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PubMed2006

Umbilical serum concentrations of chemokines (RANTES and MGSA/GRO-alpha) in preterm and term neonates.

BACKGROUND: The objective of this study was to explore the relationship between labor (preterm and term) and umbilical blood serum regulated on activation, normal T cell expressed and secreted (RANTES) and melanoma growth stimulatory activity/growth-related oncogene-a (MSGA/GRO-alpha) concentration, and to determine whether early sepsis and pneumonia are associated with changes in concentrations of the chemokines (RANTES and MSGA/GRO-alpha) in umbilical blood serum. METHODS: Umbilical blood was obtained from 67 neonates in the following groups: (i) preterm neonates with early sepsis; (ii) preterm neonates with pneumonia; (iii) non-infected preterm neonates; and (iv) full-term healthy neonates. RANTES and MGSA/GRO-alpha concentrations were determined by use of a commercially available immunoassay kit. RESULTS: Non-infected preterm neonates had lower RANTES concentrations than healthy term neonates. Preterm infected neonates (pneumonia or sepsis) did not have higher RANTES concentrations than non-infected preterm neonates. In contrast, non-infected preterm neonates had higher MSGA/GRO-alpha concentrations than full-term healthy neonates. And preterm neonates with sepsis had higher MGSA/GRO-alpha concentrations than preterm ones with pneumonia and non-infected preterm ones. CONCLUSIONS: Preterm neonates had constitutively lower RANTES concentrations than term ones and it seems that during infection RANTES concentrations did not increase. MGSA/GRO-a concentrations were constitutively higher in preterm than term neonates, and septic events further increased its concentrations in preterm neonates.

Bacteremia↗
PubMed1998

Longitudinal evaluation of salivary cortisol levels in full-term and preterm neonates.

The aim of the present study was to test the practicability of sequential cortisol determinations in saliva of low birth weight neonates and to evaluate the impact of systemic and inhaled glucocorticoid therapy on saliva concentrations of cortisol in preterm neonates with bronchopulmonary dysplasia (BPD). Salivary cortisol levels were measured by RIA in saliva samples from 10 full-term and 10 preterm healthy neonates and from 20 preterm neonates with BPD during systemic [dexamethasone (DEX); n = 10] or topical steroid therapy [budesonide (BUD); n = 10]. Saliva samples of each individual were collected on 3 consecutive days at 06.00, 12. 00, 18.00 and 24.00 h. Cortisol levels in saliva ranged from 0.8 to 60.6 nmol/l (median 6.5 nmol/l) in full-term neonates, from 0.6 to 52.1 nmol/l (median 5.5 nmol/l) in preterm neonates, from 0.4 to 14. 0 nmol/l (median 1.0 nmol/l) in preterm neonates treated with DEX and from 0.4 to 15.2 nmol/l (median 2.5 nmol/l) in preterm neonates treated with BUD. Autocorrelation analysis revealed a distinct endogenous cortisol rhythm in 2 of the 10 healthy full-term neonates and in 3 of the 10 healthy preterm neonates with a wavelength of 12-30 h. Salivary cortisol levels in preterm neonates treated with DEX or BUD were significantly lower than those measured in healthy preterm neonates. These results demonstrate that the measurement of salivary cortisol levels is a reliable and practicable way of assessing adrenal function in full-term and preterm neonates. This study also shows for the first time that some neonates display an endogenous cortisol rhythm which is not coupled to the exogenous day/night cycle. Furthermore, systemic and nebulized glucocorticoids suppress adrenal function in low-birth-weight neonates. After treatment these children should be closely monitored for potential adrenal insufficiency.

Administration, Topical↗
PubMed1985

Imprinting of growth hormone secretion, body growth, and hepatic steroid metabolism by neonatal testosterone.

The influence of endogenous sex steroids and exogenous testosterone treatment on pulsatile GH secretion, body weight, longitudinal bone growth, and hepatic steroid metabolism was studied in male and female adult rats. Blood samples were obtained from the tip of the tail, and maximum and minimum GH levels were determined in individual rats to evaluate pulse heights and baseline levels. Longitudinal bone growth was measured using the intravital marker tetracycline, and hepatic steroid metabolism was evaluated by determining the enzyme activities of 16 alpha-hydroxylase and 5 alpha-reductase. Neonatal, but not prepubertal, gonadectomy of male rats suppressed maximum and mean plasma GH levels during adult life. The body weight and the rate of longitudinal bone growth were also decreased. Testosterone treatment neonatally reversed all of these effects. Neonatal gonadectomy of male rats also caused an elevation of minimum plasma GH levels, an effect, however, which was not reversed by testosterone replacement during neonatal life. Neonatally gonadectomized females treated with testosterone neonatally or during adult life increased their maximum and decreased their minimum GH levels. Their longitudinal bone growth was increased. The body weight of these rats was increased by neonatal, but not adult, testosterone treatment. There was no effect of neonatal ovariectomy on plasma GH levels in 3- to 4-month-old female rats. However, neonatal ovariectomy did increase the maximum and mean plasma GH levels immediately postpubertally, suggesting that the effect of the ovaries on GH secretion differs among mature female rats of different ages. Prepubertal gonadectomy of male rats feminized their hepatic steroid metabolism by decreasing 16 alpha-hydroxylase and increasing 5 alpha-reductase activities. Neonatal gonadectomy caused an even more pronounced feminization, which was partly reversed in rats given testosterone replacement therapy neonatally. In neonatally gonadectomized female rats, treatment with testosterone during adult life increased 16 alpha-hydroxylase and decreased 5 alpha-reductase to levels seen in intact male rats. The present results indicate that neonatally secreted testicular androgens imprint the high amplitude pulses characteristic of GH secretion in adult male rats. Neonatal androgens also stimulate somatic growth and partially account for the masculinized hepatic steroid metabolism in the adult animal. It is proposed that imprinting of the GH secretory pattern contributes to the influence of neonatal testicular androgens on body growth and hepatic steroid-metabolizing enzymes.

Animals↗
PubMed1987

Inhibitory effect of the ovaries on neonatal androgen imprinting of growth hormone secretion in female rats.

The effect of neonatal androgen treatment on the GH secretory pattern was examined in intact and ovariectomized adult female rats. Neonatal ovariectomy or sham operation was performed at 1-2 days of age; thereafter, the animals were immediately given testosterone propionate (250 micrograms) or vehicle. Other rats, also treated neonatally with testosterone, were ovariectomized 15-22 days before blood sampling. Plasma GH was measured in blood samples obtained from indwelling intraatrial cannulae every 20 min for 8 h when the animals were 100-140 days old. Plasma GH secretory patterns were analyzed by a pulse analysis computer program (PULSAR). Neonatal testosterone treatment did not affect the GH secretory pattern of female rats with intact ovaries. In contrast, neonatal androgen treatment enhanced GH pulse height as well as mean GH concentration in neonatally ovariectomized female rats to levels comparable to those in intact male rats. Neonatal testosterone administration also significantly increased GH pulse height and mean plasma GH concentration in female rats that were ovariectomized during adulthood. However, the GH secretory pattern of ovariectomized female rats given testosterone neonatally still differed markedly from that of normal males, in that GH pulses occurred less regularly and baseline levels were higher. Pituitary GH content and concentration in neonatally ovariectomized female rats were increased to levels indistinguishable from those in male rats by neonatal testosterone treatment. No significant effect of neonatal testosterone was observed in sham-operated females. Neonatal ovariectomy decreased basal plasma GH levels, but did not affect plasma GH pulse height or pituitary GH levels. The serum estradiol concentration was markedly decreased in ovariectomized female rats, but was unchanged in sham-operated rats given neonatal testosterone, raising the possibility that serum estradiol secretion mediated the antagonistic effect of the ovaries on neonatal androgen imprinting. These results indicate that the presence of ovaries can prevent the stimulatory effect of neonatal androgen exposure on GH storage and secretion in adult female rats.

Androgens↗
PubMed2001

The promoter polymorphism of the interleukin-6 gene regulates interleukin-6 production in neonates but not in adults.

In the promoter region of the IL-6 gene there is a single base exchange (G --> C) polymorphism at position -174. Recent findings suggest that this polymorphism may affect the transcription rate of the IL-6 gene and IL-6 plasma levels. To analyse its biological significance, we examined IL-6 plasma levels in cord blood and IL-6 production by neonatal cells after LPS-stimulation in relation to the presence of the IL-6G and IL-6C alleles. We hypothesized that since healthy neonates lack a previous exposure to exogenous antigens, their cytokine production could be genetically regulated. We also assumed that the normal labour-related stress could provide a physiological stimulus for IL-6 production. Cord blood was collected from 50 healthy, full-term neonates after normal vaginal delivery (VD) and from 42 healthy, full-term neonates after elective caesarean section (ECS). Adult samples were obtained from 450 healthy adult controls. The -174 polymorphism was analysed using PCR. IL-6 plasma levels and in vitro IL-6 production were measured using an ELISA method. Generally, IL-6 plasma levels in neonates were significantly higher than those in adults (neonates born by VD versus adults p < 0.001 and neonates born by ECS versus adults p < 0.001); the median value for neonates born by VD was 11.4 pg/ml (4.5-45.9), for neonates born by ECS 2.9 pg/ml (1.9-6.4) and for adults, 1.2 pg/ml (0.7-2.0). Surprisingly, cord blood IL-6 levels after VD differed significantly from those after ECS (p < 0.001). An analysis was carried out to ascertain if there was a genetic association between different IL-6 genotypes and IL-6 plasma levels in neonates. In the group of VD neonates with the CC genotype, non-carriers of the G allele, secreted significantly more IL-6 than carriers of the G allele (p < 0.03); 21.4 pg/ml (9.5-81.3) and 9.6 pg/ml (3.5-36.2) respectively. In line with this, ECS newborns with the CC genotype had higher IL-6 plasma levels than carriers of the G allele (p < 0.02); respective median values were 6.3 pg/ml (2.2-12.9) and 2.7 pg/ml (1.7-4.1). These findings were also supported when in vitro IL-6 production by neonatal mononuclear cells was compared carriers of the G allele and non-carriers of the G allele. IL-6 levels were significantly lower in carriers of the G allele than in non-carriers (p < 0.04); respective median values were 6,980 pg/ml (4,175-16,800) and 17,425 pg/ml (11,400-33,900). In vivo or in vitro production of IL-6 of adult controls was not associated with the IL-6 -174 polymorphism. The difference between cord blood IL-6 levels after VD and after ECS suggests that normal labour-related stress induces IL-6 production. Our data also suggest that the -174 polymorphism of the IL-6 gene participates in the regulation of IL-6 responses in both groups of neonates. Furthermore, the naive IL-6 response of stimulated neonatal cells is associated with the -174 polymorphism of the IL-6 gene. In healthy adults, the regulation of IL-6 responses differs from that of healthy neonates, since baseline and inducible IL-6 levels in adults were not associated with this polymorphism. This indicates that the genetic regulation of IL-6 production can be observed in naive cells, while in adult cells previous contact with exogenous antigens probably modifies their responses.

Adult↗
PubMed1986

Deformability and intrinsic material properties of neonatal red blood cells.

Whole cell and membrane deformability are essential for red blood cell (RBC) survival and for effective blood flow. Neonatal RBCs display several specific properties (eg, large size, high hemoglobin F) that could influence their deformation characteristics and contribute to their shortened life span. The present study was designed to compare selected rheologic properties (cellular deformability, pressure required to aspirate RBC into micropipettes, static and dynamic viscoelastic material properties) of neonatal and adult RBCs. RBC deformability, as studied by a rheoscope, was similar for neonates and adults over a shear stress range of 2.5 to 500 dyn/cm2. The pressure required to aspirate RBCs completely into 3.3-micron diameter pipettes was 129 +/- 87 dyn/cm2 for neonatal RBCs and 71 +/- 37 dyn/cm2 for adult RBCs. The aspiration pressure for neonatal and adult RBCs increased with increasing RBC volume, suggesting that the increased mean aspiration pressure for neonatal RBCs resulted from their larger volume. When RBCs with same volume and diameter were compared, the aspiration pressure tended to be smaller for neonatal RBCs than for adult cells. To characterize material properties determining RBC deformability, we measured membrane extensional (shear) and bending elastic moduli, the time constant for elastic recovery from extensional deformation and hemoglobin viscosity (ie, cytoplasmic viscosity) of neonatal and adult RBCs. Membrane surface viscosity and time constant for recovery from bending deformation were calculated. The extensional and bending moduli of neonatal RBCs were slightly smaller (10% and 16%, respectively) compared with adult cells. This suggests that the static resistance of neonatal RBC membrane to deformation and failure in response to a given force is slightly smaller. The time constant for recovery from extensional deformation of neonatal RBCs was larger by 14%, compared with adult cells. The time constant for bending deformation related to the RBC diameter and surface area was increased by 18% in the neonates. Membrane surface viscosity and hemoglobin viscosity were similar for both cell types. These results indicate that the deformability and viscoelastic properties of neonatal RBCs deviate only slightly from those of adult RBCs and that the increased aspiration pressure of neonatal RBCs is solely due to their large size. Some of the specific deformation characteristics observed in this study (increased aspiration pressure, decreased resistance to elastic deformation) may contribute to the shortened life span of neonatal RBCs.

Adult↗
PubMed2005

Detection and clinical evaluation of antineutrophil antibodies in neonates who had a blood transfusion or exchange transfusion.

BACKGROUND: The aim of this study was to detect and investigate the clinical effects of antineutrophil antibodies in neonates who had received a blood transfusion or exchange transfusion. METHODS: Venous blood samples were drawn from 34 neonates at pretransfusion (sample 0), immediately after transfusion (sample 1), 2-3 weeks (sample 2) and 8-12 weeks (sample 3) after transfusion. Ten healthy neonates were in the control group. Antineutrophil antibodies were detected using flow cytometric assay. RESULTS: Antineutrophil antibody was detected in the sera of 20 (58.8%) neonates in the study group. Of these 20 neonates, nine had antineutrophil antibodies in serum samples 0, 1 and 2, which were probably due to the passive transfer of maternal antibodies. Nine neonates had antineutrophil antibodies in serum samples 1 and 2, which were probably due to neutrophil antibodies being present in the donor's blood. In two neonates, antineutrophil antibodies were not detected in samples 0 and 1, but appeared in sample 2, which were probably actively produced by the neonates. All of the antineutrophil antibodies disappeared in the serum samples, except in one neonate. Only one preterm newborn developed neutropenia, which resolved spontaneously in a week. The presence of antineutrophil antibody in transfused neonates was significantly higher than in non-transfused neonates. CONCLUSIONS: The presence of neutrophil specific antibodies in transfused neonates is not rare and antineutrophil antibodies may be found more often in transfused neonates compared to non-transfused neonates. The clinical significance of those antibodies needs to be assessed since they are transient and their clinical effects are not evident.

Anemia, Neonatal↗
PubMed1993

Relationship between periventricular intraparenchymal echodensities and germinal matrix-intraventricular hemorrhage in the very low birth weight neonate.

The pathogenesis of the periventricular intraparenchymal echodense lesion (IPE) observed in association with germinal matrix-intraventricular hemorrhage (GM-IVH) in premature neonates is unclear. The objectives of this study were to determine (1) the temporal characteristics of GM-IVH and IPE, (2) the basic characteristics of the IPE, and (3) the relationship of clinical events, including surfactant administration, to IPE. One hundred twenty-four neonates of less than 1250 g birth weight were prospectively evaluated. IPE was defined as an echodensity greater than 1 cm in diameter by cranial sonography. Fifteen (12%) neonates developed IPE in association with GM-IVH (group 1); 33 neonates developed GM-IVH only (group 2) and 76 neonates without GM-IVH served as comparison group (group 3). IPE was essentially an asymmetrical lesion; both sides of cerebrum were equally affected. The lesion was diffuse in 9 neonates and focal in 5. IPE occurred both early, at 36 hours or before (n = 8), and later, ie, between 48 and 96 hours (n = 6). In one neonate IPE was diagnosed at autopsy. GM-IVH and IPE were noted simultaneously in neonate with the earlier onset IPE (diagnosed within 36 hours); GM-IVH preceded the IPE by 6 to 48 hours when the lesion was of a later onset. Surfactant was administered to 13 (87%) group 1, 24 (73%) group 2, and 35 (46%) group 3 neonates. Pulmonary hemorrhage developed in 9 (60%) of group 1, 3 (9%) group 2, and no group 3 neonates. Symptomatic patent ductus arteriosus occurred in 12 (75%) group 1, 15 (45%) group 2, and 15 (20%) group 3 neonates. The onset of symptoms associated with patent ductus arteriosus was earlier in group 1 vs group 2 or group 3 neonates, ie, 70 vs 172 hours. Nine (60%) group 1 neonates, 6 (18%) group 2, and 5 (7%) group 3 neonates died. The cranial sonogram was markedly abnormal in all 6 group 1 survivors. Stepwise polytomous logistic regression indicated that birth weight, gestational age, and emergent cesarean section were the best predictors of GM-IVH + IPE.(ABSTRACT TRUNCATED AT 250 WORDS)

Apgar Score↗
PubMed2005

Genetic differences in the production of male neonates in Daphnia magna exposed to juvenile hormone analogs.

We studied the susceptibility of three genetically different strains of the cyclical parthenogen Daphnia magna (Cladocera, Crustacea) in producing male neonates following exposure to juvenile hormone analogs. In experiment 1, NIES, Clone A, and Belgium A strains were exposed to the insect growth regulators (IGRs) fenoxycarb or epofenonane in a 21-day reproduction experiment. Fenoxycarb exposure decreased the total number of neonates and increased production of male neonates in a concentration-dependent manner in the NIES strain. The decrease in the total number of neonates was so great in Clone A following fenoxycarb exposure that male neonates were not observed, even at the highest concentration, where the total number of neonates was only 2% of the control. In the Belgium A strain, male neonates were observed at a rate of about 20% following exposure to the highest fenoxycarb concentration, but the total number observed was small. Epofenonane did not decrease reproduction in the NIES and Belgium A strains as dramatically as did fenoxycarb, but the neonatal sex ratio changed in a concentration-dependent manner. Although the ratio of males was as low as about 10%, induction of male neonates was also observed in Clone A following epofenonane exposure. In experiment 2, gravid females were exposed to high concentrations (5 or 10 microg/l) of fenoxycarb or pyriproxyfen for 12h. These treatments induced the production of male neonates in all strains, with a small decrease in the total number of neonates. Although induction of male neonates by juvenile hormones and their analogs was universal among genetically different strains, care is needed in interpreting the results of the 21-day reproduction tests, because decreased numbers of neonates at higher concentrations could obscure the presence of male neonates.

Animals↗
PubMed1996

Reticulated platelet values in normal and thrombocytopenic neonates.

OBJECTIVES: Reticulated platelets (RPs) are newly synthesized platelets with increased ribonucleic acid content. The percentage of RPs is elevated in adults with thrombocytopenia as a result of increased platelet destruction. The objectives of this study were to determine normal RP values in neonates at birth and to determine whether neonates with thrombocytopenia as a result of increased platelet destruction have an increased percentage of RPs. STUDY DESIGN: The RP percentages were measured at birth in 89 neonates without thrombocytopenia in three gestational age groups (<30,30 to 36, and >36 weeks), six neonates with immune thrombocytopenia, and one neonate with thrombocytopenia as a result of decreased platelet production. RESULTS: The RP percentages in neonates without thrombocytopenia >36 weeks and 30 to 36 weeks of gestation were 4.0% +/- 2.4% (mean +/- SD) and 4.6% +/- 1.7%, respectively, similar to values reported in healthy adults. Neonates younger than 30 weeks of gestation had significantly higher RP percentages (8.8% +/- 5.1%) than older neonates (p </= 0.0001). Term neonates with immune thrombocytopenia had significantly higher RP percentages (38.3% +/- 23.1%) than term neonates without thrombocytopenia (p = 0.0001), with no overlap in RP values. A lower RP percentage (1.5%) and significantly lower absolute RP count were measured in the one neonate with decreased platelet production. CONCLUSIONS: These preliminary data establish normal RP percentages in term and preterm neonates at birth and demonstrate elevated RP percentages in neonates with immune platelet destruction. The RP values may be helpful in evaluating the causes of neonatal thrombocytopenia.

Blood Platelet Disorders↗
PubMed1998

Neonatal morbidity and mortality associated with triplet pregnancy.

OBJECTIVE: To compare neonatal morbidity and mortality in a large cohort of triplet pregnancies with singleton and twin neonates managed at a single tertiary center over a short time. METHODS: Records from all triplet pregnancies managed and delivered from 1992 to 1996 were reviewed for neonatal outcome data. Pregnancies delivered before 20 weeks' gestation and neonates with lethal congenital anomalies were excluded. The comparison group comprised all singleton and twin neonates managed in the same neonatal intensive care unit (NICU) during the same period. RESULTS: During the 5-year period, 55 triplet pregnancies and their resulting 165 neonates were managed and delivered at this center. Their outcomes were compared with those of 959 singleton and 357 twin neonates born at similar gestational ages. The median gestational age at delivery for triplets was 32.1 weeks, and 149 of the 165 infants were admitted. Sixteen triplet neonates were not admitted to our neonatal intensive care unit, 12 because of previable gestational age, three because of stillbirth, and one because of a lethal congenital anomaly. The crude perinatal mortality rate in triplets was 121 per 1000 births, and there was no significant difference in outcome based on triplet birth order. There were no significant differences in survival rates between singleton, twin, and triplet neonates, with an overall neonatal survival of 95%, 95%, and 97%, respectively. The only significant differences in morbidity were an increased incidence of mild intraventricular hemorrhage (relative risk [RR] 6.20; 95% confidence interval [CI] 2.64, 14.61), mild retinopathy of prematurity (RR 20.05; 95% CI 3.59, 111.79), and severe retinopathy of prematurity (RR 46.69; 95% CI 6.25, 348.85) in triplets compared with singletons, and severe retinopathy of prematurity (RR 6.83; 95% CI 1.24, 37.56) in triplets compared with twins. CONCLUSION: When stratified by gestational age, triplet neonates delivered at 24-34 weeks' gestation have similar outcomes as singleton and twin neonates, with the only clinically significant difference being an increased incidence of retinopathy of prematurity in triplets.

Female↗
PubMed2002

Comparison of single and repeated antenatal corticosteroid therapy to prevent neonatal death and morbidity in the preterm infant.

INTRODUCTION: In the case of threatened preterm delivery, repeat administration of antenatal corticosteroids is a common practice in women who have not delivered 7-14 days after the first course of corticosteroids. However, the benefits of this policy as compared to single-course administration have not been proven. AIM: Our purpose was to compare neonatal death and morbidity after repeat antenatal courses of corticosteroids with neonatal death and morbidity after a single course. METHODS: We performed a cohort study with matched controls. Neonates treated with repeat antenatal courses of corticosteroids were matched with neonates treated with a single course. Matching criteria were sex, single or multiple gestation, route of delivery, gestational age at delivery and year of birth. Intrauterine growth-restricted infants were matched separately. We excluded neonates with congenital malformation and neonates with an unknown number of antenatal corticosteriod courses. Outcome measures were the incidences of neonatal death, respiratory distress syndrome, intraventricular haemorrhage and necrotizing enterocolitis. RESULTS: From the neonates treated with two or three courses of antenatal corticosteroids, 56 appropriate grown neonates and 24 intrauterine growth-restricted neonates could be matched. The incidences of neonatal death, respiratory distress syndrome, intraventricular haemorrhage and necrotizing enterocolitis did not show statistically significant differences after single and repeat courses of corticosteroids. Appropriate grown and intrauterine growth-restricted neonates showed the same results. CONCLUSION: From our study, it can be concluded that in preterm neonates, repetition of antenatal corticosteroids seems not to improve neonatal outcome.

Adult↗
PubMed2005

Why do neonates die in rural Gadchiroli, India? (Part II): estimating population attributable risks and contribution of multiple morbidities for identifying a strategy to prevent deaths.

OBJECTIVES: The understanding about why neonates die in rural areas in developing countries is limited. In the first year (1995 to 1996) of the field trial of home-based neonatal care in rural Gadchiroli, India, we prospectively observed a cohort of neonates in 39 villages. In Part I of this article, we presented the primary causes of death. The data were further analyzed: To estimate the population attributable risk (PAR) of death for the main causes of neonatal mortality. To evaluate the effect of a multiplicity of morbidities and to identify which morbidity combinations cause neonatal deaths. To develop a hypothesis about how best to reduce neonatal mortality. STUDY DESIGN: We analyzed the observational data by logistic regression to estimate the PAR of death for six major morbidities. The effect of the number of morbidities per neonate on case fatality (CF) was estimated. Then we identified the main combinations of morbidities as the component causes leading to death. We estimated the excess deaths attributable to sepsis. RESULTS: This cohort included 763 neonates among whom 40 neonatal deaths occurred. Six major morbidities were associated with the following proportion of deaths: preterm, 62.5%; sepsis, 60%; intrauterine growth restriction (IUGR), 27.5%; asphyxia, 25%; hypothermia, 22.5%, and feeding problems, 15%. The estimated PARs were: preterm, 0.74; IUGR, 0.55; sepsis, 0.55; asphyxia, 0.35; hypothermia, 0.08, and feeding problems, 0.04. The CF associated with the number of morbidities per neonate was: with no morbidity, 0.3%; one morbidity, 2.1%; two morbidities, 15.3%; three or more morbidities, 41.4% (p<0.001). In all, 82.5% of all deaths occurred in neonates with two or more morbidities. The proportion of total deaths associated with only preterm was 7.5%, and with only IUGR was 2.5%; however, with the main morbidity combinations it was preterm+sepsis, 35%; IUGR+sepsis, 22.5%; preterm+asphyxia, 20%; preterm+hypothermia, 15%; and preterm+feeding problem, 12.5%. The % CF with low birth weight (LBW) <2500 g alone was 5.2% and with infection alone was 1.9%, but with LBW+infection it was 31.9%. The estimated excess deaths caused by sepsis over and above LBW was 44% of the total deaths. CONCLUSIONS: Preterm and IUGR are ubiquitous components, but usually not sufficient to cause death. Most deaths occur due to a combination of preterm or IUGR with other comorbidities. If preterm birth or IUGR cannot be prevented, the strategy should be to ensure neonatal survival by addressing comorbidities, that is, infections, asphyxia, hypothermia, and feeding problems in that order of priority. We hypothesize that the prevention and/or management of neonatal infections will reduce neonatal mortality by 40 to 50%.

Cause of Death↗
PubMed2002

Myeloid hematopoietic growth factors and their role in prevention and/or treatment of neonatal sepsis.

Sepsis continues to be an important cause of morbidity and mortality among both full-term and preterm infants, secondary to an immaturity in neonatal host defense. The incidence of neonatal sepsis ranges from 30% in very low birth weight infants to 0.4% in preterm neonates and 0.1% in term neonates. The dysregulation of the expression and production of hematopoietic cytokines in the neonate contributes to quantitative and qualitative deficiencies in neonatal myeloid progenitor activity and decreased availability and function of mature effector neutrophils. These abnormalities contribute in large part to the increased incidence and mortality associated with neonatal sepsis. In this review, we have summarized and analyzed the studies investigating the dysregulation, expression and production of myelopoietic growth factors in neonates, the preclinical in vivo effects of myelopoietic growth factors in neonatal animals, the preclinical in vivo effects of myelopoietic growth factors during experimental sepsis in neonatal animals, the in vitro effects of growth factors on human neonatal phagocytic immunity, and clinical results of myelopoietic growth factors in human neonates. Future studies should be focused on investigating other abnormalities of neonatal host defense and multiple and simultaneous approaches to circumvent identified defects to attempt to reduce both the incidence and severity of neonatal host defense.

Adult↗
PubMed2000

Role of graft interleukin-10 expression in the tolerogenicity of neonatal skin allografts.

BACKGROUND: Allografts of skin from neonatal donors survive longer than those from adult donors and can induce tolerance in mice that are treated with short-term immunosuppression. Neonatal (< or =24 hr old) epidermal cells (EPC) secrete high levels of interleukin-(IL) 10 and include abundant class II- immature Langerhans cells (LC). In this study, the role of IL-10 in the tolerogenicity of neonatal skin grafts was examined. METHODS: After a preliminary experiment established that tolerogenesis by neonatal grafts could be supported by monoclonal antilymphocyte antibodies, B10.A(5R) recipients were immunosuppressed with anti-CD4 plus anti-CD8 (days 0, +2) and adult C57B1/6 bone marrow cells (day +7). Recipients were grafted with adult or neonatal C57B1/6 skin from wild-type or IL-10 deficient ("knockout" donors). EPC from wild-type and knockout neonatal skin were compared by flow cytometry, before and after 48 hr culture, to adult cells in terms of class II and costimulatory molecule expression. RESULTS: Grafts from knockout neonates survived longer than those from adult donors (median survival, MST=81 vs. 61 days), but not as long as those from wild-type neonates (MST=100 days; P<0.05). As with normal neonatal EPC, neonatal knockout EPC expressed little class II antigen. Both types of neonatal EPC acquired class II in culture, and up-regulated CD80 and CD86 in an adult pattern, but failed to up-regulate class II antigen to the high level seen among cultured adult cells. CONCLUSIONS: The tolerogenicity of neonatal skin grafts derives in part from natural expression of IL-10 by the graft. Another possible contribution to tolerogenicity may be the inability of neonatal antigen presenting cells to up-regulate class II fully. Low expression of class II by neonatal cells is not attributable to epidermal IL-10 secretion.

Animals↗
PubMed2006

Survival rates and mode of delivery for vertex preterm neonates according to small- or appropriate-for-gestational-age status.

OBJECTIVE: The goal was to characterize the relationship between cesarean section delivery and death for preterm vertex neonates according to intrauterine growth. METHODS: Maternal and infant data from the National Center for Health Statistics for 1999 and 2000 were analyzed. Neonates with gestational ages of 26 to 36 weeks were characterized as small for gestational age (<10th percentile) or appropriate for gestational age (10th to 90th percentile). Mortality rates at 28 days and relative risks were calculated for each gestational age group according to mode of delivery. RESULTS: Cesarean section rates were higher for small-for-gestational-age neonates compared with appropriate-for-gestational-age neonates, most prominently from 26 weeks to 32 weeks of gestation, at which small-for-gestational-age neonates had cesarean section rates of 50% to 67%, whereas appropriate-for-gestational-age neonates had rates of 22% to 38%. Small-for-gestational-age neonates at gestational ages of <31 weeks had increased survival rates associated with cesarean section, whereas small-for-gestational-age neonates at >33 weeks and appropriate-for-gestational-age neonates overall had decreased survival rates associated with cesarean section. After adjustment for sociodemographic and medical factors, the survival advantage for small-for-gestational-age neonates at gestational ages of 26 to 30 weeks persisted. CONCLUSIONS: Cesarean section delivery was associated with survival for preterm small-for-gestational-age neonates but not preterm appropriate-for-gestational-age neonates. We speculate that vaginal delivery may be particularly stressful for small-for-gestational-age neonates. We found no evidence that prematurity alone is a valid indication for cesarean section for preterm appropriate-for-gestational-age neonates.

Adult↗
PubMed1997

Renal pyelectasis in fetuses and neonates: diagnostic value of renal pelvis diameter in pre- and postnatal sonographic screening.

OBJECTIVE: Pre- and postnatal pyelectasis detected by sonographic screening is of questionable pathologic importance. Therefore, we defined the natural course and diagnostic value of renal pelvis diameter (RPD) during fetal life and the neonatal period as such dilatation was revealed on routine sonography. MATERIALS AND METHODS: Routine sonography in pregnant women was obtained between gestational weeks 22 and 30. Sonograms were obtained for 1021 fetuses, of which 15 could not be followed up as neonates. The remaining 1006 fetuses also underwent neonatal sonography. All neonates with an RPD larger than 5 mm were followed up sonographically. Neonates with an RPD larger than 9 mm or persistent widening (> 5-9 mm) were examined by voiding cystourethrogram, radionuclide renogram, or both. RESULTS: Thirty fetuses (3%) had an RPD larger than 5 mm. Nine of these fetuses also had an RPD larger than 5 mm as neonates. Of these nine neonates, one had bilateral grade II vesicoureteric reflux (VUR) and two had urinary tract obstructions (one posterior urethral valve and one ureteropelvic junction obstruction). Forty-nine neonates whose results on fetal sonograms had been normal showed an RPD larger than 5 mm on neonatal sonograms. Grade III VUR was found in one boy, and ureteropelvic junction obstruction was found in two boys. The kidneys of 54 neonates who showed an RPD larger than 5 mm without urinary tract obstruction were followed up until an RPD of 0-5 mm was evident. RPD normalized within 1 year of birth, whether VUR was present or not. Symptomatic urinary tract infection was diagnosed in 17 infants who had no renal pelvis dilatation seen on pre-or postnatal screening during the observation period. Seven of the 17 neonates had VUR. Conversely, none of the infants with pre- postnatal dilatation presented with symptomatic urinary tract infection. However, in one neonate an asymptomatic urinary tract infection without VUR was diagnosed by routine urinalysis. CONCLUSION: In our study, we linked renal pelvis dilatation on pre- and postnatal sonograms to obstructive uropathies rather than to vesicoureteric reflux. Prenatal sonography proved less sensitive than postnatal sonography in revealing obstructive uropathies. An RPD smaller than 10 mm on neonatal sonography was of no pathologic significance because renal collecting systems normalized spontaneously in all infants within 1 year of birth. These neonates and infants had no significant risk for urinary tract infection and did not need further evaluation.

Dilatation, Pathologic↗
PubMed2003

The burden of disease from neonatal mortality: a review of South Asia and Sub-Saharan Africa.

OBJECTIVE: To assess the burden of neonatal mortality in two developing regions. DESIGN: Review of secondary data collated through literature review. SETTING: Community and facility based studies and national health surveys. POPULATION: Neonatal (<28 days) population of South Asia and Sub-Saharan Africa. METHODS: Data on neonatal mortality were gathered from peer-reviewed literature, reports of the Demographic and Health Surveys and websites of country-based organisations. The base year for this study is 1995. For each country, a weighted mean neonatal mortality rate was calculated and the total number of neonatal deaths estimated. Country data were summarised over each region to estimate annual regional neonatal deaths and rates. The burden of disease from neonatal mortality was determined using a summary measure of health--healthy life years. MAIN OUTCOME MEASURES: Numbers of deaths and healthy life years (HeaLYs). RESULTS: Neonatal mortality rate for South Asia ranged from 41.9 to 56.9 per 1000 live births for 1995. Sri Lanka was an exception with a neonatal mortality rate between 16.3 and 18.6 per 1000 live births. The estimated regional neonatal mortality rate for South Asia was 46.27 per 1000 live births for 1995. There was a significant lack of data from Sub-Saharan Africa, resulting in highly variable neonatal mortality rates, ranging from 13 per 1000 live births in Kenya to 108 per 1000 live births in Senegal. The mean regional neonatal mortality for Sub-Saharan Africa for 1995 was estimated at 38.8 per 1000 live births. CONCLUSION: The burden of neonatal mortality in only these two regions of the developing world represents more than 2 million annual deaths. A call for greater investments in neonatal research and health programs is a logical extension to this review of evidence.

Adult↗