Abstract

Previous etiologic studies have defined intrauterine growth restriction (IUGR) based on a single cutoff. To assess the relative importance of known etiologic determinants for different degrees (mild versus severe) and timing (preterm versus term) of fetal growth restriction. Hospital-based cohort study. Tertiary-care university hospital. Sixty-five thousand two hundred eighty inborn singleton infants without major congenital anomalies delivered between January 1, 1978 and March 31, 1996. Comparison of adjusted odds ratios (ORs) and 95% confidence intervals for mild IUGR (defined as birth weight 75% to <85% of the mean for gestational age, the latter cutoff equivalent to the 9.9th percentile for this cohort) and severe IUGR (<75% of mean, or 2.3rd percentile), after controlling for maternal age, education, marital status, and other potential determinants by means of multiple logistic regression. Maternal prepregnancy overweight (body mass index [BMI] >26.0-29.0 kg/m2) and obesity (BMI >29.0 kg/m2) had stronger protective effects against mild IUGR than against severe IUGR, but most of the determinants showed the opposite pattern. This was especially true for pathologic determinants; ORs (and 95% confidence intervals) for severe versus mild IUGR were 18.5 (14.5-23.8) vs 4.6 (3.6-5.8) for severe pregnancy-induced hypertension (PIH), 3.5 (2.2-5.5) vs 2.3 (1. 5-3.4) for prepregnancy hypertension, and 3.4 (2.9-3.9) vs 2.2 (2. 0-2.4) for smoking >/=11 cigarettes/day. Primiparity, short stature, prepregnancy BMI, maternal weight gain, and cigarette smoking had significantly larger effects on term IUGR, whereas the effect of severe PIH was more than twice as large for preterm IUGR (OR = 9.7 [7.3-13.0]) as for term IUGR (OR = 4.0 [3.0-5.3]). Pathologic determinants of IUGR such as prepregnancy and PIH and cigarette smoking predispose to more severe fetal growth retardation, and PIH in particular seems to do so before 37 weeks. Growth-restricted newborns are not, therefore, all created equal(ly).

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