Intrauterine growth restriction (IUGR) [5] describes a fetus whose weight is less than expected based on gestational age and sex, as determined by population standards; frequently chosen cutoffs point are below the 10th percentiles on these curves (1). Causes for IUGR are still unknown, although several determinants have been identified (1). On the basis that thrombophilic polymorphism' could affect placental circulation and thus fetal growth, we recently investigated the role of such maternal and newborn polymorphism' on IUGR. Results for the C677T and A1298C polymorphism' in the 5,10-methylenetetrahydrofolate reductase (MTHFR) gene showed that IUGR risk did not increase with these variants except among women who were homozygous carriers for the C677T variant and who were not taking vitamin supplements during pregnancy (2). We had also hypothesized that higher plasma homocysteine concentrations would be associated with a greater risk of IUGR or a reduction in birthweight through a thrombotic placental effect, regardless of the relative contribution of hrombophilic polymorphisms on maternal and newborn homocysteine concentrations. Mild hyperhomocysteinemia has been associated with pregnancy outcomes such as abruptio placentae, preeclampsia, and fetal loss (3, 4). However, results on the association between plasma total homocysteine (tHcy) and atherothrombotic conditions in general are not consistent (5), and some authors have even suggested that the association is an effect rather than a cause, e.g., the increase in plasma homocysteine could be caused by the decrease in renal function that is common in atherosclerosis (6).
