Debora Lattuada1, Francesca Crovetto2, Laura Trespidi1, Sveva Mangano2, Barbara Acaia1, Edgardo Somigliana3, Luigi Fedele2, Giorgio Bolis2. 1. Dept. Obstet-Gynecol, Fondazione Cà Granda, Ospedale Maggiore Policlinico, Via della Commenda 12, 20122 Milan, Italy. 2. Dept. Obstet-Gynecol, Fondazione Cà Granda, Ospedale Maggiore Policlinico, Via della Commenda 12, 20122 Milan, Italy; Università degli Studi di Milano, Via Commenda 12, 20122 Milan, Italy. 3. Dept. Obstet-Gynecol, Fondazione Cà Granda, Ospedale Maggiore Policlinico, Via della Commenda 12, 20122 Milan, Italy. Electronic address: dadosomigliana@yahoo.it.
Abstract
OBJECTIVE: To test the hypothesis that a quantitative defect of maternal cellular mitochondria would play a role in the pathogenesis of HELLP syndrome. STUDY DESIGN: Peripheral 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 MEASURE: Peripheral blood Mt-DNA. RESULTS: The 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). CONCLUSIONS: Attenuated maternal mitochondrial function may favor HELLP syndrome development.
OBJECTIVE: To test the hypothesis that a quantitative defect of maternal cellular mitochondria would play a role in the pathogenesis of HELLP syndrome. STUDY DESIGN: Peripheral 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 MEASURE: Peripheral blood Mt-DNA. RESULTS: The 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). CONCLUSIONS: Attenuated maternal mitochondrial function may favor HELLP syndrome development.