; P=0.024).ConclusionMost of preterm infants (98.9%) had vitamin D insufficiency and half of them were severely vitamin D deficient. Younger gestational age did not increase the risk of vitamin D deficiency, but gestational number was associated with severe vitamin D deficiency.

Early Human Development: An international journal concerned with the continuity of fetal and postnatal life

Traditional treatment of respiratory distress syndrome in preterm infants consisted of early intubation, mechanical ventilation and intra-tracheal administration of exogenous surfactant. Recently, non-invasive ventilation, which has shown some advantages in short- and long-term outcomes, has gained popularity for the initial management of respiratory insufficiency in preterm infants. However, non-invasive ventilation from the outset poses difficulties in relation to administration of exogenous surfactant. The customary INSURE technique requires tracheal intubation, surfactant administration, and rapid extubation, but the latter is not always possible. As a more elegant approach, several minimally invasive techniques of delivering surfactant have been developed for babies spontaneously breathing on CPAP. The most extensively studied have been those in which the trachea is briefly catheterized with a nasogastric tube or vascular catheter, and exogenous surfactant is administered. Although results seem promising they are not yet conclusive, and further studies will be needed to answer a number of outstanding questions.© 2014 Elsevier Ireland Ltd. All rights reserved.

Administration of surfactant using less invasive techniques as a part of a non-aggressive paradigm towards preterm infants

Traditional treatment of respiratory distress syndrome in preterm infants consisted of early intubation, mechanical ventilation and intra-tracheal administration of exogenous surfactant. Recently, non-invasive ventilation, which has shown some advantages in short- and long-term outcomes, has gained popularity for the initial management of respiratory insufficiency in preterm infants. However, non-invasive ventilation from the outset poses difficulties in relation to administration of exogenous surfactant. The customary INSURE technique requires tracheal intubation, surfactant administration, and rapid extubation, but the latter is not always possible. As a more elegant approach, several minimally invasive techniques of delivering surfactant have been developed for babies spontaneously breathing on CPAP. The most extensively studied have been those in which the trachea is briefly catheterized with a nasogastric tube or vascular catheter, and exogenous surfactant is administered. Although results seem promising they are not yet conclusive, and further studies will be needed to answer a number of outstanding questions.

Adrenal and thyroid function in the fetus and preterm infant.

Adrenal and thyroid hormones are essential for the regulation of intrauterine homeostasis, and for the timely differentiation and maturation of fetal organs. These hormones play complex roles during fetal life, and are believed to underlie the cellular communication that coordinates maternal-fetal interactions. They serve to modulate the functional adaptation for extrauterine life during the perinatal period. The pathophysiology of systemic vasopressor-resistant hypotension is associated with low levels of circulating cortisol, a result of immaturity of hypothalamic-pituitary-adrenal axis in preterm infants under stress. Over the past few decades, studies in preterm infants have shown abnormal clinical findings that suggest adrenal or thyroid dysfunction, yet the criteria used to diagnose adrenal insufficiency in preterm infants continue to be arbitrary. In addition, although hypothyroidism is frequently observed in extremely low gestational age infants, the benefits of thyroid hormone replacement therapy remain controversial. Screening methods for congenital hypothyroidism or congenital adrenal hyperplasia in the preterm neonate are inconclusive. Thus, further understanding of fetal and perinatal adrenal and thyroid function will provide an insight into the management of adrenal and thyroid function in the preterm infant.

Biotin and carnitine profiles in preterm infants in Japan

Biotin plays an important role as a covalently bound coenzyme for carboxylases. Carnitine is essential in β-oxidation to transport long-chain fatty acids across the inner mitochondrial membrane. The present study was conducted to assess the risk of biotin and carnitine deficiencies in preterm infants who received enteral feeding with maternal milk and/or standard infant formula made in Japan. Forty-six infants were enrolled in the study. Urine and serum samples and dried blood spots were collected at 1 week and 1 month of age. Additionally, samples were collected at 40 and 44 weeks post-menstrual age (PMA) in preterm infants. Free carnitine and C5-OH acylcarnitine, which consist of 3-hydroxyisovalerylcarnitine as a major isomer, were measured in serum samples and dried blood spots using tandem mass spectrometry. Urine 3-hydroxyisovaleric acid (3-HIVA) was measured using gas chromatography/mass spectrometry. The free carnitine levels in preterm infants were significantly lower than those in term infants, but increased with PMA in serum samples and dried blood spots. C5-OH acylcarnitine and urinary 3-HIVA levels, which were very low in term infants, were increased with PMA in preterm infants. The present results may indicate chronic biotin deficiency in preterm infants fed maternal milk and/or standard infant formula. Analyses of carnitine profiles of dried blood spots and urine 3-HIVA are relatively non-invasive and useful for the early detection of biotin deficiency in preterm infants.

1021 Characterization of Key Enzymes of the Steroid Biosynthesis in Preterm Infants

BackgroundA suspected cause for relative adrenal insufficiency in preterm infants is the immaturity of adrenal key enzymes for steroid synthesis (3ß-hydroxysteroiddehydrogenase (3ß-HSD), 11ß-hydroxylase (11ß-HYD)). The fetus lacks 3ß-HSD activity until...