Y L. Guo

Epidemiology of Congenital Anomalies in a Population-based Birth Registry in Taiwan, 2002

BACKGROUND/PURPOSE Congenital anomalies are important medical and public health conditions. However, the occurrence rates of congenital anomalies and their risk factors are unknown in Taiwan. We used the medical-practitioner-reported birth registry in 2002 to determine the occurrence of individual congenital anomalies and their associated risk factors, such as maternal age, fetal sex, and plurality. METHODS The birth registry was started in 2001 in Taiwan. We obtained the data for 2002 from the Department of Health, and translated the coding of congenital anomalies to International Classification of Diseases 9th revision-clinical modification (ICD-9-CM). The occurrence rates of individual congenital anomalies were calculated. The effects of maternal age, fetal sex, and plurality were calculated as odds ratios (ORs) by logistic regression analysis. RESULTS A total of 1775 infants were diagnosed as having congenital anomalies among 242,140 live and deceased newborn infants delivered in Taiwan in 2002.The occurrence rates of congenital anomalies of the nervous system, eyes and face, cardiovascular, digestive, urogenital, musculoskeletal and respiratory systems, and chromosomes were 0.67 per thousand, 1.86 per thousand, 1.47 per thousand, 0.62 per thousand, 0.71 per thousand, 2.05 per thousand, 0.07 per thousand and 0.79 per thousand, respectively. Sex chromosomal anomalies, Down syndrome, and trisomy 18 were associated with maternal age of > or = 35 years (OR, 15.9, 4.6, and 2.3, respectively). Such elevation was even more prominent for maternal age > or = 40 years (OR, 35.5, 22.2, and 11.62, respectively). A milder and borderline significant maternal age (> or = 40 years) effect was seen with cleft lip, with or without cleft palate (OR, 2.1). Female births had more cleft palates (OR, 1.6). There was no relationship between plurality and anomalies. CONCLUSION The occurrence rates for individual congenital anomalies in Taiwan were reported. Older maternal age was a risk factor for the occurrence of chromosomal and orofacial anomalies. More active prenatal screening and further investigation of causal factors of congenital anomalies are of major importance.

THE ASSOCIATION BETWEEN GLUTATHIONE S-TRANSFERASE P1, M1 POLYMORPHISMS AND ASTHMA IN TAIWANESE SCHOOLCHILDREN

STUDY OBJECTIVES Genetic polymorphisms in the glutathione S-transferase P1 gene (GSTP1) and the glutathione S-transferase M1 gene (GSTM1) have been implicated as risk factors for asthma. However, their roles in asthma pathogenesis and the interaction between these two genes have not been extensively investigated. This study, therefore, examined the relationship among GSTP1 and GSTM1 genotypes and childhood asthma, and evaluated their gene-gene interactions. SETTING The population from three southern Taiwan communities of a 2001 national survey. SUBJECTS AND METHODS Two hundred sixty-six fourth-grade to ninth-grade schoolchildren were recruited for oral mucosa samplings based on questionnaire information. Polymerase chain reaction-based assays were performed to determine GSTP1 and GSTM1 genotypes among asthmatic subjects and nonasthmatic control subjects. Multiple logistic regression was used to adjust for potential confounding factors. RESULTS All of the participants were homozygous at the GSTP1 Ala-114 locus. After controlling for age, sex, and atopic eczema, compared with participants carrying any Val-105 allele, children who were homozygotic for GSTP1 Ile-105 had a significantly increased risk of physician-diagnosed asthma (adjusted odds ratio [adjOR], 1.94; 95% confidence interval [CI], 1.08 to 3.59). A positive risk for childhood asthma was also noted on the GSTM1 null genotype but did not reach statistical significance (adjOR, 1.37; 95% CI, 0.80 to 2.38). Among children with GSTM1 present genotypes, GSTP1-105 polymorphisms were associated with the increased risk of asthma. However, the reduced and statistically insignificant asthma risk was observed among those with GSTM1 null genotype. CONCLUSIONS We concluded that GSTP1-105 was a predictor for childhood asthma, whereas GSTM1 polymorphism might modify the risk. Our study also suggested a competitive effect for homozygous GSTP1 Ile-105 and GSTM1 null genotypes on childhood asthma.