Etiology

There is clearly a familial tendency to the development of neural tube defects, although this is probably a polygenic mechanism. Siblings of an affected individual have an approximately ten times greater chance of also being affected (2.5% vs approximately 0.2% risk in the general population - see above). The children of healthy siblings of an affected child are known also to be at increased risk.

Nutritional factors are thought to play a role and may explain partly the social class differences in incidence. The use of preconception folic acid stems from the concept that low maternal folate intake is implicated in the etiology of neural tube defects (see above). Numerous teratogens have been identified in animal models, including anticonvulsants such as valproate and phenytoin, other folate antagonists such as aminopterin, hypervitaminosis A, alcohol and mitomycin C. The extent to which these factors operate in humans remains uncertain.

Recently, abnormalities in homeobox genes have been implicated in the genesis of neural tube defects in mice. In particular, the human analogue of the mouse Pax3 gene has been identified. It is unknown, however, whether this is a sine qua non in humans [3].

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The term vaginitis is one that is applied to any inflammation or infection of the vagina, and there are many different conditions that are categorized together under this ‘broad’ heading, including bacterial vaginosis, trichomoniasis and non-infectious vaginitis.

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