Details

Autor(en) / Beteiligte

• Romero, Roberto, MD
• Velez Edwards, Digna R., PhD
• Kusanovic, Juan Pedro, MD
• Hassan, Sonia S., MD
• Mazaki-Tovi, Shali, MD
• Vaisbuch, Edi, MD
• Kim, Chong Jai, MD
• Chaiworapongsa, Tinnakorn, MD
• Pearce, Brad D., PhD
• Friel, Lara A., MD, PhD
• Bartlett, Jacquelaine, MS
• Anant, Madan Kumar, PhD
• Salisbury, Benjamin A., PhD
• Vovis, Gerald F., PhD
• Lee, Min Seob, PhD
• Gomez, Ricardo, MD
• Behnke, Ernesto, MD
• Oyarzun, Enrique, MD
• Tromp, Gerard, PhD
• Williams, Scott M., PhD
• Menon, Ramkumar, PhD

Titel

Identification of fetal and maternal single nucleotide polymorphisms in candidate genes that predispose to spontaneous preterm labor with intact membranes

Ist Teil von

• American journal of obstetrics and gynecology, 2010-05, Vol.202 (5), p.431.e1-431.e34

Ort / Verlag

New York, NY: Mosby, Inc

Erscheinungsjahr

2010

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• Objective The purpose of this study was to determine whether maternal/fetal single nucleotide polymorphisms (SNPs) in candidate genes are associated with spontaneous preterm labor/delivery. Study Design A genetic association study was conducted in 223 mothers and 179 fetuses (preterm labor with intact membranes who delivered <37 weeks of gestation [preterm birth (PTB)]), and 599 mothers and 628 fetuses (normal pregnancy); 190 candidate genes and 775 SNPs were studied. Single locus/haplotype association analyses were performed; the false discovery rate was used to correct for multiple testing. Results The strongest single locus associations with PTB were interleukin-6 receptor 1 (fetus; P = .000148) and tissue inhibitor of metalloproteinase 2 (mother; P = .000197), which remained significant after correction for multiple comparisons. Global haplotype analysis indicated an association between a fetal DNA variant in insulin-like growth factor F2 and maternal alpha 3 type IV collagen isoform 1 (global, P = .004 and .007, respectively). Conclusion An SNP involved in controlling fetal inflammation (interleukin-6 receptor 1) and DNA variants in maternal genes encoding for proteins involved in extracellular matrix metabolism approximately doubled the risk of PTB.