RESUMO
OBJECTIVE: To evaluate the usefulness of serum lipid peroxide (LPO) for hypoxic ischemic encephalopathy (HIE) in full-term neonates. STUDY DESIGN: Diagnostic test evaluation forming three groups: (1) healthy full-term neonates (n=59), (2) at-risk full-term neonates without HIE (n=57) and (3) at-risk full-term neonates with HIE (n=57). HIE diagnosis was made using the Finer clinical classification at 48 h after birth. Serum LPO was taken at 4 h after birth and determined by spectrophotometry. RESULT: One hundred seventy-three full-term neonates were studied. Fifty-one of the at-risk full-term neonates with HIE (51/57) had high serum LPO and two of the at-risk full-term neonates without HIE (2/57) (P<0.001). Serum LPO level had 89% sensitivity, 96% specificity, 96% positive predictive value, 90% negative predictive value, 24 positive probability ratio, 0.11 negative probability ratio and 92% diagnostic usefulness. CONCLUSION: Serum LPO level could be a useful test for early diagnosis of HIE in full-term neonates.
Assuntos
Asfixia Neonatal/sangue , Asfixia Neonatal/diagnóstico , Hipóxia-Isquemia Encefálica/sangue , Hipóxia-Isquemia Encefálica/diagnóstico , Peróxidos Lipídicos/sangue , Índice de Apgar , Estudos de Coortes , Feminino , Humanos , Recém-Nascido , Unidades de Terapia Intensiva Neonatal , Masculino , Valor Preditivo dos Testes , Fatores de Risco , EspectrofotometriaRESUMO
OBJECTIVES: HIF-1 alpha (hypoxia-inducible factor-1 alpha) mediates the responses of mammalian cells to hypoxia/ischemia by inducing the expression of adaptive gene products (e.g., vascular endothelial growth factor (VEGF) and erythropoietin (EPO)). Persistent pulmonary hypertension of the newborn (PPHN) and cyanotic congenital heart disease (CCHD) are common neonatal diseases considered as paradigms of hypoxemia. Since the expression HIF-1 alpha, VEGF and EPO in newborns diagnosed with these diseases has yet to be studied, we set out to define the expression of these genes in peripheral blood from newborn infants diagnosed with PPHN and CCHD. DESIGN AND METHODS: The mRNA transcripts encoding HIF-1 alpha, VEGF and EPO were measured by RT-PCR in healthy newborn infants and infants diagnosed with PPHN and CCHD. RESULTS: An important increase in HIF-1 alpha expression was observed in both pathological conditions, accompanied by significant increases in VEGF and EPO expression when compared to healthy infants. CONCLUSIONS: HIF-1 alpha mRNA expression increases in newborn infants with PPHN or CCHD, as does the expression of its target genes VEGF and EPO.
Assuntos
Eritropoetina , Cardiopatias , Subunidade alfa do Fator 1 Induzível por Hipóxia , Hipóxia , Síndrome da Persistência do Padrão de Circulação Fetal , Fator A de Crescimento do Endotélio Vascular , Eritropoetina/sangue , Eritropoetina/genética , Cardiopatias/sangue , Cardiopatias/congênito , Cardiopatias/fisiopatologia , Humanos , Hipóxia/sangue , Hipóxia/patologia , Subunidade alfa do Fator 1 Induzível por Hipóxia/sangue , Subunidade alfa do Fator 1 Induzível por Hipóxia/genética , Lactente , Recém-Nascido , Síndrome da Persistência do Padrão de Circulação Fetal/sangue , Síndrome da Persistência do Padrão de Circulação Fetal/genética , Fator A de Crescimento do Endotélio Vascular/sangue , Fator A de Crescimento do Endotélio Vascular/genéticaRESUMO
INTRODUCTION: There is some evidence that retinopathy of prematurity is due to excessive oxidative stress on the developing retina caused by high free radical production or reduced ability to eliminate these radicals. OBJECTIVE: To determine the relationship between high levels of oxidative stress and retinopathy of prematurity. MATERIAL AND METHODS: A prospective cohort study was designed. Fifty premature infants of less than 33 weeks' gestational age were included. Serum lipoperoxide levels were determined as a measure of oxidative stress. Samples were taken once a week for 1 month, starting from the first week of life. The results of all four samples were compared between infants who developed any degree of retinopathy of prematurity and those without it. Ophthalmological examinations were performed after the fourth week of life. RESULTS: The incidence of retinopathy of prematurity was 22 % (11/50). The mean values of all the samples showed a significant difference between infants who developed retinopathy of prematurity (5.44 +/- 1.30 nmol/ml) and those who did not (2.94 +/- 0.89 nmol/ml, p = 0.0001). The relative risk of developing retinopathy of prematurity with high serum lipoperoxide levels was 5.15, 5.63, 4.15 and 12.70 for each of the weekly samples. CONCLUSIONS: There is an association between high serum lipoperoxide levels, as a measure of oxidative stress, and the incidence of retinopathy of prematurity.
Assuntos
Peróxidos Lipídicos/sangue , Estresse Oxidativo , Retinopatia da Prematuridade/sangue , Humanos , Lactente , Recém-Nascido , Recém-Nascido Prematuro , Estudos Prospectivos , Retinopatia da Prematuridade/etiologiaRESUMO
Adriamycin (ADM) is an oncostatic of the anthracycline family with confirmed experimental and clinical efficiency. This antitumoral drug has been reported to stimulate macrophage activity and is able to induce apoptosis (AP) in some tumour cells. The objective of the present work was to investigate if in vivo administration of ADM to mice induces AP in their peritoneal macrophages (PM). AP was expressed by the apoptotic index (AI) of peritoneal macrophages observed under fluorescence microscope after ethidium bromide and acridine orange staining and confirmed by detection of the ladder pattern on DNA electrophoresis, indicates DNA fragmentation in 80-120 bp characteristic of apoptotic state. 24 hours after i.p. ADM administration, AP was observed in PM. The effect was best visible after the injection of 5 mg/kg ADM. (Al: 76.3+/-8.9 vs untreated control group AI: 2.8+/-1.1). In the ADM treated group a DNA ladder electrophoretic pattern was observed while DNA from normal PM was genomic. Since ADM toxicity has been attributed to reactive oxygen species generation, we investigated its possible participation in AP induction by pretreating mice with antioxidants: (+)-alpha-tocopherol acid succinate (30 IU/mouse per os) for 3 days before ADM administration with E. coli lipopolysacharide (0.15 microg/mouse i.p.) 24 hours before ADM administration or with superoxide dismutase (10,000 IU/mouse i.p.) 1 hour before ADM administration. AI was significantly decreased, with values close to those of the untreated control group (AI: 15+/-5.7, 9.6+/-8.0 and 32.9+/-6.9, respectively). Antioxidants given before ADM treatment significantly increased the live cell index (p < or = 0.001) in PM the groups while inactivated antioxidants no longer protect PM against the ADM AP induction. DNA analysis confirmed the effect: in the untreated control and in the antioxidant protected groups DNA was genomic while in either ADM or inactivated-antioxidants + ADM treated groups, DNA presented the ladder pattern. AP can thus be induced in PM by ADM and inhibited by antioxidants. These observations may have clinical applications.