OBJECTIVE: To evaluate exposure to intrauterine infection as an independent risk factor for spastic cerebral palsy (CP) among very prematurely born infants. STUDY DESIGN: Retrospective case-control study. METHODS: Singleton children with gestational ages less than 32 weeks and birth weights less than 1999 g who survived to age 2 years and were born from 1988 to 1994 in a level 2 or 3 hospital in California were included in the study. Cases were children with congenital spastic CP (n = 170). Controls were children randomly sampled within 250-g birth weight intervals (n = 270). Gestational age was controlled through multiple logistic models. Major analyses were controlled for preeclampsia and short time between admission and delivery. RESULTS: Neither clinical nor histologic indicators of intrauterine infection were associated with total spastic CP or spastic diplegia in these infants. Although not predicted by prior hypothesis, we observed an approximate doubling of risk for infants of infected mothers among children born to white women, whereas no association was noted among children born to women of other races/ethnicities. White controls had lower frequency of all measured infection indicators compared with white cases and cases and controls of other races/ethnicities. CONCLUSION: Exposure to intrauterine infection was not an independent risk factor for CP in very premature infants when gestational age and other confounders were tightly controlled.
OBJECTIVE: To evaluate exposure to intrauterine infection as an independent risk factor for spastic cerebral palsy (CP) among very prematurely born infants. STUDY DESIGN: Retrospective case-control study. METHODS: Singleton children with gestational ages less than 32 weeks and birth weights less than 1999 g who survived to age 2 years and were born from 1988 to 1994 in a level 2 or 3 hospital in California were included in the study. Cases were children with congenital spastic CP (n = 170). Controls were children randomly sampled within 250-g birth weight intervals (n = 270). Gestational age was controlled through multiple logistic models. Major analyses were controlled for preeclampsia and short time between admission and delivery. RESULTS: Neither clinical nor histologic indicators of intrauterine infection were associated with total spastic CP or spastic diplegia in these infants. Although not predicted by prior hypothesis, we observed an approximate doubling of risk for infants of infected mothers among children born to white women, whereas no association was noted among children born to women of other races/ethnicities. White controls had lower frequency of all measured infection indicators compared with white cases and cases and controls of other races/ethnicities. CONCLUSION: Exposure to intrauterine infection was not an independent risk factor for CP in very premature infants when gestational age and other confounders were tightly controlled.
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