ABSTRACT
BACKGROUND: Early-onset neonatal sepsis (EONS) remains one of the leading causes of morbidity and mortality related to premature birth, and its diagnosis remains difficult. Our goal was to evaluate the intestinal microbiota of the first meconium of preterm newborns and ascertain whether it is associated with clinical EONS. METHODS: In a controlled, prospective cohort study, samples of the first meconium of premature infants with a gestational age (GA) ≤32 weeks was obtained at Hospital de Clínicas de Porto Alegre and DNA was isolated from the samples. 16S rDNA based microbiota composition of preterm infants with a clinical diagnosis of EONS was compared to that of a control group. RESULTS: 40 (48%) premature infants with clinical diagnosis of EONS and 44 (52%) without EONS were included in the analysis. The most abundant phylum detected in both groups, Proteobacteria, was more prevalent in the sepsis group (p = .034). 14% of variance among bacterial communities (p = .001) correlated with EONS. The genera most strongly associated with EONS were Paenibacillus, Caulobacter, Dialister, Akkermansia, Phenylobacterium, Propionibacterium, Ruminococcus, Bradyrhizobium, and Alloprevotella. A single genus, Flavobacterium, was most strongly associated with the control group. CONCLUSION: These findings suggest that the first-meconium microbiota is different in preterm neonates with and without clinical EONS.
Subject(s)
Infant, Premature, Diseases , Microbiota , Neonatal Sepsis , Premature Birth , Sepsis , Female , Humans , Infant , Infant, Newborn , Infant, Premature , Infant, Premature, Diseases/diagnosis , Meconium/microbiology , Neonatal Sepsis/diagnosis , Pregnancy , Prospective Studies , Sepsis/diagnosis , Sepsis/microbiologyABSTRACT
OBJECTIVES: Myeloperoxidase (MPO) polymorphism -463 has been related to higher cardiovascular risk. This study was conducted to test whether the MPO promoter polymorphism -463A/G and MPO plasma levels are associated with coronary artery disease (CAD) severity. DESIGN AND METHODS: Patients submitted to elective coronariography were enrolled, CAD severity was assessed and blood samples collected to identify the MPO polymorphism and its plasma levels. RESULTS: Genotypes were determined in 118 patients. Among these patients, 12 (10%) were homozygous for AA, 69 (58%) for GG and 37 (32%) were heterozygous. Mean MPO plasma levels were 8.6+/-4.7 ng/mL for AA, 8.6+/-7.0 ng/mL for AG and 9.4+/-5.6 ng/mL for GG genotypes. The CAD severity was not associated with MPO genotypes (p=0.43), however, patients with higher CAD score presented higher MPO levels (p=0.02). CONCLUSION: We found no association between MPO polymorphism and CAD severity, although a relation was observed for MPO plasma levels and extension of CAD.
