Late-onset Pregnancy-induced Hypertension Research Articles

Histopathological findings of pregnancy-induced hypertension: histopathology of early-onset type reflects two-stage disorder theory.

The placental tissues of pregnancy-induced hypertension (PIH) patients exhibit multiple infarctions, acute atherosis, distal villous hypoplasia, and increased syncytial knots. However, these findings are not observed in all cases of PIH; thus, the significance of these changes in PIH is still unclear. We studied the frequency of histopathological changes of placental tissue in the subgroups of PIH, such as mild and severe PIH and early-onset (< 34weeks) and late-onset (≥ 34weeks) PIH. One hundred seven cases of PIH diagnosed at the Shinshu University Hospital, Matsumoto, Japan, between 2008 and 2014 were collected. PIH includes preeclampsia and gestational hypertension. The pathologic changes evaluated in the placenta were multiple infarctions, acute atherosis, distal villous hypoplasia, and increased syncytial knots. Placental tissues of patients with early-onset PIH demonstrated acute atherosis resulting from the incomplete remodeling of the spiral arteries and distal villous hypoplasia and increased syncytial knots reflecting placental hypoxia/ischemia much more frequently than those with late-onset PIH (all p < 0.001). The frequencies of multiple infarctions did not show a statistical difference between early-onset PIH and late-onset PIH. Moreover, there were no significant differences in the frequencies of histopathological features of placental tissue between mild PIH and severe PIH. Early-onset PIH exhibited histopathological changes of placental tissue consistent with the two-stage disorder theory more frequently than late-onset PIH. These findings support the idea that early-onset PIH and late-onset PIH are distinct entities or different extremes of the PIH spectrum.

Maternal history and uterine artery wave form in the prediction of early-onset and late-onset preeclampsia: A cohort study

Pregnancy induced hypertension (PIH) is a significant cause of maternal morbidity and mortality. Pregnancy-induced-hypertension can be prevented by identification of prenatal and antenatal factors. The uterine artery Doppler waveform transforms into a high flow with low resistance at 22-24 wk. To study the maternal risk factors and uterine artery Doppler waveform in singleton mid-trimester pregnancy and predict the occurrence of pregnancy-induced hypertension. This is a cohort study comprising of Doppler ultrasound examination of the uterine arteries at 20-23 wk gestation in 697 women with singleton pregnancies attending a routine target scan. The pregnant women were followed up. PIH was recorded in 57 (8.18%) of all pregnancies. Maternal age >34 yr, primiparity, the presence of chronic hypertension was also associated with increased risk of PIH. High pulsatility index (>95th percentile) as compared to low pulsatility index was a good tool for the detection of PIH (sensitivity 91.23% and specificity 99.06%, p<0.05). Presence of high pulsatility was a significant risk factor for early-onset PIH as compared to late-onset PIH. Uterine artery Doppler can be safely performed at the time of routine target anomaly scan in the second trimester. It is simple, economical, feasible and with good detection rates.

Usefulness of placental volume on three-dimensional ultrasound and Doppler findings in uterine artery to predict early and late onset pregnancy-induced hypertension

Usefulness of placental volume on three-dimensional ultrasound and Doppler findings in uterine artery to predict early and late onset pregnancy-induced hypertension

Re: Prediction of early- and late-onset pregnancy-induced hypertension using placental volume on three-dimensional ultrasound and uterine artery Doppler. T. Arakaki, J. Hasegawa, M. Nakamura, S. Hamada, M. Muramoto, H. Takita, K. Ichizuka and A. Sekizawa. Ultrasound Obstet Gynecol 2015; 45: 539-543.

Linked Comment: Ultrasound Obstet Gynecol 2015; 45: 539–543

Expression of Angiotensin II Receptor-like 1 in the Placentas of Pregnancy-induced Hypertension

Angiotensin II receptor-like 1 (APJ), a G protein-coupled receptor that was identified as a homologue of angiotensin II type 1 (AT1) receptor, exerts antagonistic effects on AT1-mediated vasoconstriction. Studies on pregnancy-induced hypertension (PIH) revealed aberrant activation of AT1 downstream signaling. In contrast, little is known about APJ in the pathophysiology of human pregnancy. In this study, we investigated APJ expression in normal human and PIH placentas. mRNAs were extracted from 50 placental villous tissues of 18 cases with severe PIH (8 late-onset, 4 early-onset, and 6 superimposed PIH) and 32 control pregnancies (including 6 preterm cases). Histopathologic studies were conducted using paraffin-embedded placental tissues from 12 control placentas (from 23 to 39 wk) and 23 PIH placentas (from 24 to 41 wk). Reverse transcriptase-polymerase chain reaction showed that APJ was cooperatively expressed with its ligand apelin and AT1 in controls and in late-onset PIH placentas but was significantly downregulated in early-onset PIH placentas with poor fetal growth. Quantitative reverse transcriptase-polymerase chain reaction analysis revealed upregulated APJ in late-onset PIH placentas but significantly downregulated APJ in early-onset PIH. In immunohistochemical staining, APJ was detected strongly in villous capillary endothelial cells and trophoblasts of late-onset PIH placentas. In contrast, APJ was poorly stained in endothelial cells of hypoplastic villi of early-onset PIH placentas. Collective data indicate that the apelin-APJ system is involved in fetoplacental circulation during human pregnancy. Impaired APJ expression in early-onset PIH placentas may reflect an aggravated placental condition with poor fetal growth.

The effects of smoking and hypertensive disorders on fetal growth

BackgroundIt is well known that smoking and pregnancy induced hypertension (PIH) are associated with decreased fetal growth. It has been reported that in preeclampsia the fetal growth deficit attributable to smoking is higher, which has been contradicted in other studies. We therefore evaluated the effects on fetal growth of early- and late onset PIH and chronic hypertension and how cigarette smoking modify these effects. We also quantified the proportion of small for gestational age (SGA) cases attributable to PIH, chronic hypertension, and smoking.MethodsPopulation-based study based on record of 215598 singleton pregnancies from the Medical Birth Registry of Norway.ResultsIn severe preeclampsia, mild preeclampsia, transient hypertension, and normotension in term birth, odds ratios (ORs) of SGA in smokers compared with non-smokers were 1.4 (95% confidence interval 0.9, 2.2), 1.6 (1.3, 1.9), 2.3 (1.8, 3.1), and 2.0 (1.9, 2.1), respectively. For preterm births, corresponding ORs were 1.3 (0.9, 2.0), 1.8 (1.1, 3.0), 4.1 (1.9, 9.0), and 1.7 (1.4, 2.0), respectively. The effect of early onset PIH was stronger than that in term births, while the effect of smoking was equal in preterm and term newborns. Only in non-smokers who delivered at term, the rates of SGA significantly increased with the severity of PIH (ORs = 1.3 (1.1, 1.5), 1.8 (1.7, 2.0), and 2.5 (2.2, 3.0) for transient hypertension, mild-, and severe preeclampsia, respectively). The combined effects of smoking and hypertension were generally not synergistic. The effect of smoking was not stronger in women who had chronic hypertension. Nor were the effects of chronic hypertension stronger in smokers. PIH explained 21.9 and 2.5% of preterm and term cases of SGA, respectively, while smoking explained 12% of SGA cases.ConclusionThe effects of hypertensive disorder and smoking were generally not synergistic, which suggest that they may exert their main actions on separate sites or work through separate mechanisms within or outside the placenta. If smoking were eliminated in pregnant women, the number of SGA cases would be reduced by 12%.

A randomised placebo controlled trial of labetalol in the treatment of mild to moderate pregnancy induced hypertension

To determine the need for, and efficacy of, treatment with labetalol in women with mild-to-moderate pregnancy induced hypertension (PIH). Prospective double-blind randomised placebo controlled study. Maternity units of five hospitals in the Trent Region. 144 women (86 primigravid) who developed PIH after 20 weeks gestation. Treatment with oral labetalol up to 600 mg daily or placebo with subsequent care of treatment failures in accordance with the attending obstetrician's practice. Number of days spent as an antenatal inpatient; the development of proteinuria; the perceived need for induction of labour or elective caesarean section; and gestation age at delivery. Labetalol significantly lowered the blood pressure and reduced the incidence of proteinuria. However, neither the number of days spent as an antenatal inpatient, nor the perceived need for induction of delivery or elective caesarean section, nor the gestation age at delivery differed significantly between the two treatment groups. Post-randomisation consideration of early (< or = 32 weeks) and late (> 32 weeks) onset groups showed the placebo treated early-onset group (n = 15) to have more patients with severe hypertension (> 150/110 mmHg) and a greater requirement for additional antihypertensive therapy prior to labour than the group treated with labetalol (n = 16). Anti-hypertensive intervention therapy in pregnancy induced hypertension has been examined using a placebo controlled randomised double-blind trial of labetalol in pregnancy. The maximum blood pressure prior to labour and the incidence of proteinuria was reduced in women on active therapy. However, the length of gestation was not significantly prolonged and indices of clinical outcome were not significantly altered. The appropriateness of pharmacological therapy for late-onset PIH may be questioned.