Conclusion
Epidemiological studies clearly confirm a genetic component to pre-eclampsia. Numerous candidate
genes have been studied that fall into groups based on their proposed pathological mechanism,
including thrombophilia, endothelial function, vasoactive proteins, oxidative stress and lipid metabolism
and immunogenetics. It is expected that no one gene will be identified as the sole risk factor for
pre-eclampsia, as in the general population pre-eclampsia represents a complex genetic disorder.
Interactions between numerous SNP either alone or with combination with predisposing environmental
factors, are most likely underpin the genetic component of this disorder. We must be cautious
in our approach to genetics and acknowledge that we are still in the infancy of this research. Following
on from GWAS, further fine mapping studies to delineate SNP that are causal from those that are in
linkage disequilibrium, followed by functional laboratory studies will be required. Only when we have
a better understanding of how the environment interacts with genes will we be in a better position to
target treatment for women, for example knowing that women with a certain genotype will benefit
from losing weight, enabling us to yield clinical benefit.