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PubMed2004

Trends in sepsis-related neonatal mortality in the United States, 1985-1998.

BACKGROUND: In the United States, bacterial sepsis affects up to 32,000 live births annually. In the 1990s, intrapartum antibiotic prophylaxis (IAP) was recommended to prevent maternal-infant transmission of group B Streptococcus (GBS), a leading cause of sepsis occurring in the first week of life (early onset sepsis). Since IAP has been used, early onset GBS disease declined 70%; however, increased antibiotic use associated with IAP might lead to more severe or antimicrobial resistant etiologies of sepsis. To understand the influence of IAP on neonatal sepsis, in general, we evaluated neonatal mortality from sepsis before and after IAP recommendations were issued. METHODS: Using the National Center for Health Statistics Linked Birth/Infant Death Datasets, we compared trends in sepsis-related early neonatal mortality (<7 days) and late neonatal mortality (7-27 days) among singleton United States births from 1985 through 1991 to 1995 through 1998 [data beyond 1998 not included because of International Classification of Diseases (ICD)-10/ICD-9 coding differences]. We compared trends in mortality between the 2 time periods by estimating the average annual percent change in mortality using log linear regression and stratified by gestational age. RESULTS: Combined early and late neonatal mortality from sepsis averaged 39.6/100,000 live births from 1985 through 1991 and 31.8/100,000 live births from 1995 through 1998. Early neonatal mortality from sepsis averaged 24.9/100,000 live births from 1985 through 1991 and 15.6 from 1995 through 1998; late neonatal mortality averaged 14.8/100,000 live births from 1985 through 1991 and 16.2 from 1995 through 1998. Early neonatal mortality declined more steeply after IAP recommendations were issued, 5.0% annually from 1995 through 1998 versus 3.0% annually from 1985 through 1991. Late neonatal mortality increased more from 1995 through 1998, 5.0% annually compared with 0.5% from 1985 through 1991. CONCLUSIONS: Lower mortality rates and greater declines in early neonatal mortality from sepsis during 1995-1998 indicate greater survival of infants beyond 7 days of life and suggest an association with GBS disease prevention efforts. Thus these findings provide some evidence for continuing IAP for GBS-colonized women. Our findings of apparent increasing trends in late neonatal mortality from sepsis necessitate follow-up with clinical studies.

Female↗
PubMed2005

Interleukin-6 in preterm premature rupture of membranes as an indicator of neonatal outcome.

BACKGROUND: The aim of this study was to investigate whether the levels of interleukin-6 (IL-6) can be used as markers of adverse outcome in preterm neonates born after preterm premature rupture of membranes (PPROM). METHODS: This study involved 109 preterm neonates and their mothers. The PPROM group consisted of 58 neonates who were born after PPROM, and the control group consisted of 51 neonates. IL-6 levels were measured in umbilical cord blood, maternal blood sampled during delivery and in neonatal blood taken on the fourth day of life. RESULTS: In the PPROM group, IL-6 concentrations in maternal blood, cord blood, and neonatal blood were significantly higher in neonates with sepsis, compared with those without sepsis (P < 0.001). Choosing 108.5 pg/ml as a cut-off concentration of IL-6 in umbilical cord blood for neonatal sepsis resulted in sensitivity 95%, specificity 100%, positive predictive value 100%, and negative predictive value 97.4%. Concerning IL-6 in maternal blood, a cut-off concentration of 81 pg/ml showed sensitivity 90%, specificity 97.4%, positive predictive value 94.7%, and negative predictive value 94.9%. Eighteen of 20 neonates with early sepsis and seven of nine neonates, who died in the PPROM group, were born of mothers with IL-6 levels above the cut-off concentration in their blood during delivery. CONCLUSIONS: IL-6 in umbilical cord blood was the most significant variable for predicting early onset sepsis in preterm neonates. IL-6 in maternal blood was indicative of intrauterine environmental threats and might be used to identify pregnancies where intervention would be appropriate.

Biomarkers↗
PubMed2006

High prevalence of mannose-binding lectin (MBL) deficiency in premature neonates.

Mannose-binding lectin (MBL) is a component of innate immunity and thus particularly important in neonates in whom adaptive immunity is not yet completely developed. Promoter polymorphisms and structural exon-1 mutations in the MBL2 gene cause reduced or deficient MBL plasma concentrations. The aim of our study was to determine the prevalence of MBL deficiency in neonates admitted to the neonatal intensive care unit (NICU). Eighty-five NICU patients (69 premature) were included in the study. We measured MBL concentrations in umbilical cord and neonatal blood within 24 h after birth by ELISA technique. MBL2 genotypes (n = 67) were determined by Taqman analysis. MBL concentrations were measured longitudinally during three weeks in 26 premature neonates. The association between pre- and intra-partum clinical data and MBL concentrations was investigated. At birth, 29 (42%) premature and six (38%) term neonates had MBL plasma concentrations < or = 0.7 microg/ml which was regarded as deficient. Twenty-one (38%) premature and four (36%) term neonates had variant MBL2 haplotypes, corresponding to exon-1 mutations and the LXPA haplotype. MBL concentrations increased over time in neonates with wild-type MBL2 haplotypes, but not in neonates with variant haplotypes. Low MBL plasma concentrations were related to lower gestational age and variant MBL2 haplotypes. Umbilical cord and neonatal MBL plasma concentrations appeared to be similar. In conclusion, almost half of our NICU patients, especially the premature ones, were MBL-deficient at birth. These infants may be at increased risk of neonatal infections. MBL concentration can reliably be measured in umbilical cord blood and it is positively correlated with gestational and postnatal age.

Area Under Curve↗
PubMed2003

DEC-205lo Langerinlo neonatal Langerhans' cells preferentially utilize a wortmannin-sensitive, fluid-phase pathway to internalize exogenous antigen.

Antigen treatment of neonatal epidermis results in antigen-specific immune suppression. Compared with adult counterparts, neonatal Langerhans' cells (LC) demonstrate an impaired ability to transport antigen to the lymph node (LN). As it is possible that neonatal LC have a reduced ability to endocytose antigen, we evaluated the acquisition of endocytic function, the expression of uptake receptors and the internalization of soluble and small particulate antigens in neonatal, juvenile and adult mice. Although LC from 4-day-old mice were weakly positive for the mannose-type receptor, Langerin, they were capable of internalizing fluorescein isothiocyanate (FITC)-dextran, but to a lesser extent than LC from 6-week-old mice. However, when ratio data were calculated to account for variations in fluorescence intensity at 4 degrees, it was demonstrated that neonatal LC continued to internalize antigen over a longer period of time than adult mice and, as the ratios were much higher, that neonatal cells were also relatively more efficient in antigen uptake. When receptors for mannan and mannose were competitively blocked, LC from neonatal mice, but not adult mice, could still efficiently internalize FITC-dextran. Consequently, the uptake of FITC-dextran, in part, occurred via alternative receptors or a receptor-independent fluid-phase pathway. A feasible pathway is macropinocytosis, as LC from 4-day-old mice demonstrated a reduction in FITC-dextran internalization by the macropinocytosis inhibitor, wortmannin. Evidence of a functional macropinocytosis pathway in neonatal LC was further supported by internalization of the soluble tracer Lucifer Yellow (LY). We conclude that neonatal LC preferentially utilize a wortmannin-sensitive, fluid-phase pathway, rather than receptor-mediated endocytosis, to internalize antigen. As neonatal LC are capable of sampling their environment without inducing immunity, this may serve to avoid inappropriate immune responses during the neonatal period.

Androstadienes↗
PubMed1996

Impact of increased neonatal survival on postneonatal mortality in the United States.

Neonatal intensive care has increased neonatal survival, but has also led to postponement of some of the neonatal deaths to the postneonatal period, particularly in very low birthweight (< 1.5 kg) infants. Our report assesses the impact of the increased neonatal survival and the accompanying delayed deaths on the crude postneonatal mortality rate of the US, using the national livebirth cohort data of 1960, 1980, and 1986. With increased neonatal survival, very low birthweight infants comprised 0.68% of all neonatal survivors in 1986, compared with only 0.31% in 1960. However, postneonatal mortality was increased in infants with birthweights < 1.0 kg from 69 per 1000 neonatal survivors in 1960 to 116 per 1000 in 1986. All other birthweight groups (> 1.0 kg) showed significant reductions in their postneonatal mortality, although the 1.0-1.5 kg group showed the least improvement. Thus, in 1986, 12.1% of all postneonatal deaths were from the very low birthweight neonatal survivors, as compared with 2.7% in 1960. If there had been no improvement in neonatal survival of very low birthweight infants since 1960, the crude postneonatal mortality rate of the US would have been 5.5% and 7.9% less than the actual rates of 3.65 and 3.45 per 1000 neonatal survivors in 1980 and 1986, respectively. However, the impact of these delayed deaths in very low birthweight infants was far less than the increase in their neonatal survival: an additional 416 per 1000 very low birthweight infants survived to 1 year of age in 1986 as compared with 1960. Delayed deaths in the 1.5-2.5 kg birthweight group had a very small effect on postneonatal mortality and there was no such effect of delayed deaths in the > 2.5 kg birthweight group.

Age Distribution↗
PubMed2006

Trend and causes of neonatal mortality in the Kassena-Nankana district of northern Ghana, 1995-2002.

OBJECTIVES: To describe the trend and causes of neonatal deaths in a rural district in northern Ghana. METHODS: Descriptive analysis of data collected from the Navrongo Demographic Surveillance System and verbal autopsies conducted on all neonatal deaths from 1995-2002. RESULTS: Of 1118 recorded neonatal deaths 1068 (95.5%) could be analysed. Only 13.2% of deaths occurred at the health facility; 62.7% occurred in the early neonatal period, with prematurity (38%) and birth injuries (19%) as leading causes. Infectious causes (66%) were the major contributors to late neonatal deaths. Infanticide accounted for 4.9% of all neonatal deaths. The cause-specific mortality rate for neonatal tetanus remained under 2.5% throughout the 8-year period. Overall, the neonatal mortality rate declined at an average of 2.5 per 1000 live births per year: Down by nearly 50% from 40.9 (95%C.I. 34.1-46.8) in 1995 to 20.5 (95%C.I.17.3-22.7) in 2002. CONCLUSION: The various health interventions undertaken in this district have had the collateral effect of causing decline in neonatal mortality. Neonatal mortality could be further reduced by preventing and treating neonatal infections, having skilled attendance at delivery and the elimination of infanticide. Data from demographic surveillance sites may be useful in monitoring trends in child mortality.

Birth Injuries↗
PubMed2004

Determinants of neonatal IgE level: parity, maternal age, birth season and perinatal essential fatty acid status in infants of atopic mothers.

OBJECTIVE: The hygiene hypothesis suggests that the protective 'siblings effect' against atopic diseases such as atopic dermatitis, allergic asthma and hay fever is a result of recurrent infections during early childhood. A recent study and review have indicated that this protective effect may already arise in utero. Lower n-3 essential fatty acid (EFA) status is associated with increased parity, and EFA status has also been related to atopy. The present study confirms the negative association between parity and neonatal immunoglobulin E (IgE) levels and further unravel the role of perinatal EFA status. METHODOLOGY: In a prospective cohort study in 184 atopic mothers and their neonates, we simultaneously measured serum total IgE and EFA levels in plasma phospholipids, both in the mother at 34-36 weeks of gestation and in the neonate at the age of 1 week. Linear regression analysis was used to estimate the effect of parity on maternal and neonatal IgE and EFA status, and the independent effects of parity and EFA status on IgE, controlling for confounding factors such as maternal age and birth season. RESULTS: Parity was associated with lower neonatal IgE level (P < 0.01), as well as with lower docosahexanoic acid (DHA, 22:6n-3) status of the mother (P = 0.01) but not of the neonate (P > 0.69). In the multivariate analysis, higher parity, higher maternal IgE, lower maternal age and birth in the first 3 months of the year were independently associated with neonatal IgE level. No association was detected between maternal or neonatal EFA status and neonatal IgE. CONCLUSIONS: As neonatal total serum IgE is predictive of later atopy, our results support the hypothesis that the sibling effect in atopy is already being programmed in utero. Our data also confirm earlier findings that DHA status is lower in multiparous women, but this did not confound the relation between parity and neonatal IgE.

Fatty Acids, Essential↗
PubMedDate not supplied

Neonatal presentations to a Mixed Emergency Department.

AIMS: To investigate the characteristics of neonates presenting to a metropolitan Mixed Emergency Department (MED). To examine whether there are maternal and neonatal characteristics which increase the risk of presentation to the ED in the neonatal period. METHODS: A retrospective chart review was performed of all neonatal presentations occurring between July 2002 and June 2003 to Liverpool Hospital Emergency Department, a Level 6 MED located in south-western Sydney, New South Wales, Australia, seeing approximately 45,000 presentations annually of which 20% are paediatric. Comparisons of maternal and neonatal characteristics were made with Liverpool Hospital, Area Health Service and New South Wales Mothers and Babies data, and with other paediatric presentations to the MED. RESULTS: 179 neonates made 194 neonatal presentations. Compared with all paediatric presentations, the neonatal triage category assignment, admission and transfer proportions were significantly higher, although just over half had 'primary care type illnesses'. Mothers of neonates presenting to this MED were more likely to be younger and first time mothers in comparison to the general population of mothers and newborns. This study did not find an over-representation of neonates who were discharged within 48 h after birth. CONCLUSION: The implications of these results for practice include a consideration of the availability and appropriateness of after-hours service available to new mothers. Further studies investigating parental reasons for neonatal ED presentation are recommended.

Adolescent↗
PubMed1995

Clinical study of heavy-for-dates neonates.

Incidence and morbidity rates of heavy-for-dates (HFD) term neonates were examined to elucidate whether HFD neonates are at high risk. At the same time the criteria for HFD, defined by the fetal growth curve published in 1983 by the Ministry of Health and Welfare, were evaluated. A sample of 15,377 term neonates who were born between 1984 and 1990 were obtained. Still-births and neonates from non-Japanese mothers were excluded. The overall incidence of HFD neonates was 5.13%. The morbidity rate excluding idiopathic hyperbilirubinemia was 10.0%, which increased with gestational age and was accompanied by an increment of birth trauma. The main diagnosis of hospitalization of HFD neonates was birth trauma followed by respiratory disorders. The incidences of hypoglycemia and polycythemia, regarded as major problems of HFD neonates, were low. The main causes of hospitalization of HFD neonates are associated with difficulty at delivery due to their heavy weight. There were no significant differences in the morbidity rate of neonates defined by the deviation of birth-weight from the mean +1.3 s.d. to +2.5 s.d. On the other hand, neonates of birth weight over 3750 g had significantly high morbidity rates. Criteria defined by the absolute birth-weight of over 3750 g are more appropriate to screen risk neonates with heavy weight rather than the criteria for HFD as being above mean birth-weight +1.5 s.d.

Birth Injuries↗
PubMed2005

Aminoglycoside extended interval dosing in neonates is safe and effective: a meta-analysis.

OBJECTIVES: To review the evidence from controlled clinical trials of neonates given equal daily aminoglycoside doses as extended interval dosing (dosage interval typically 24 hours in term and 36-48 hours in immature neonates) compared with traditional dosing (dosage interval typically 8-12 hours in term and 12-24 hours in immature neonates). DESIGN: Systematic review and meta-analysis of controlled trials found in electronic databases, trial registers, and references in reviews and selected trials. SETTINGS: The selected trials were blinded and assessed for methodological quality. Each trial's own predefined criteria for treatment failure, nephrotoxicity, ototoxicity, and therapeutic serum drug concentrations were used. SUBJECTS: Controlled trials of neonatal aminoglycoside treatment in which equal aminoglycoside daily doses were given at traditional and extended dosage intervals. MAIN OUTCOME MEASURES: Serum drug concentrations outside the therapeutic range. Treatment failure and toxicity. RESULTS: Sixteen trials involving 823 neonates met the inclusion criteria for the systematic review. Twelve trials involving 698 neonates were included in the meta-analysis of the pharmacokinetics. Compared with traditional dosing, extended interval dosing was associated with a significantly lower risk of both peak (summary risk ratio 0.50, 95% confidence interval 0.26 to 0.94) and trough (0.36, 0.25 to 0.56) serum drug concentrations outside the therapeutic range. Accurate information on treatment failure was obtained in nine trials involving 555 neonates. One trial reported treatment failure. In this trial two neonates in the traditional dosing group did not respond to treatment within 72 hours. Nephrotoxicity was investigated in 589 neonates in 12 trials and ototoxicity in 210 neonates in four trials, with no significant differences between the two dosing regimens. CONCLUSIONS: Extended interval dosing of aminoglycosides in neonates is safe and effective, with a reduced risk of serum drug concentrations outside the therapeutic range.

Aminoglycosides↗
PubMed2004

Adult sterol metabolism is not affected by a positive sterol balance in the neonatal Golden Syrian hamster.

Dietary components impact metabolism early in life. Some of the diet-induced effects are long lasting and can lead to various adult-based diseases. In the current studies, we examined the short-term effects of dietary cholesterol on neonatal hepatic sterol metabolism and the long-term effects that those early-life diets had on sterol metabolism in adulthood. Neonatal hamsters began consuming solid food as a supplement to milk by 5 days of age; diets contained 0 or 2% added cholesterol (wt/wt). By 10 days of age, plasma and liver cholesterol concentrations were 3.2- and 2.5-fold greater, respectively, in the neonates fed cholesterol. Hepatic sterol synthesis rates were suppressed 65% in cholesterol-fed neonates compared with control neonates. By 20 days of age, plasma and liver cholesterol concentrations were still greater and sterol synthesis rates were now suppressed maximally in neonates fed cholesterol compared with control neonates. The expression level of an apolipoprotein B-containing lipoprotein receptor (low-density lipoprotein receptor-related protein) was greater and the mature form of the sterol regulatory element-binding protein-2 was similar in livers of 20-day-old control neonates compared with control neonates at 10 days of age. To test whether the change in sterol balance in the neonatal period had a lasting effect on hepatic sterol metabolism, all animals were weaned on a low-cholesterol diet. At 70 days of age, hepatic sterol synthesis rates, plasma lipoprotein and liver cholesterol concentrations, and bile acid pool sizes and compositions were measured. Sterol balance in the adults was similar between animals fed either diet early in life, as demonstrated by a lack of difference in any parameter measured. Thus, even though dietary cholesterol suppressed hepatic sterol synthesis rates dramatically in the neonatal hamster, the change has little impact on sterol balance later in life.

Aging↗
PubMed2005

Elevation of cytokine concentrations in asphyxiated neonates.

BACKGROUND: Various cytokines are reportedly associated with many neonatal diseases. Asphyxia is considered to result in ischemia-reperfusion injuries and induces abnormal inflammatory responses involving excessive cytokine production. OBJECTIVES: To evaluate alteration in sera levels of various cytokines/chemokines in case of perinatal asphyxia at birth. METHODS: In order to determine the concentrations of various cytokines/chemokines in sera, we used a highly sensitive fluorescence microsphere method. We measured the concentration of 8 types of cytokines/chemokines in sera obtained from 17 cases of asphyxia, 10 normal neonates, and 6 healthy adults. RESULTS: The concentrations of IL-6, IL-8, and IL-10 in the sera of asphyxiated neonates were higher than those in the normal neonates. Irrespective of the presence or absence of asphyxia, sera concentrations of IL-2, IL-4, IFN-gamma, and TNF-alpha were higher in the neonates than those in the adults. The concentration of IFN-gamma in the asphyxiated neonates was lower than that in the normal neonates. Sera levels of IL-10 were higher in the asphyxiated cases than those in the normal neonates. The sera levels of IL-6, IL-8, and IL-10 in asphyxiated neonates with either a poor outcome or death were higher than those without poor outcomes. CONCLUSIONS: The concentrations of various types of cytokines/chemokines were different in neonatal sera and some of them increased drastically during asphyxia. The concentration of an anti-inflammatory cytokine IL-10 was elevated in asphyxiated neonates immediately after birth, thereby suggesting that IL-10 might be associated with neuroprotective functions.

Asphyxia Neonatorum↗
PubMed1989

Anticoagulant effects of heparin in neonatal plasma.

Available data on the anticoagulant effects of heparin in neonatal plasma are scarce and conflicting: relative to adult plasma, neonatal plasma has been reported to show both resistance as well as sensitivity to heparin. We explored this apparent paradox by comparing how well heparin accelerated inhibition of exogenous thrombin and prevented thrombin generation in defibrinated neonatal and adult plasmas. Using amidolytic assays, we determined the effects of heparin on 1) the neutralization of exogenous human alpha-thrombin and on 2) the formation of endogenous thrombin activity after contact activation and recalcification. Neonatal plasma proved resistant to heparin (0.05 U/mL) during inhibition of added thrombin (15 NIH U/mL). Inhibition of thrombin in heparinized neonatal plasma became as efficient as in adult plasma only after raising the AT III activity to normal adult values. However, de novo generation of thrombin activity was very susceptible to inhibition by heparin, even in neonatal plasmas with physiologically low AT III levels. Peak thrombin activity generated in neonatal plasma in the absence of heparin was 50% or less of peak adult activity, and this already reduced ability of neonatal plasma to generate thrombin activity upon prothrombin activation was further decreased by heparin (0.05-0.2 U/mL). We conclude that due to the neonatal AT III deficiency, added thrombin is inactivated less effectively by heparin in neonatal than in normal adult plasma. Yet, the generation of thrombin activity is impaired in neonatal plasma and easily suppressed by heparin. We speculate that newborn infants may be resistant to heparin therapy during overt thrombotic disease, when neutralization of abnormal thrombin activity is the therapeutic goal.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

The effect of hyperoxic exposure on antioxidant enzyme activities of alveolar type II cells in neonatal and adult rats.

Neonatal animals of several species are more tolerant of hyperoxic exposure than are adults, but the mechanisms of increased neonatal tolerance are unknown, as are the cell types, if any, that contribute to oxygen resistance. We studied the effect of in vivo exposure to 85% oxygen for 72 h on the activities of the antioxidant enzymes, glutathione peroxidase, catalase and superoxide dismutase (SOD), in alveolar type II cells and whole lung from adult and neonatal rats. Baseline antioxidant enzyme activities were generally lower in neonatal type II cells compared with adults. Baseline enzyme activities did not differ in neonatal type II cells and lung homogenates except for lower catalase activity in type II cells. Hyperoxic exposure resulted in 35-38% increases in antioxidant enzyme activities in neonatal whole lung. In neonatal type II cells, SOD activity increased by 170% after hyperoxia, whereas catalase and glutathione peroxidase were not significantly changed. In the adult whole lung, hyperoxic exposure resulted in increases in only glutathione peroxidase activity, whereas in adult type II cells there was a significant decrease in SOD activity after O2 exposure. Therefore, although baseline antioxidant enzyme activities were not higher in neonatal type II cells compared with whole lung, there were differences in the antioxidant enzyme responses of adult and neonatal type II cells to hyperoxia, particularly with respect to SOD. The ability of the neonatal type II cell to respond to hyperoxia with an early increase in SOD activity may contribute to the enhanced oxygen tolerance of the neonate.

Animals↗
PubMed2002

Intestinal permeability and carrier-mediated monosaccharide absorption in preterm neonates during the early postnatal period.

Immaturity of intestinal epithelial barrier function and absorptive capacity may play a role in the pathophysiology of intestinal complications in preterm neonates during the early postnatal period. We determined the intestinal permeability and carrier-mediated absorption of monosaccharides in preterm neonates during the first 2 wk after birth. Fifty-nine preterm neonates born between 25 and 32 wk gestation were included within 24 h of birth. Neonates received exclusively parenteral nutrition during the first 7 d after birth; enteral feeding was initiated at d 8. An intestinal permeability-absorption test was performed at 1, 4, 7, and 14 d after birth. The lactulose-to-rhamnose ratio was determined as a marker of intestinal permeability. Urinary excretion percentages of D-xylose and 3-O-methyl-D-glucose were determined as markers of passive and active carrier-mediated monosaccharide absorption, respectively. Intestinal permeability transiently increased between d 1 and 7 in all neonates (p < 0.05). Carrier-mediated monosaccharide absorption increased between d 1 and 14 in neonates of 28-30 wk (p < 0.05) to the level observed in the neonates of 30-32 wk gestation. In neonates <28 wk, intestinal permeability at d 7 was higher (p < 0.05) and carrier-mediated monosaccharide absorption at d 14 was lower (p < 0.01) as compared with neonates >or=28 wk. The barrier function of the intestinal epithelium transiently decreases during the first week after birth in preterm neonates who are not enterally fed. Diminished barrier function and low monosaccharide absorptive capacity, particularly in neonates <28 wk, may predispose these patients to the development of intestinal complications during the early postnatal period.

Female↗
PubMed2003

Comparison of L-selectin and CD11b on neutrophils of adults and neonates during the first month of life.

The newborn infant is particularly susceptible to infection in the first weeks of life and this may be, in part, related to functional impairment of neonatal neutrophils in regard to adherence, chemotaxis, and migration. Differences in expression of the neutrophil adherence molecules, L-selectin and CD11b/CD18 (Mac-1), have been previously demonstrated in cord blood and in very young infants (</= 48 h) compared with adults, but it is unknown for how long these differences persist. We measured surface expression of neutrophil L-selectin and CD11b using flow cytometry in healthy term human newborns from 24 h through 4 wk of age. We also measured levels of soluble L-selectin using an ELISA in neonates though the age of 4 wk. Compared with adults, neonates expressed significantly less L-selectin on resting neutrophils through 4 wk of age, with the lowest levels being at 24 h. Expression of L-selectin on the neutrophil after activation with N-formyl-methionyl-leucyl-phenylalanine was less in the neonate than in the adult (p < 0.05) for the first week of life. Soluble L-selectin showed a steady increase with age in the neonates. Soluble L-selectin was significantly lower in the 24-h neonate compared with the adult and was higher in the 4-wk neonate compared with the adult. CD11b expression was similar between neonates and adults on unstimulated neutrophils, but upon activation, the neonatal neutrophil demonstrated significantly lower up-regulation of CD11b on the neutrophil surface through 4 wk of age compared with adults (p < 0.05 for all ages except 1 wk). These findings that differences in expression of L-selectin and CD11b from that in adults persist throughout the neonatal period provide further evidence that these differences may play a role in the neutrophil defects observed during the neonatal period.

CD11b Antigen↗
PubMed2003

Association between heat shock protein 72 gene polymorphism and acute renal failure in premature neonates.

Heat shock protein (HSP)70 plays an important role in the ischemic tolerance of fetal and neonatal kidney. We have investigated the association of genetic polymorphisms of the constitutive HSP70 (HSP73) and the inducible HSP70 (HSP72) encoding genes with the risk of acute renal failure (ARF) in very low birth weight (VLBW) neonates. Thirty-seven VLBW neonates with ARF and 93 VLBW neonates without ARF were enrolled in the study. The presence of HSP72 (1267)AG and HSP73 (190)GC polymorphism was analyzed from dried blood samples by PCR and restriction length fragment polymorphism. Allelic prevalence was related to reference values obtained in 131 healthy adults. Stepwise binary logistic regression was applied to determine the independent effect of the established risk factors to the development of ARF. Sixteen of 37 VLBW neonates with ARF and 18 of 93 VLBW neonates without ARF were homozygous for HSP72 (1267)G allele (p </= 0.01). The association between HSP72 (1267)GG genotype and ARF remained at the level of significance (p = 0.05) when it was adjusted for established risk factors of neonatal ARF. Prevalence of HSP72 (1267)GG was also higher in VLBW neonates than in the reference population (p < 0.05) and in VLBW neonates with infant respiratory distress syndrome than in those without (p < 0.001). We found that in VLBW neonates carrying HSP72 (1267)GG genetic variation, which is associated with low inducibility of HSP72, the risk of ARF was increased. Therefore, VLBW neonates with (1267)GG might express less HSP72 and might be less protected against ARF.

Acute Kidney Injury↗
PubMed1987

Differential effects of neonatal and adult androgen exposure on the growth hormone secretory pattern in male rats.

The interactive effects of androgen exposure during neonatal and adult life on the pattern of GH secretion in adult male rats was investigated. Neonatal rats were orchidectomized or sham-operated on days 1-2 of life and injected immediately postoperatively with testosterone propionate (250 micrograms, sc) or vehicle. At 90-130 days of age the rats were bled every 20 min between 9 and 17 h from an indwelling intraatrial catheter. Some neonatally gonadectomized, testosterone- or vehicle-treated rats were also given depot testosterone (15 mg/kg, im) 5-10 days before blood sampling. Plasma GH concentrations were measured by RIA, and the pulsatile secretory patterns were analyzed by the PULSAR computer program. Neonatal orchidectomy resulted in a marked suppression (50-75%) of both the height and duration of GH secretory episodes, while baseline GH levels were higher in neonatally gonadectomized males than in sham-operated controls. Neonatal testosterone replacement therapy restored high amplitude GH pulses. However, the GH pulses of these animals were of significantly shorter duration and occurred more frequently, and baseline GH levels were markedly higher than those in intact male rats. In contrast, neonatally gonadectomized rats treated with testosterone both neonatally and during adulthood exhibited a GH pattern indistinguishable from that in normal males, with high amplitude and long-lasting (103 +/- 8 min) pulses at regular intervals (178 +/- 9 min). A similar masculine GH pattern was seen in neonatally gonadectomized rats given testosterone only during adult life. The present results indicate that high amplitude GH pulses can be induced by either neonatal or adult androgen exposure. However, while neonatal androgens irreversibly cause stimulation of overall GH secretion, only the continuous presence of androgens during adult life can induce a GH secretory pattern, consisting of large surges at regular 3-h intervals separated by a low baseline that is characteristic of normal male rats.

Aging↗