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1.
Early Hum Dev ; 93: 33-8, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26759989

RESUMO

AIMS: To determine whether the brain disturbances develop in late-onset intrauterine growth restriction (IUGR) before blood flow redistribution towards the fetal brain (detected by Doppler measurements in the middle cerebral artery and umbilical artery). Further, to evaluate predictive values of Doppler arterial indices and umbilical cord blood gases and pH for early functional and/or morphological brain disturbances in late-onset IUGR. STUDY DESIGN: This cohort study included 60 singleton term pregnancies with placental insufficiency caused late-onset IUGR (IUGR occurring after 34 gestational weeks). Umbilical artery resistance index (URI), middle cerebral artery resistance index (CRI), and cerebroumbilical (C/U) ratio (CRI/URI) were monitored once weekly. Umbilical blood cord samples (arterial and venous) were collected for the analysis of pO2, pCO2 and pH. Morphological neurological outcome was evaluated by cranial ultrasound (cUS), whereas functional neurological outcome by Amiel-Tison Neurological Assessment at Term (ATNAT). RESULTS: 50 fetuses had C/U ratio>1, and 10 had C/U ratio≤1; among these 10 fetuses, 9 had abnormal neonatal cUS findings and all 10 had non-optimal ATNAT. However, the total number of abnormal neurological findings was much higher. 32 neonates had abnormal cUS (53.37%), and 42 (70.00%) had non-optimal ATNAT. Furthermore, Doppler indices had higher predictive validity for early brain disturbances than umbilical cord blood gases and pH. C/U ratio had the highest predictive validity with threshold for adverse neurological outcome at value 1.13 (ROC analysis), i.e., 1.18 (party machine learning algorithm). CONCLUSION: Adverse neurological outcome at average values of C/U ratios>1 confirmed that early functional and/or structural brain disturbances in late-onset IUGR develop even before activation of fetal cardiovascular compensatory mechanisms, i.e., before Doppler signs of blood flow redistribution between the fetal brain and the placenta.


Assuntos
Encéfalo/fisiopatologia , Desenvolvimento Infantil , Retardo do Crescimento Fetal/diagnóstico por imagem , Insuficiência Placentária/diagnóstico por imagem , Encéfalo/crescimento & desenvolvimento , Encéfalo/patologia , Circulação Cerebrovascular , Feminino , Humanos , Recém-Nascido , Circulação Placentária , Gravidez
2.
J Matern Fetal Neonatal Med ; 29(9): 1520-4, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-26103779

RESUMO

OBJECTIVE: To determine whether as a result of an assumed advanced maturation late preterm twin infants have a more favorable perinatal outcome than singleton late preterm infants. METHODS: Over a 36-month period (from September 2011 to September 2014), 277 late preterm infants (153 from singleton and 124 from twin pregnancies) were hospitalised in NICU, University Hospital Center "Sisters of Mercy" Zagreb, Croatia, and were retrospectively studied by review of maternal and neonatal charts for gestational age, sex, birth weight, mode of delivery, 5-min Apgar score and for several outcome variables expected for preterm infants, until the day of discharge. RESULTS: There was statistically no significant difference in the incidence of any of the observed and compared outcomes, except in the incidence of phototherapy which was higher in singletons group (49.01 versus 13.7%, p < 0.0001). The mean birth weight, as expected, was smaller in the twin group. CONCLUSIONS: We found no evidence to support the traditional belief that twin late preterm infants have accelerated maturation and better neonatal outcome compared with singleton late preterm infants. Our findings suggest that late preterm twins have a prognosis similar to that of singleton late preterm infants born at the same gestational age.


Assuntos
Doenças do Prematuro/epidemiologia , Recém-Nascido Prematuro/crescimento & desenvolvimento , Gravidez de Gêmeos/fisiologia , Gêmeos/estatística & dados numéricos , Feminino , Humanos , Recém-Nascido , Masculino , Gravidez , Estudos Retrospectivos
3.
J Matern Fetal Neonatal Med ; 27(8): 844-50, 2014 May.
Artigo em Inglês | MEDLINE | ID: mdl-23981182

RESUMO

OBJECTIVE: The etiology of jaundice in otherwise healthy breastfed newborns that can present as early-onset exaggerated physiologic jaundice, or late breast milk jaundice (BMJ), is not yet entirely understood. This study tested the hypothesis that molecular marker for Gilbert's syndrome (GS), UGT1A1 TATA-box polymorphism, is associated with this disorders. METHODS: We have investigated the UGT1A1 polymorphism frequency and its relation to severity of hyperbilirubinemia and jaundice duration among 220 exclusively breastfed term newborns; 57 of them with non-physiologic hyperbilirubinemia (NH), and 163 with BMJ, and in 187 healthy controls. RESULTS: Significant differences in TA7/7 genotype frequency were established. The highest frequency was observed among the newborns with BMJ (42.0%), intermediate in the NH group (24.6%), while the controls had the lowest TA7/7 frequency (12.8%). Linear increase in TA7/7 frequency was observed depending on the duration of jaundice, peaking at 42.4% in newborns with the longest jaundice duration. Positive correlation between the serum bilirubin levels and the TATA-box length was established in all groups. CONCLUSION: This study provides evidence that UGT1A1 TATA-box polymorphism is an important risk factor for developing jaundice in term breastfed newborns, presented as either early non-physiologic hyperbilirubinemia or breast milk jaundice. These results further support the original Odell's idea of neonatal jaundice as an early presentation of GS.


Assuntos
Aleitamento Materno , Doença de Gilbert/genética , Glucuronosiltransferase/genética , Icterícia Neonatal/genética , Polimorfismo Genético , TATA Box/genética , Idade de Início , Estudos de Casos e Controles , Diagnóstico Precoce , Feminino , Frequência do Gene , Predisposição Genética para Doença , Idade Gestacional , Doença de Gilbert/diagnóstico , Doença de Gilbert/epidemiologia , Humanos , Recém-Nascido , Masculino , Regiões Promotoras Genéticas
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