Search

The diagnosis of preeclampsia in China currently relies on limited clinical signs and unspecific laboratory findings. These are inadequate predictors of preeclampsia development, limiting early diagnosis and appropriate management. Previously, the Prediction of Short-Term Outcome in Pregnant Women with Suspected Preeclampsia Study (PROGNOSIS) and PROGNOSIS Asia demonstrated that a soluble fms-like tyrosine kinase 1 (sFlt-1)/placental growth factor (PlGF) ratio of ≤38 can be used to rule out preeclampsia within 1 week, with negative predictive values of 99.3 and 98.6%, respectively. This is an exploratory sub-analysis of the Chinese cohort (n = 225) of the PROGNOSIS Asia study. The primary objectives were to assess the predictive performance of using the sFlt-1/PlGF ratio to rule out preeclampsia within 1 week and to rule in preeclampsia within 4 weeks. The sFlt-1/PlGF ratio was also examined for short-term prediction of fetal adverse outcomes, maternal adverse outcomes, and time to delivery. The overall prevalence of preeclampsia was 17.3%. With the use of an sFlt-1/PlGF ratio of ≤38, the negative predictive value for ruling out preeclampsia within 1 week was 97.3% [95% confidence interval (CI), 93.8–99.1], with a sensitivity of 64.3% and specificity of 85.3%. With the use of an sFlt-1/PlGF ratio of >38, the positive predictive value for ruling in preeclampsia within 4 weeks was 35.0% (95% CI, 20.6–51.7), with a sensitivity of 50.0% and specificity of 86.8%. In the analyses of the sFlt-1/PlGF ratio and fetal adverse outcomes, the area under the receiver operating characteristic curve was 92.8% (95% CI, 83.5–98.7) for ruling out fetal adverse outcomes within 1 week and 79.9% (95% CI, 68.1–90.3) for ruling in fetal adverse outcomes within 4 weeks. An sFlt-1/PlGF ratio of >38 increased the likelihood of imminent delivery 3.3-fold compared with a ratio of ≤38 [hazard ratio, 3.3 (95% CI, 2.1–5.1)]. This sub-analysis confirms the high predictive performance of the sFlt-1/PlGF ratio cutoff of 38 for short-term prediction of preeclampsia in Chinese women, which may help prevent unnecessary hospitalization of women with low risk of developing preeclampsia.

Today the only effective “treatment” for preeclampsia is to deliver at the optimal time for both maternal and foetal well-being. Studies reported that severe preeclampsia can benefit from the expectant management including mild preeclampsia between 34 and 37 weeks. However it is unclear whether mild preeclampsia before 34 weeks also benefits from the expectant management. Data on 274 women with mild preeclampsia before 37 weeks of gestation were retrospectively collected and analysed. Blood pressure and proteinuria at time of onset were not clinically associated with delivery time. For women who developed preeclampsia before 34 weeks, the median latency from onset to delivery or from onset to admission to hospital or from admission to hospital to delivery was 27 or 21 or 3 days, respectively. There were four women (2%) who delivered within 48 h after onset, 28 (14%) FGR and 14 (7%) stillbirths. The median birth-weight was 2240 g. For women who developed preeclampsia between 34 and 37 weeks, the median latency from onset to delivery or from onset to admission to hospital or from admission to hospital to delivery was 11 or 7 or 2 days, respectively. There were seven women (10%) who delivered within 48 h after onset and eight (12%) FGR. The median birth-weight was 2880 g. Our study demonstrates that mild preeclampsia before 37 weeks has benefits from expectant or outpatient management with a median prolongation of over 11 days dependent on the time of onset, but it increases the risk for stillbirths before 34 weeks.

To date, data on postpartum management of preeclampsia including the optimal time for discharge are limited. The aims of this study were to investigate the appropriate time for discharge after delivery, and factors that could affect the time for discharge. Data on 210 preeclamptic women including the severity or time of onset and days in the ward after delivery were collected and analysed. In total, 167 (73%) patients were followed up for at least 16 months and none of them developed any complications after delivery. The mean days in the ward after delivery in preeclamptic women with vaginal delivery or with caesarean section was 3.4 or 5.8 days, respectively. After adjusting for delivery modes and parity, women with severe or early onset preeclampsia or preeclamptic women complicated with IUGR were in the ward longer than women with mild or late onset of preeclampsia or preeclamptic women without IUGR. In addition, women with severe preeclampsia or with IUGR delayed the time for blood pressure to return to normal range. Our descriptive data reported that preeclamptic women stayed in the ward for 4-6 days after delivery, dependent on the delivery modes. Preeclamptic women with severe or early onset form or complicated with IUGR delayed the improvement of clinical symptoms after delivery. We further found that women with severe preeclampsia, and preeclampsia complicated with IUGR delayed blood pressure returning to normal range. These pre-discharge checklists may help obstetricians and midwives decide when to discharge.

Fetal growth restriction (FGR) is a well-known risk factor for cognitive dysfunction, especially for learning and memory abilities. However, knowledge about prevention and treatment methods of learning and memory abilities of fetal are limit. Here, Morris water maze and passive avoidance tests showed zinc supplementation could protect the impairment of the learning and memory abilities caused by FGR. As accumulating evidence suggested that insufficiency of placental trophoblast cell invasion was closely related to FGR fetal neurodevelopmental dysplasia, we further explored the relationship between zinc supplementation during pregnancy and placental trophoblast. Microarray identified 346 differently expressed genes in placental tissues with and without zinc supplementation, and GO and KEGG analyses showed these differently expressed genes were highly enriched in cell invasion and migration and STAT3 pathway. Protein-protein interaction(PPI) analysis found that STAT3 interacted with matrix metalloproteinase-2/9 (MMP-2/9). In vivo, western blot results authenticated that the expression levels of phospho-STAT3, STAT3, MMP-2 and MMP-9 were up-regulated in placental tissues after zinc treatment. To validate whether zinc could promotes trophoblast cell invasion and migration via enhancing STAT3-MMP-2/9 activity. In vitro, Transwell assay was performed, and we observed that abilities of invasion and migration were obviously increased in zinc treated trophoblast cells. And phospho-STAT3, STAT3, MMP-2 and MMP-9 expression levels were correspondingly increased in zinc treated trophoblast cells, which were dose-dependent. Moreover, gain–of-function and loss-of-function of STAT3 confirmed that zinc promotes cell invasion and migration via regulating STAT3 mediated up-regulation of MMP-2/9 activity. We propose that activation of MMP-2/9 mediated by STAT3 may contribute to invasion and migration of trophoblast cells, which improved neurodevelopmental impairment of FGR rats probably via contributing to placental development. Our findings are the first to show a possible mechanism of reversing neurodevelopmental impairment of FGR rats by zinc supplementation, holding promise for the development of novel therapeutic modalities for learning and memory abilities impairment caused by FGR.

// Xia Ying 1, 2 , Su-xia Han 3 , Chen-chen He 3 , Cong-ya Zhou 1 , Yi-ping Dong 3 , Meng-jiao Cai 1 , Xin Sui 3 , Cheng-xian Ma 1 , Xiao Sun 3 , Yuan-yuan Zhang 1 , Wen-li Gou 4 , Clifford Mason 5 , Qing Zhu 1 1 Department of Oncology, The Second Affiliated Hospital of Xi'an Jiaotong University Medical College, Xi’an, Shannxi, P.R. China 2 Department of Gynecological Oncology, Women’s Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, P.R. China 3 Department of Oncology, The First Affiliated Hospital of Xi’an Jiaotong University Medical College, Xi’an, Shannxi, P.R. China 4 Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xi’an Jiaotong University Medical College, Xi’an, Shannxi, P.R. China 5 Department of Obstetrics and Gynecology, University of Kansas School of Medicine, Kansas City, Kansas, USA Correspondence to: Qing Zhu, email: newzhuqing1972@yahoo.com Keywords: heptocellular carcinoma (HCC), tumor associated antigens (TAA), proteomics, autoantibodies, biomarker Received: June 03, 2016 Accepted: December 05, 2016 Published: February 08, 2017 ABSTRACT Purpose: To identify Heptocellular carcinoma (HCC) associated antigens by proteomics, and validate whether autoantibodies against tumor-associated antigens (TAAs) could be used for diagnosis and conditional monitoring. Results: The 78 kDa glucose regulated protein (GRP78) was selected as a candidate TAA. The titers of autoantibodies against 78 kDa glucose regulated protein (GRP78) from patients with HCC, liver cirrhosis (LC), and chronic hepatitis (CH) were significantly higher than that from normal controls ( P

Preeclampsia is clinically divided into early onset and late onset preeclampsia based on the gestational age at delivery. Although the diagnostic criteria are the same in each subgroup of preeclampsia, it has been suggested that the maternal and perinatal mortalities of early onset and late onset preeclampsia are different. However, studies that compare clinical parameters or laboratory biomarkers between early onset and late onset preeclampsia are limited. Data on 177 women with early or late preeclampsia with severe hypertension were collected from a University Teaching Hospital from January 2010 to January 2011 and analysed. Data included all the clinical parameters and laboratory biomarkers of liver and renal function. 63 women and 114 women were diagnosed with early and late preeclampsia with severe hypertension, respectively. There was no difference in the maternal age and the incidence of clinical symptoms including edema, vision disturbance, severe headache and stillbirth between two groups. There was a decrease in alkaline phosphatase levels in early preeclampsia with severe hypertension but other markers of liver function were not altered. However, renal function including blood urea nitrogen, creatinine and uric acid were significantly higher in early preeclampsia with severe hypertension. Umbilical artery systolic velocity/diastolic velocity ratio was significantly higher in early preeclampsia with severe hypertension. Our data demonstrates that the laboratory biomarkers of renal function differ between early and late preeclampsia with severe hypertension. The severity of renal dysfunction correlated with the time of delivery in preeclampsia with severe hypertension.

Today the only effective "treatment" for preeclampsia is to deliver at the optimal time for both maternal and foetal well-being. Studies reported that severe preeclampsia can benefit from the expectant management including mild preeclampsia between 34 and 37 weeks. However it is unclear whether mild preeclampsia before 34 weeks also benefits from the expectant management. Data on 274 women with mild preeclampsia before 37 weeks of gestation were retrospectively collected and analysed. Blood pressure and proteinuria at time of onset were not clinically associated with delivery time. For women who developed preeclampsia before 34 weeks, the median latency from onset to delivery or from onset to admission to hospital or from admission to hospital to delivery was 27 or 21 or 3 days, respectively. There were four women (2%) who delivered within 48 h after onset, 28 (14%) FGR and 14 (7%) stillbirths. The median birth-weight was 2240 g. For women who developed preeclampsia between 34 and 37 weeks, the median latency from onset to delivery or from onset to admission to hospital or from admission to hospital to delivery was 11 or 7 or 2 days, respectively. There were seven women (10%) who delivered within 48 h after onset and eight (12%) FGR. The median birth-weight was 2880 g. Our study demonstrates that mild preeclampsia before 37 weeks has benefits from expectant or outpatient management with a median prolongation of over 11 days dependent on the time of onset, but it increases the risk for stillbirths before 34 weeks.

Preeclampsia is a leading cause of maternal and perinatal morbidity and mortality globally and proteinuria can be one of the cardinal features of this disease. However, studies about the association of the amount of proteinuria and the severity of preeclampsia, and perinatal outcomes are limited. Data on 239 women with preeclampsia were retrospectively collected from a university teaching hospital from September 2011 to June 2013 and analysed. Data included all clinical parameters and proteinuria in a 24h urine collection. In cases of severe preeclampsia, significantly fewer patients had proteinuria levels0.3g/L in comparison to any of the other groups with proteinuria0.3g/L, but there was no difference in cases of severe preeclampsia when proteinuria levels were0.3g/L. Furthermore, when proteinuria levels were0.3g/L, the frequency of severe preeclampsia in each group was significantly higher than the frequency of mild pre-eclampsia cases. Time of onset was significantly earlier in patients with proteinuria3g/L in a 24h urine collection, but time between the onset of preeclampsia and delivery was not correlated with the amount of proteinuria. The birth weight was significantly lower in patients with proteinuria3g/L. The incidence of fetal growth restriction or stillbirth was significantly higher in patients with proteinuria5g/L. Our data demonstrate that the amount of proteinuria is not associated with the severe of preeclampsia, once proteinuria is detected, but is related to the severity of preeclampsia. The adverse fetal outcomes appear to be the function of prematurity rather than proteinuria itself.

Approximately 60% of ovarian cancers are positive for the estrogen receptor (ER); however, ER-targeted treatment is disappointing due to drug resistance as compared with breast cancer. In estrogen-sensitive cancers, estrogen activates Src to phosphorylate p27 promoting its degradation and increasing cell cycle progression. Since Src is frequently activated in ovarian cancers, we investigated whether combined Src and ER blockade by saracatinib and fulvestrant would circumvent anti-estrogen resistance. In 20 out of 40 enrolled patients with immunohistochemically ER-positive ovarian cancer, phosphorylated Src (p-Src) at the site of 416 tyrosine was expressed with a propensity for metastasis and a poorer disease-free survival (DFS) at 3 years following ER antagonist treatment. The effects of ER and Src blockade on cell cycle were assayed in estrogen receptor α (ERα)-positive ovarian cancer. We observed that Src activity was fairly greater in anti-estrogen-resistant ovarian cancer cells than that in the anti-estrogen-sensitive cell line. Estrogen activated Src via ER-Src binding and ER translocation from cytoplasm to nucleus. Mitogenesis was mediated via ERα, not ERβ. Combined saracatinib and fulvestrant increased p27 and inhibited cell cycle progression. Furthermore, dual therapy induced autophagy and inhibited ovarian cancer xenograft growth more effectively than monotherapy. Saracatinib facilitated the therapeutic effects of fulvestrant by antagonizing the estrogen-mediated Src activation. These are supportive of further preclinical assessment of combined fulvestrant and saracatinib in patients with ovarian cancer.

Introduction Pre-eclampsia (PE) is the most serious syndrome of human pregnancy and it is potentially life-threatening for both mother and fetus. The aim of the study was to identify the role of high temperature requirement A1 (HtrA1) in pre-eclampsia. Material and methods One hundred consecutive pregnancies complicated by PE and 100 normal controls were included in our study. The changes in serum HtrA1 and fetal growth restriction were recorded. The placentae after delivery was also obtained for laboratory analyses. Results High temperature requirement A1 expressed positively in all placenta tissues, but showed higher expression from control, PE with AGA (pre-eclamptic pregnancies with appropriate-for-gestational-age newborns) to PE with fetal growth restriction (FGR) groups. Early-onset PE happened more frequently while in PE with AGA, late-onset PE was more common. Additionally, we found that only during ∼28-32 gestational weeks, sera HtrA1 level of PE with AGA and PE with FGR was increased significantly compared with the control group (p < 0.05). In contrast, there was no significant difference between groups in other gestational ages in the third trimester (p > 0.05). Conclusions HtrA1 could potentially affect trophoblast migration and invasion during placentation, resulting in the shallow invasion noted in pre-eclampsia. HtrA1 may play an important role in the etiology and severity of PE and FGR. But the actual mechanism still needs deep research.

Objective Throughout the world, fetal growth restriction(FGR) is one of the most severe complications occurring during pregnancy. It is subsequently associated with neurologic abnormalities in chldren. Our aim was to investigate the spatial learning and memory ability of rat offspring born with FGR. Methods A rat model of FGR was constructed using the method of passive smoking. Spatial learning and memory were studied in rat offspring born with FGR by assessing the animals' performance using the Morris water maze task. Results At 1- and 2-months of age, both female and male offspring rats showed impairment of performance, while at 4 months of age, only female rats showed impaired performance. The FGR offspring spent a longer time swimming and used inefficient strategies( P P Conclusion The Morris water maze performance decreased in rat offspring born with FGR. It is suggested that FGR can cause impairments of spatial learning and memory in young animals.

Objective To study effects of behavior training on learning, memory and the expression of NR2B, GluR1 in hippocampus of rat' s offspring with fetal growth restriction(FGR). Methods The rat model of FGR was established by passive smoking method. The rats offspring were divided into the FGR group and the control group, then randomly divided into the trained and untrained group, respectively. Morris water maze test was proceeded on postnatal month(PM2/4) as a behavior training method, then the learning-memory of rats was detected through dark-avoidance and step-down tests. The expressions of NR2B and GluR1 subunits in hippocampal CA1 and CA3 areas were detected by immunohistochemical method. Results In the dark-avoidance and step-down tests, the performance record of rats with FGR was worse than that of control rats, and the behavior-trained rats was better than the untrained rats, when the FGR model and training factors were analyzed singly. The model factor and training factor had significant interaction(P Conclusion These findings suggested that the effect of behavior training on the expressions of NR2B and GluR1 subunits in CA1 area should be the mechanistic basis for the training-induced improvement in learning-memory abilities.

Objective: To study the significance of Leptin and the activity of erythrocyte membrane Ca(superscript 2+)-ATPase(EMCA) in the development of hypertensive disorder complicating pregnancy. Methods: Radioimmunoassay was used to test the level of serum Leptin, and the activity of EMCA was determined chemically in 38 pregnant women with hypertensive disorder complicating pregnancy and 36 normotensive pregnant women. Results: The level of serum Leptin in hypertensive disorder complicating pregnancy (gestational hypertension: 13.76±3.46 ng/ml; preeclampsia: 15.76±5.47 ng/ml; eclampsia: 18.32±6.38 ng/ml) was significantly higher than that in normotensive pregnant women (11.33±2.93 ng/ml), respectively. The average EMCA activity of patients with hypertensive disorder complicating pregnancy (gestational hypertension: 1.65±0.24 μmol•pi/mg•h; preeclampsia: 1.37±0.19 μmol•pi/mg•h; eclampsia: 1.12±0.14 μmol•pi/mg•h) was significantly lower than that of normotensive pregnant women (1.83±0.38 μmol•pi/mg•h), respectively. There was a negative correlation between the level of serum Leptin and the activity of RMCA in hypertensive disorder complicating pregnancy (r=-0.63). Conclusion: Inhibition of EMCA activity of erythrocyte in hypertensive disorder complicating pregnancy may increase cytoplasmic free calcium, which contributes to the development of hypertensive disorder complicating pregnancy. The negative correlation between the level of serum Leptin and the activity of EMCA, also suggested that serum Leptin and the activity of EMCA may play a role in the development of hypertensive disorder complicating pregnancy.

Objective To investigate the value of PAPP-A (pregnancy assouated plasma protein-A) in the diagnosis and prognosis of gestational trophoblastic disease (GTD). Methods The serum β-HCG(β-human chorionic gonadotropin) and PAPP-A levels of 25 normal pregnant women, 28 patients with complete hydatidiform mole and 38 patients with invasive mole were measured by enzyme linked immunosorbent assay (ELISA) during the periods of diagnosis, treatment and follow-up. Results Compared with control group, patients with complete mole and invasive mole had higher levels of β-HCG ( P P > 0.05). The PAPP-A level of complete mole group was significantly higher than that of control group ( P P P Conclusion The PAPP-A level can give us some help not only in early diagnosis of hydatidiform mole and invasive mole, but also in the prognosis of malignant sequelae.

Introduction Preeclampsia is a pregnancy-specific disorder and placental factor(s) contribute to the pathogenesis of preeclampsia. Turnover of villous trophoblast is affected by impaired placental perfusion in preeclampsia. Expression and localisation of cadherins and cytokeratins are involved in the pathogenesis of preeclampsia. However, studies describing the associations between cadherins and cytokeratins in preeclampsia are limited. The aim of this study was to investigate the expression of E-cadherin, N-cadherin, cytokeratin 18 and cytokeratin 19 in placentae from women with preeclampsia in order to determine whether their expression differs with disease severity. Methods 29 preeclamptic placentae and 25 normotensive placentae were included in this study. The expression of E-cadherin, cytokeratin 18, cytokeratin 19 andN-cadherin was quantified by immunohistochemistry and western blotting. Results E-cadherin, cytokeratin 18 and cytokeratin 19 were expressed predominantly in the syncytiotrophoblast of the placenta and the expression of E-cadherin, cytokeratin 18 and cytokeratin 19 was significantly increased in preeclampsia compared to normotensive pregnancies. However, there was no significant difference in expression between severe preeclampsia and mild preeclampsia. In addition, there was no difference in the expression of N-cadherin between preeclampsic and normotensive pregnancies. Discussion Our data demonstrated increased expression of E-cadherin, cytokeratin 18 and cytokeratin 19 in the syncytiotrophoblast of preeclamptic placentae, but this increase was not correlated with disease severity. Conclusion Our data suggests that E-cadherin and cytokeratins are involved in the pathogenesis of preeclampsia.

The aim of the present study was to characterize the role of microRNA (miR)-155 in the pathogenesis of severe preeclampsia (PE). A total of 19 severe preeclampsic and 22 normal placentas were collected to measure miR-155 and endothelial nitric oxide synthase (eNOS) expression using quantitative (q)PCR and western blot analysis. The results demonstrated a significant increase in the levels of miR-155 and decreased eNOS expression in the severe preeclampsic placentas, as compared with the normal controls. In order to examine the function of miR-155 in the human placenta, the HTR8/Svneo cell line was transiently transfected with an miR-155 mimic or its inhibitor, anti-miR-155. It was confirmed that miR-155 may suppress the expression of eNOS in HTR-8/SVneo cells. Furthermore, a transwell insert invasion assay demonstrated that miR-155 inhibited cell invasion in trophoblast cells, and the effect was rescued by over expression of eNOS. The present study revealed that miR-155 has a negative regulatory role in the migratory behavior of HTR-8/SVneo cells via modulating eNOS.

To investigate the expression and changes of high-temperature requirement A1 (HtrA1) during pregnancy and the use of this value in predicting preeclampsia.Serum samples were collected from pregnant mothers at different gestational weeks, and double-antibody sandwich enzyme-linked immunosorbent assay was employed to describe the changes in HtrA1 in serum during pregnancy.(i) In Xi'an area of China, the incidence of preeclampsia was 4.95%, including 0.85% of early-onset type and 4.10% of late-onset type; (ii) the HtrA1 showed a lognormal distribution during pregnancy in the maternal serum, with the peak at 17-20 weeks of pregnancy; (iii) the HtrA1 levels in preeclampsia mothers peaked at 13-16 weeks of pregnancy, followed by acute decline until 21-24 weeks, then remained stable; (iv) the HtrA1 levels in preeclampsia mothers were higher than the control group in 13-16 weeks and lower than that in 21-24 weeks (p0.05); (v) the criteria using lgHtrA1 level at 1.684 during 13-16 weeks of pregnancy could predict hypertension disorders complicating pregnancy (HDCP) with sensitivity of 62.1% and specificity of 53.7%. This could be improved to 85 and 83%, respectively, when combined with body mass index as well as education background of the mother.(i) HtrA1 showed lognormal distribution during pregnancy for all populations; (ii) HtrA1 level peaked at 17-20 weeks in normal group of pregnant mothers, and the increase of HtrA1 level in 13-16 weeks could predict the risk of preeclampsia; (iii) the risk calculation formula for preeclampsia: p (%) = eY/(1 + eY) (Y = -15.87 + 3.706 × lgHtrA1 + 0.134 × mean arterial pressure (MAP) - 1.4 × education level code); e = 2.718.

Introduction Preeclampsia is a major complication of pregnancy affecting maternal and fetal health. Although the pathogenesis of preeclampsia is unclear, it is believed that trophoblast apoptosis plays an important role in the pathogenesis of preeclampsia during pregnancy. Survivin is a member of the inhibitor of apoptosis protein family that uniquely promotes trophoblast proliferation. In this study we investigated the alteration of survivin levels during pregnancy and compared the survivin protein and mRNA between preeclampsia and normal pregnancy. Methods The mRNA level of survivin in first, second and third trimester placentae was measured by Real-time PCR. The expression of survivin in preeclamptic placentae (including severe and mild preeclampsia) and in age-matched normal placentae was measured by immunohistochemistry. The mRNA levels of survivin in preeclamptic or normal placentae were measured by Real-time PCR. Results The mRNA level of survivin was significantly reduced throughout gestation. The mRNA level of survivin in preeclamptic placentae was significantly reduced compared to that in normal placenta. The mRNA level of survivin in severe preeclamptic placentae was further significantly reduced compared to that in mild preeclamptic placentae. In addition, survivin was expressed on syncytiotrophoblasts and cytotrophoblasts and the expression of survivin was significantly decreased in preeclamptic placenta compared to that in normal placenta ( p = 0.01). Furthermore the expression of survivin in severe preeclamptic placentae was significantly lower than that in mild preeclamptic placentae. Conclusion Our current data suggests lower placental expression of survivin may be associated with the severity of preeclampsia.

To study the relationship between human leucocyte antigen (HLA), parents' sharing rate and the incidence of pregnancy induced hypertension (PIH), and investigate its immunopathogenetic roles to severe PIH.Newborn's and their parents' peripheral blood DNA was extracted and HLA phenotypes were studied by sequence-specific primers polymerase chain reaction (SSP-PCR) in 57 with PIH and 46 normal pregnancy.The frequency of DRB1 * 0306, DRB1 * 0405, DRB1 * 0315, DRB1 * 0403, DRB1 * 1304, QB1 * 03032/33, DQB1 * 0502 in women with PIH was increased significantly and the frequency of DRB1 * 0407, DRB1 * 0317, DQB1 * 05031 were lower than controls. And the risk to PIH of women with DRB1 * 0306, DRB1 * 0405, DQB1 * 0502 were higher than others (RR: 9.76, 6.34, 4.20), and its gene-frequency was higher than controls (P0.01). Frequency of DQB1 * 0502, DRB1 * 0405 in PIH's newborns were higher than controls (P0.05), but DRB1 * 1304, DQB1 * 05031 were lower than controls, with significant difference (P0.05); The gene-frequency of fathers of the two groups weren't different. The HLA sharing rate of mothers or fathers of the two groups weren't different. But that of mother-fetus was higher in PIH than controls. Two locus alleles of PIH group constructed haplotype, and the DRB1 * 0315-DQB1 * 0502, DRB1 * 0405-DQB1 * 06012 antibody was positive with hypertension and protenuria (P0.05).PIH is associated with HLA, and the over expression of HLA genes was a severe cause of PIH.