• Fumihiro Sata, Hideto Yamada, Kana Suzuki, Yasuaki Saijo, Takashi Yamada, Hisanori Minakami, and Reiko Kishi.
• Department of Public Health, Hokkaido University Graduate School of Medicine, Sapporo, Japan. fsata@med.hokudai.ac.jp
• Pharmacogenet. Genomics. 2006 Nov 1; 16 (11): 775-81.

ObjectivesThe pathophysiologic processes that occur at the cellular and molecular levels in intrauterine fetal growth restriction are largely unknown. Catechol-O-methyltransferase (COMT) is a phase II enzyme that inactivates catechol estrogens by transfer of a methyl group. A functional Val158Met polymorphism in the COMT gene has been known as a susceptible marker for breast cancer. The aim of this study was to examine the association between this polymorphism and fetal growth.MethodsA consecutive series of 412 women who experienced singleton deliveries was assessed in the birth cohort study. Genotyping of COMT and CYP17A1 polymorphisms was determined by allelic discrimination using fluorogenic probes and the 5'nuclease assay.ResultsThe adjusted odds ratio for the risk of low birth weight (<2.500 g) in women with homozygous low-activity (COMT-L) alleles was 2.98 (95% confidence interval, 1.10-8.11). The mean birth weight of infants whose mothers were homozygous for COMT-L was less than that of infants whose mothers had at least one high-activity (COMT-H) allele (2.610 versus 2.800 g, P=0.07). The odds ratio for the risk of intrauterine fetal growth restriction, defined as birth weight <10th percentile or ConclusionOur findings suggest that the allele encoding low-activity COMT may be a susceptible marker for intrauterine fetal growth restriction.

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