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Association between maternal Group B Streptococcus (GBS) colonization diagnosed between 35 and 37 weeks of gestation and early term birth (between 37 and 39 weeks) and maternal-fetal inflammatory response associated with this condition were tested. In this cohort study of women delivering at term at Centennial Women's Hospital in Nashville, TN, GBS status and other clinical and demographic data were obtained from medical records. Exposed women were those testing positive for GBS (GBS positive [n = 490]) and the unexposed tested negative for GBS (GBS negative [n = 1,127]). To determine the inflammatory response associated with GBS, a cross sectional study, maternal and fetal plasma biomarkers (IL-1β, IL-2, IL-6, IL-8, and TNF-α) were measured in the same cohort. T-tests and logistic regression determined association between GBS status, biomarker concentrations and early term birth. Gestational age was reduced to 271.1 (95% CI 270.4, 271.1) for cases compared to 274.7 (95% CI 274.4, 275.1) days for controls (p < 0.0001). The odds of early term birth was increased by threefold in cases (OR 3.28; 95% CI 2.60-4.15; p < 0.0001). The mean birth weight in cases (3285.3 g) (95% CI 3242.6, 3327.9) was lower than the controls, 3373.8 g (95% CI 3348.9, 3398.7) (p = 0.0004). Maternal IL-1β was greater in cases (22.8 ng/ml; range 5.2-157.7 ng/ml) compared to controls (5.7; range 2.4-69.5 ng/ml; p < 0.0001). IL-1β was higher in fetal plasma in cases vs. controls (20.33 vs. 8.18 ng/ml; p = 0.01). A 10 ng/ml increase in maternal IL-1β was associated with increased risk for GBS infection (OR: 1.628, CI: 1.163-2.278; p = 0.0045). GBS colonization shortened gestational age at term and IL-1β concentration in maternal plasma is an indicator of GBS status.

Purpose: To investigate differences in pre-pregnancy BMI status in patients with spontaneous preterm birth (PTB) compared with term birth and assess the role of ethnicity as a risk modifier in BMI-associated PTB., Methods: A case-control study involving self-reported African American and Caucasian women delivering singletons in Nashville, TN, USA, 2003-2009. Maternal pre-pregnancy BMI was recorded in 447 PTB-cases (African American = 145, Caucasian = 302) and 1315 term-birth controls (African American = 522; Caucasian = 793). Crude and adjusted odds ratio (OR and AOR) for PTB were calculated using normal BMI (18.5-24.9 kg/m(2)) as reference. Age, education, marital status, income, smoking, parity, previous PTB and pregnancy weight gain were included as covariates in logistic regression., Results: No significant differences were noted in the OR for PTB among different BMI categories when women of different ethnicity were combined. Odds of PTB were greater in obese than in normal weight Caucasian women, even after adjusting for confounders (AOR = 1.84, 95%CI [1.15, 2.95]). Obese African American women had a decreased crude OR for PTB, although this was not significant after adjusting for confounders (AOR = 0.72, 95%CI [0.38, 1.40]). The odds for early PTB (<32 weeks) were decreased in obese compared with normal weight African American women (OR = 0.23, 95%CI [0.08, 0.70]), whereas they were increased in obese compared with normal weight Caucasian women (OR = 2.30, 95%CI [1.32, 4.00])., Conclusion: The risk for PTB in women with different pre-pregnancy BMI categories differs according to ethnicity.

Objective: To document racial disparity in biomarker concentrations in maternal/fetal plasma and amniotic fluid between African Americans and European Americans with spontaneous preterm birth (PTB; cases) and normal term birth (controls), and their contribution to distinct pathophysiological pathways of PTB., Design: Nested case-control study., Setting: The Perinatal Research Center, Nashville, Tennessee, USA., Sample: Maternal and fetal plasma and amniotic fluid samples were collected from 105 cases (59 African American and 46 European American) and 86 controls (40 African American and 46 European American)., Methods: Thirty-six biomarkers were analysed using the protein microarray approach., Main Outcome Measures: Differences in biomarker concentrations between cases and controls of different races in maternal, fetal and intra-amniotic compartments, and the risk of PTB. Dysregulated biomarker-induced PTB pathways associated with PTB in each race were determined using ingenuity pathway analysis (IPA)., Results: Racial disparity was observed in biomarker concentrations in each compartment between cases and controls: amniotic fluid, IL8 and MIP1α differed between case and controls in European Americans, whereas ANGPT2, Eotaxin, ICAM-1, IL-1β, IL1RA, RANTES and TNFα differed between case and controls in African Americans. In both races the FAS ligand, MCP-3 and TNFR-I differed between cases and controls. For fetal plasma, ANGPT2, Eotaxin, FGF basic, ICAM-1, IGF-I, IL10, IL-1β, IL2, IP10 KGF, MCP-3, MIP1α, PDGF-BB, TGFα, TGFβ1, TIMP1, TNFα, TNFR-I, TNFR-II and VEGF differed between cases and controls in European Americans, whereas only MMP7 differed between cases and controls in African Americans. IL-8 differed between cases and controls in both races. For maternal plasma, IL1RA, MMP7 and VEGF differed between cases and controls in European Americans, whereas ANGPT2, FGF basic, IL-1β, IL5, IL6R, KGF, MCP-3, MIP1α, TIMP1 and TNFα differed between cases and controls in African Americans. ANG, IL8 and TNFR-I differed between cases and controls in both races., Conclusions: We conclude that: (1) biomarker concentrations in maternal, fetal and intra-amniotic compartments differ between cases and controls; (2) there is racial disparity in the biomarker profile in each of the compartments; (3) substantial numbers of dysregulated fetal plasma biomarkers contribute to PTB in European Americans, whereas maternal plasma biomarkers contribute to PTB in African Americans; and (4) both inflammation and haematological functions are associated with PTB in European Americans, but maternal proinflammatory changes dominate PTB in African Americans. Biomarker analyses document racial disparity and the distinct pathophysiological contributions from different compartments that can determine pregnancy outcome., (© 2012 The Authors BJOG An International Journal of Obstetrics and Gynaecology © 2012 RCOG.)

Catechol-O-methyltransferase (COMT) activity has been reported to be higher in African Americans (AA) than Caucasians (Cau). COMT converts 2- and 4-hydroxy (OH) estrogens to 2- and 4-methoxyestrogens, respectively, and can increase estrogenic milieu locally in tissues. To assess whether the increased incidence of preterm birth (PTB) among AA women is associated with single-nucleotide polymorphism (SNP) in the COMT gene, we examined variations in maternal and fetal COMT genes and their association with pregnancy outcomes (term vs preterm pregnancies) using 4 functional SNPs: rs4633, rs4680, rs4818, and rs6269 in both AA and Cau. We analyzed samples from 267 AA women (191 term and 76 preterm pregnancies) and 339 Cau (194 term and 145 preterm pregnancies) in this study. The results showed a significant difference (P < .05) in allele and genotype frequencies between term and preterm AA and Cau women in 3 SNPs in both maternal and fetal DNA. The analysis revealed that in AA fetal COMT genes, SNP rs4818 is associated with PTB at the allele (C; P < .001), genotype (C/C; P < .01), and 2- (P < .03) and 3 (P < .04)-window haplotype levels. Multidimensionality reduction analysis also showed a significant (P < .01) association between rs4818 and PTB. In conclusion, our study demonstrated that a synonymous polymorphism, rs4818 in the fetal COMT gene, is associated with PTB in AA.

Spontaneous preterm birth (PTB; <37 weeks gestation) is a major risk factor for neonatal morbidity and mortality. The exact cause of PTB is unknown but oxidative stress may play an important role. Genetic studies have recently begun to elucidate the role of genetic variation in PTB but these studies have overlooked the mitochondrial genome/gene(s) as a plausible PTB candidate. In the present study, we sought to document association between nonsynonymous mitochondrial DNA (mtDNA) variants A4917G, G10398A and T4216C and PTB. We performed a case (PTB; <36 weeks gestation)-control (normal term) analysis of these mtDNA markers and examined their potential interaction with smoking in PTB. A sample of 422 pregnant Caucasian women (220 preterm and 202 terms) was examined for association. Haplogroup T marker A4917G was identified as a possible candidate for association with PTB after adjusting for smoking (OR=1.99 [95% CI 0.93-4.24]) as was T4216C (OR=1.63 [95% CI 0.93-2.83]). No significant multi-locus interactions or interactions with other environmental variables were observed. Our data, although preliminary, support the hypothesis that mitochondrial genome polymorphisms may play a significant role in PTB through an interaction with smoking.