RESUMEN
<p><b>OBJECTIVE</b>To analyze the maternal outcomes of pregnant women with pernicious placenta previa (PPP).</p><p><b>METHODS</b>Clinical data of 470 patients with placenta previa admitted in Women's Hospital Zhejiang University School of Medicine from August 2012 to August 2014 were collected and retrospectively analyzed. The patients were divided into pernicious group(n=101) and non-pernicious group(n=369) according to the history of cesarean section and location of placenta attached to the uterine. The general profiles, maternal outcomes of two groups were compared.</p><p><b>RESULTS</b>The age, gravidity and rate of recurrent cavity surgery of pernicious group [(32.5 ± 4.1) y, 3.4 ± 1.2, 28.7%] were higher than those of non-pernicious group [(30.7 ± 4.5) y, 2.1 ± 1.4,13.6%] (P<0.05). The gestational age of pernicious group was (35.6 ± 2.7) weeks, less than that of non-pernicious group [(36.7 ± 2.7) weeks, P<0.001]. Rate of postpartum massive hemorrhage, rate of blood transfusion, rate of placental implantation and hysterectomy in pernicious and non-pernicious group were 29.7%, 35.6%, 27.7%, 11.9% and 8.1%, 10.8%, 5.7%, 0.8%, respectively (P<0.05). Multiple regression analysis showed that placenta accrete was significantly associated with postpartum massive hemorrhage in pernicious group (P<0.05).</p><p><b>CONCLUSION</b>The awareness of the danger of pregnant women with PPP before operation and paying more attention to antenatal care are key measures to decrease the adverse maternal outcomes of pregnant women with placenta previa.</p>
Asunto(s)
Adulto , Femenino , Humanos , Embarazo , Cesárea , Edad Gestacional , Placenta Previa , Epidemiología , Patología , Hemorragia Posparto , Epidemiología , Resultado del Embarazo , Estudios Retrospectivos , Factores de RiesgoRESUMEN
<p><b>OBJECTIVE</b>In this study, we assayed promoter hypermethylation and protein expression of the mismatch repair gene (MMR) hMLH1 and hMSH2 in gestational trophoblastic diseases to understand the significance of MMR promoter methylation and expression in the pathogenesis and malignant transformation of hydatidiform mole.</p><p><b>METHODS</b>DNA was extracted from chorion of early pregnancies, partial hydatidiform moles, complete hydatidiform moles, and invasive moles were over digested by methylation sensitive endonuclease Hpa II. Then the promoters were amplificated by polymerase chain reaction. The protein was detected by immunohistochemistry.</p><p><b>RESULTS</b>In the normal placenta, neither hMLH1 nor hMSH2 promoter methylation was detected. Expression of hMLH1 and hMSH2 in cytotrophoblasts was strongly positive, and that was negative or weakly positive in syncytiotrophobasts. In all normal chorion, expression of hMLH1 and hMSH2 in cytotrophoblasts was strongly positive. In partial hydatidiform mole and complete hydatidiform mole, the methylation of hMLH1 and hMSH2 promoters was significantly higher than that of early placenta (P < 0.05), and the protein expression in cytotrophoblasts was significantly lower (P < 0.05). In the invasive mole, hMLH1 and hMSH2 promoter methylation were not significantly different as compared with the partial hydatidiform mole and complete hydatidiform mole (P > 0.05). Expression of hMLH1 in the invasive mole (54.5%, 6/11) was not significantly different as compared with the partial hydatidiform mole and complete hydatidiform mole (P > 0.05). But expression of hMSH2 in the invasive mole (36.4%, 4/11) was weaker than that in complete hydatidiform mole (P = 0.044). Promoter methylation and less expression of hMSH2 had correlations in complete hydatidiform mole or invasive mole.</p><p><b>CONCLUSIONS</b>Strong expressions of hMLH1 and hMSH2 in the cytotrophoblasts of normal placenta may keep the genome stability. Promoter methylation and down-regulation of hMLH1 and hMSH2 are probably involved in the pathogenesis of hydatidiform mole.</p>