Search

BACKGROUND Knowledge of patterns in prevalence of congenital heart defects (CHDs) is important for clinical care, etiologic research, and prevention. We evaluated temporal and racial/ethnic trends in the birth prevalence of CHDs in metropolitan Atlanta from 1978 to 2005. METHODS Cases of CHDs were obtained from the Metropolitan Atlanta Congenital Defects Program among live born infants, stillborn infants, and pregnancy terminations of at least 20 weeks gestation. We calculated birth prevalence per 10,000 live births and used joinpoint regression analysis to calculate the average annual percent change for total CHDs and for 23 specific subtypes in the total population and among whites and blacks. To evaluate racial/ethnic variations, we calculated prevalence ratios among blacks and Hispanics compared with whites. RESULTS Between 1978 and 2005, 7301 infants and fetuses with major structural CHDs were ascertained among 1,079,062 live births (67.7 per 10,000). The prevalence of all CHDs in aggregate increased from 50.3 per 10,000 in 1978–1983 to 86.4 per 10,000 in 2000–2005. The prevalence of septal defects and vascular rings increased and the prevalence of tricuspid atresia decreased, while other CHD prevalences were stable. Racial/ethnic prevalence differences were found for all CHDs combined and muscular ventricular septal defects, aortic stenosis, and atrioventricular septal defects. CONCLUSIONS The prevalence of total CHDs, primarily common, less severe types, are increasing, with some racial/ethnic differences. Further studies could clarify the possible reasons for such variations including differences in ascertainment, risk factors, or susceptibility. Birth Defects Research (Part A) 2013. © 2013 Wiley Periodicals, Inc.

A 10-year-old boy with osteosarcoma and normal renal function manifested laboratory evidence of impending renal toxicity and extreme elevation of aspartate aminotrasferase and alanine aminotransferase within 2 hours after the completion of a 4-hour infusion of high-dose methotrexate (MTX) (12 g/m2), and went on to develop acute renal failure with life-threatening hyperkalemia 29 hours later. Although his renal function recovered completely with high-dose leucovorin, hemodialysis, charcoal hemoperfusion, and carboxypeptidase G2, we present this case to emphasize that signs of renal toxicity may be present as early as 2 hours after the completion of a 4-hour MTX infusion, and to suggest that monitoring for MTX toxicity should perhaps begin within a few hours after the completion of 4-hour MTX infusion.