Lewis Marilyn W, Misra Sonya, Johnson Helen L, Rosen Tove S
Alcohol Research Center, University of Connecticut School of Medicine, Farmington, Connecticut, USA.
Am J Drug Alcohol Abuse. 2004 May;30(2):299-320. doi: 10.1081/ada-120037380.
Second generation studies of prenatal cocaine exposure failed to find gross deficits after controlling for confounders. Concern remained that exposure could cause subtle deficits. This prospective, cohort study evaluated effects of cocaine on development at 12, 18, 24, and 36 months. From 1991-1993, 361 mother-infant pairs were recruited from the Children's Hospital of New York, Presbyterian Medical Center's prenatal clinic or delivery room suite. Mothers were assigned to the cocaine group based on report of prenatal cocaine use or positive urine toxicology. Control mothers were enrolled from the same clinic and matched for age and socioeconomic status (SES). Women with serious medical problems were excluded from either group. Of the retained cohort, at 12 months, 147 infants were exposed and 89 were unexposed case controls. Both groups were raised in impoverished environments with few supports. Developmental evaluations were conducted blinded to group. Cross-sectional analysis revealed cocaine-related deficits in neurological exams and speech across all time periods, in spite of catch up in weight, length, and head circumference. Overall analysis of development was evaluated using Generalized Estimating Equations regression analysis. Bayley Mental [Badj = -6.5 (CI--9.4, -3.5, p < or = 0.001)] and Psychomotor [Badj = -3.9 (CI--7.4, -0.5, p = 0.02)] Developmental Indices showed deficits after controlling for confounders. Males were more vulnerable to cocaine exposure for height, motor development, and emotional regulation. Dose-response relationships existed for abnormal neurological exams (Ptrends < 0.08), Mental Development Index (MDI) (Ptrend < 0.001), and Psychomotor Development Index (PDI) (Ptrend < 0.001) deficits. Although nonexposed children performed poorly, cocaine-exposed children showed worse performance. Both groups showed declines at 18 months in mental and psychomotor development from which only nonexposed children rebounded. Overall, cocaine exposure adds an additional risk to disadvantaged children's development. Cocaine-exposed children are less resilient to effects of these multiple risks.
第二代关于产前可卡因暴露的研究在控制混杂因素后未发现明显缺陷。人们仍然担心这种暴露可能会导致细微的缺陷。这项前瞻性队列研究评估了可卡因对12、18、24和36个月时发育的影响。1991年至1993年期间,从纽约长老会医学中心儿童医院的产前诊所或产房招募了361对母婴。根据产前可卡因使用报告或尿液毒理学检测呈阳性,将母亲分配到可卡因组。对照母亲从同一诊所招募,并在年龄和社会经济地位(SES)方面进行匹配。患有严重医疗问题的女性被排除在两组之外。在留存的队列中,12个月时,有147名婴儿暴露于可卡因,89名未暴露的病例对照。两组都在几乎没有支持的贫困环境中成长。发育评估在对分组不知情的情况下进行。横断面分析显示,尽管在体重、身长和头围方面有所追赶,但在所有时间段的神经检查和言语方面都存在与可卡因相关的缺陷。使用广义估计方程回归分析对发育进行总体分析。贝利智力发育指数[校正后差值=-6.5(可信区间为-9.4,-3.5,p≤0.001)]和心理运动发育指数[校正后差值=-3.9(可信区间为-7.4,-0.5,p=0.02)]在控制混杂因素后显示出缺陷。男性在身高、运动发育和情绪调节方面更容易受到可卡因暴露的影响。在异常神经检查(趋势p<0.08)、智力发育指数(MDI)(趋势p<0.001)和心理运动发育指数(PDI)(趋势p<0.001)缺陷方面存在剂量反应关系。尽管未暴露的儿童表现不佳,但暴露于可卡因的儿童表现更差。两组在18个月时的智力和心理运动发育都出现下降,只有未暴露的儿童有所反弹。总体而言,可卡因暴露给处于不利地位的儿童的发育增加了额外风险。暴露于可卡因的儿童对这些多重风险的影响恢复力较弱。