Liu Shiliang, Joseph K S, Luo Wei, León Juan Andrés, Lisonkova Sarka, Van den Hof Michiel, Evans Jane, Lim Ken, Little Julian, Sauve Reg, Kramer Michael S
From Maternal, Child and Youth Health, Surveillance and Epidemiology Division, Centre for Chronic Disease Prevention, Public Health Agency of Canada, Ottawa, ON, Canada (S. Liu, W.L., J.A.L.); Department of Obstetrics and Gynaecology, University of British Columbia and the Children's and Women's Hospital of British Columbia, Vancouver, BC, Canada (K.S.J., S. Lisonkova, K.L.); School of Population and Public Health, University of British Columbia, Vancouver, BC, Canada (K.S.J.); Department of Obstetrics and Gynaecology, Dalhousie University, NS, Canada (M.V.d.H.); Department of Biochemistry and Medical Genetics, University of Manitoba, Winnipeg, MB, Canada (J.E.); School of Epidemiology, Public Health and Preventive Medicine, University of Ottawa, Ottawa, ON, Canada (J.L.); Departments of Pediatrics and Community Health Sciences, University of Calgary, Calgary, AB, Canada (R.S.); and Departments of Pediatrics and Epidemiology, Biostatistics, and Occupational Health, McGill University, Montreal, QC, Canada (M.S.K.).
Circulation. 2016 Aug 30;134(9):647-55. doi: 10.1161/CIRCULATIONAHA.116.022126.
Previous studies have yielded inconsistent results for the effects of periconceptional multivitamins containing folic acid and of folic acid food fortification on congenital heart defects (CHDs).
We carried out a population-based cohort study (N=5 901 701) of all live births and stillbirths (including late-pregnancy terminations) delivered at ≥20 weeks' gestation in Canada (except Québec and Manitoba) from 1990 to 2011. CHD cases were diagnosed at birth and in infancy (n=72 591). We compared prevalence rates and temporal trends in CHD subtypes before and after 1998 (the year that fortification was mandated). An ecological study based on 22 calendar years, 14 geographic areas, and Poisson regression analysis was used to quantify the effect of folic acid food fortification on nonchromosomal CHD subtypes (n=66 980) after controlling for changes in maternal age, prepregnancy diabetes mellitus, preterm preeclampsia, multiple birth, and termination of pregnancy.
The overall birth prevalence rate of CHDs was 12.3 per 1000 total births. Rates of most CHD subtypes decreased between 1990 and 2011 except for atrial septal defects, which increased significantly. Folic acid food fortification was associated with lower rates of conotruncal defects (adjusted rate ratio [aRR], 0.73, 95% confidence interval [CI], 0.62-0.85), coarctation of the aorta (aRR, 0.77; 95% CI, 0.61-0.96), ventricular septal defects (aRR, 0.85; 95% CI, 0.75-0.96), and atrial septal defects (aRR, 0.82; 95% CI, 0.69-0.95) but not severe nonconotruncal heart defects (aRR, 0.81; 95% CI, 0.65-1.03) and other heart or circulatory system abnormalities (aRR, 0.98; 95% CI, 0.89-1.11).
The association between food fortification with folic acid and a reduction in the birth prevalence of specific CHDs provides modest evidence for additional benefit from this intervention.
先前的研究对于含叶酸的围孕期多种维生素及叶酸食品强化对先天性心脏病(CHD)的影响得出了不一致的结果。
我们对1990年至2011年在加拿大(魁北克和曼尼托巴除外)妊娠≥20周分娩的所有活产和死产(包括妊娠晚期终止妊娠)进行了一项基于人群的队列研究(N = 5901701)。CHD病例在出生时和婴儿期被诊断出来(n = 72591)。我们比较了1998年(强制强化的年份)前后CHD亚型的患病率和时间趋势。基于22个日历年、14个地理区域以及泊松回归分析的生态研究用于在控制产妇年龄、孕前糖尿病、早产子痫前期、多胎妊娠和终止妊娠的变化后,量化叶酸食品强化对非染色体CHD亚型(n = 66980)的影响。
CHD的总体出生患病率为每1000例总出生数12.3例。除房间隔缺损显著增加外,1990年至2011年间大多数CHD亚型的患病率下降。叶酸食品强化与圆锥干畸形(调整率比[aRR],0.73,95%置信区间[CI],0.62 - 0.85)、主动脉缩窄(aRR,0.77;95% CI,0.61 - 0.96)、室间隔缺损(aRR,0.85;95% CI,0.75 - 0.96)和房间隔缺损(aRR,0.82;95% CI,0.69 - 0.95)的患病率较低相关,但与严重非圆锥干型心脏缺陷(aRR,0.81;95% CI,0.65 - 1.03)和其他心脏或循环系统异常(aRR,0.98;95% CI,0.89 - 1.11)无关。
叶酸食品强化与特定CHD出生患病率降低之间的关联为该干预措施带来的额外益处提供了适度的证据。