Article ID Journal Published Year Pages File Type
3006099 Pregnancy Hypertension: An International Journal of Women's Cardiovascular Health 2013 6 Pages PDF
Abstract

ObjectiveTo test the hypothesis that a quantitative defect of maternal cellular mitochondria would play a role in the pathogenesis of HELLP syndrome.Study designPeripheral blood mitochondrial DNA (MtDNA) was measured in 20 non-pregnant women with a history of HELLP syndrome, 40 non-pregnant control subjects who had previous physiologic pregnancies, 59 subjects carrying physiologic pregnancies, seven pregnant women with a history of HELLP syndrome and five women in the active phase of the disease.Main outcome measurePeripheral blood Mt-DNA.ResultsThe median (interquartile range) mtDNA in women with a history of HELLP syndrome, in non-pregnant women who had previous physiologic pregnancies, in subjects carrying physiologic pregnancies, in pregnant women with a history of HELLP syndrome and in women in the active phase of the disease was 115 (81–194), 229 (199–319), 174 (136–211), 101 (82–178) and 92 (39–129) copies per nuclear DNA, respectively. Non-pregnant women with a history of HELLP syndrome had significantly lower levels than non-pregnant controls (p < 0.001). Moreover, blood mtDNA was lower in pregnant women with a history of HELLP syndrome and in those in the active phase of the disease when compared to pregnant controls (p = 0.002 and p = 0.025, respectively).ConclusionsAttenuated maternal mitochondrial function may favor HELLP syndrome development.

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