A study has linked mutations in three genes with the severe pregnancy condition, pre-eclampsia. The international research team say they're the first to link genetic mutations and pre-eclampsia in women with the autoimmune disorder - lupus. The findings also link immune system dysfunction with the risk of developing the condition.
The researchers suggest this study could help find new targets for treating pre-eclampsia, which can only be stopped by delivering the baby. This can be risky if the baby is delivered prematurely.
'This study identifies the first genetic risk factors associated with pre-eclampsia in patients with lupus and also validates these risk factors in a population of patients who do not have an autoimmune disease', said study author Dr Jane Salmon from the Hospital for Special Surgery in New York, in the Daily Mail.
The international research team analysed DNA from 250 pregnant women diagnosed with lupus and other autoimmune disorders, which increase the risk of developing the condition.
To understand whether the body's immune response is associated with pre-eclampsia, the team sequenced three genes encoding proteins that play regulatory roles in the immune system. These were membrane cofactor protein (MCP), complement factor I (CFI), and complement factor H (CFH).
Of the 40 women who developed pre-eclampsia, 18 percent had heterozygous mutations in these genes. Similar genetic mutations were found among five of 59 women with pre-eclampsia who did not have an autoimmune disorder.
Professor Basky Thilaganathan from the UK's Royal College of Obstetricians and Gynaecologists said to the BBC: 'This work shows an association. At best genes like these might identify 10-15 percent of pre-eclampsia, so its relative importance may not be sensational. But it may allow us to study new treatments to prevent or delay the onset of pre-eclampsia and to know which women need closer surveillance'.
Pre-eclampsia affects four in every 100 pregnant women leading to high blood pressure and kidney dysfunction, but its exact cause is unknown. The study was published in the open-access journal PLoS Medicine.