Epidemiology of Human Congenital Malformations by Bengt Källén

Author:Bengt Källén
Language: eng
Format: epub
Publisher: Springer International Publishing, Cham

Discussion and Conclusions

The rate of children with alimentary tract atresia in this study was 0.8 per 1,000, similar to the estimate from an international study (Harris et al. 1995). The rate of oesophageal atresia (0.28 per 1,000) is higher than the average rate (0.24 per 1,000) in an international study (Nassar et al. 2012). The highest rate in that study came from South America and that was the only rate estimate with a lower 95 % confidence limit higher than the present rate.

It is often supposed in the literature that small gut atresia is a consequence of a circulatory accident, perhaps occurring relatively late during embryonic or foetal development. In an international study (Harris et al. 1995) epidemiological arguments were given for the idea that small gut atresia to a large extent were the result of an early morphogenetic disturbance, probably at the re-canalization of the gut as suggested by Kirillova et al. (1984) and Puri and Fujimoto (1988). The present observations agree with this. The three types of atresia show many similarities why it seems likely that the majority share some elements of pathogenesis and that they all originate relatively early during ontogenesis.

Maternal age seemed to play no important role for the aetiology of these malformations but 1st parity was consistently associated with a higher risk than other parities. Similar results were seen especially for oesophageal atresia by Duong et al. (2012). Smoking had no effect. In a meta-analysis (Hackshaw et al. 2011), a weak effect was seen on anal atresia which was not observed in the present material and which was not found by Zwink et al. (2011). A high maternal BMI was a risk factor in spite of the fact that pre-existing diabetes did not seem to increase the risk. This effect was most marked for anal atresia which agrees with the results of Blomberg and Källén (2010) and those of Zwink et al. (2011).

There was very little association between maternal drug use and the risk of these malformations. There was an association between maternal use of thyroxine and an increased risk for anal atresia which seems not to have been observed previously. It seems unlikely that this hormone could cause malformations, it is more likely that undertreated hypothyroidism in early pregnancy can explain the association. A high but non-significant risk for any alimentary atresia was seen after maternal use of sedatives or hypnotics. A similar observation was made by Norstedt Wikner et al. (2007) on a material which partly overlaps the present one.

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