///2010 Abstract Details
2010 Abstract Details2019-08-03T15:49:10-05:00

BETA-2 ADRENOCEPTOR GENOTYPE AND THE TIMING OF DELIVERY AFTER PRETERM LABOR

Abstract Number: 81
Abstract Type: Original Research

Richard M Smiley MD, PhD1 ; Marci Adams BS, MPH2; Jean-Louis Blouin PhD3; Vladimir Ilievski MD4; Emmet Hirsch MD5

OBJECTIVE: Homozygosity for arginine at codon 16 of the beta-2 adrenoceptor (β2AR) has been shown to have a strong protective effect against preterm delivery (PTD) in two case-control studies and a prospective treatment trial. [1-3] We examined the the influence of β2AR single nucleotide polymorphisms (SNPs) at codons 16 and 27 on preterm delivery (delivery before 36 weeks after an episode of spontaneous preterm labor (PTL)) in matched cases and controls in an large study of pretrem labor and delivery.

STUDY DESIGN: The following groups of women were compared: Group 1 (PTL del <36 wk), PTL with intact membranes delivering @ < 36 wks gestation (n=31); Group 2 (PTL del ≥ 36 wks), PTL delivering at ≥ 36 wks (n=15); Group 3 (PPROM), PPROM @ <37 weeks (n=36, randomly selected from among 110 patients with PPROM; Group 4 (CONTROL), women without PTL or ROM who delivered at term (n=85, chosen from 170 controls). PTL was defined as regular contractions with cervical change with intact membranes. Matching criteria were: race, Hispanic origin, parity, and payor status. Clinical management was per physician judgment. PTL without evidence of infection was generally treated with tocolysis up to 34 weeks. PPROM without evidence of infection was treated with 7d of antibiotics, with delivery at 34 weeks. β2AR genotype was determined from maternal blood.[3] Incidence of genotypes was compared by χ2 with p < 0.05 accepted as significant. Odds ratio for Arg16 homozygosity was calculated for Group 1 versus controls.

RESULTS: Homozygosity for arginine conferred protection from preterm delivery after an episode of PTL (see Table), but was not associated with the occurrence of PTL or PPROM. Odds ratio for Arg16 homozygosity for Group 1 versus controls (term, no PTL) was 0.13 (95% CI 0.003-0.94). There was no association with genotype at codon 27.

CONCLUSION: Consistent with previous reports, in this cohort of women homozygosity for arginine at codon 16 was again associated with a significantly decreased rate of PTD after an episode of PTL. The Arg16Arg genotype may identify clinically insignificant episodes of preterm labor. This may help guide therapy, or provide clues to the molecular mechanisms involved in many cases of spontaneous preterm labor. The physiological or pharmacological mechanisms of this genetic effect improving outcome after PTL merits further study.

REFERENCES: 1. Landau R et al. Am J Obstet Gynecol 2002; 187: 1294-8; 2. Doh K et al. J Perinat Med 200



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