Open Access
Neural tube defects in Victoria, Australia: potential contributing factors and public health implications
Author(s) -
Owen T. J.,
Halliday J. L.,
Stone C. A.
Publication year - 2000
Publication title -
australian and new zealand journal of public health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.946
H-Index - 76
eISSN - 1753-6405
pISSN - 1326-0200
DOI - 10.1111/j.1467-842x.2000.tb00521.x
Subject(s) - neural tube , public health , environmental health , medicine , biology , fishery , nursing , embryo
Abstract Objectives: To measure population prevalence and determine potential predictors of neural tube defects. Method Analysis of all births reported to a mandated collection of perinatal data, and terminations prior to 20 weeks' gestation that have been reported to a data collection of birth defects in Victoria from 1983 to 1997. Prevalence at birth and risk ratios of infant and maternal characteristics associated with neural tube defects were calculated. Results: Prevalence of spina bifida has remained steady for 15 years and was 8.8/ 10,000 in 1997. Anencephaly increased to 7.9/10,000 in 1997. After exclusion of pregnancy terminations, the 1997 birth prevalence was 4.5/10,000 for spina bifida and 2.4/10,000 for anencephaly. Neural tube defects are identified in 1 in 1600 fetuses, the risk being significantly higher for epileptic women (Adjusted Odds Ratio (AOR)= 3.70, 95% Cl 2.25–6.07), multiple births (AOR=4.56, 95%Cl 3.46–6.02), teenage mothers (AOR=1.47, 95% Cl 1.09–2.00) compared with those aged 25–29, and women with three or more previous pregnancies (AOR=1.40, 95% Cl 1.10–1.78). The risk was lower for women of East Asian (AOR=0.70, 95% Cl 0.49–1.00) and Middle Eastern origin (AOR=0.60, 95% Cl 0.35–1.02) and these differences were approaching statistical significance. Conclusion: Total prevalence of neural tube defects did not decline up to 1997. Implications: It is unlikely that targeting ‘at risk’ groups identified in this study would make a difference to neural tube defect incidence. However, consideration could be given to identifying larger ‘at risk’ groups such as those with homocysteine metabolism defects.