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| Expression level and clinical significance of ADMA and DDAH2 in earlyonset severe preeclampsia |
| ZHAO Li′na Li Jiawei LIU Guocheng |
| 1.Department of Obstetrics and Gynecology, Guangdong Maternal and Child Health Hospital, Guangdong Province, Guangzhou 510010, China |
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Abstract Objective To discuss the expression of ADMA and DDAH2 in plasma and placental and the correlation between the two factors in early onset severe preeclampsia (EPSP). To approach the possible role of DDAH2 and ADMA in the pathogenesis and progression of EPSP. And to seek the basis of early diagnosis and treatment of disease based on pathogenesis. Methods From January 2017 to January 2018, 45 cases with severe preeclampsia in Guangdong Maternal and Child Health Hospital ("our hospital" for short) were selected as the experimental group, of which 25 cases in early onset severe preeclampsia group, 20 cases in late onset severe preeclampsia group, and 35 healthy pregnant women delivery in our hospital during the same period were selected as the control group. The expression levels of ADMA and DDAH2 in sera and placenta tissues of two groups were detected with Enzyme-linked immunosorbent assay (ELISA). Spearman linear correlation analysis was used for correlation analysis. Results The expression level of ADMA in serum of early-onset severe preeclampsia was significantly higher than that of later onset severe preeclampsia and control group (P < 0.05). The expression level of ADMA of later onset severe preeclampsia in serum was significantly higher than that of control group (P < 0.05). The expression level of DDAH2 of in serum of early onset severe preeclampsia group was significantly lower than that of later onset severe preeclampsia group and control group (P < 0.05). The expression level of DDAH2 in serum of later onset severe preeclampsia group was significantly lower than that of control group (P < 0.05). The positive staining rate of ADMA in the placenta tissues of early onset severe preeclampsia was significantly higher than that of late onset severe preeclampsia (P < 0.05). The positive staining rate of ADMA in the placenta tissue of late onset severe preeclampsia was significantly higher than that of control group (P < 0.05). The positive staining rate of DDAH2 in the placenta tissues of early onset severe preeclampsia was significantly lower than that of late onset severe preeclampsia (P < 0.05). The positive staining rate of DDAH2 in the placenta tissues of late onset severe preeclampsia was significantly lower than that of control group (P < 0.05). The expression levels of DDAH2 and ADMA in serum and in the placenta tissues of earlyonset severe preeclampsia appeared in a obvious negative correlation (r = -0.77, P < 0.05). Conclusion The significantly higher expression level of ADMA and the significantly lower expression level of DDAH2 in serum and in the placenta tissue of early onset severe preeclampsia, they are negatively correlated. ADMA and DDAH2 are closely related to early onset severe preeclampsia. They may interact with each other in the process of trophoblast infiltration and participate pathogenesis of the early onset severe preeclampsia.
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