Preeclamptic Pregnancies Research Articles

Pregnancy outcomes and risk factors for preeclampsia in dichorionic twin pregnancies after in vitro fertilization: a five-year retrospective study

BackgroundBoth in vitro fertilization (IVF) and preeclampsia (PE) were associated with placental dysfunction. Although IVF can increase the incidence of PE, the pregnancy outcomes and risk factors for preeclampsia in dichorionic twin pregnancies conceived via IVF remain unclear. This study aimed to investigate the pregnancy outcomes and the risk factors for preeclampsia in dichorionic twin pregnancies conceived through IVF compared to those conceived after natural conception (NC).MethodsThis retrospective observational study enrolled 181 dichorionic twin pregnancy women with preeclampsia from 2016 to 2020. According to the mode of conception, they were allocated into IVF (n = 117) and NC groups (n = 64). The clinical characteristics of preeclampsia and pregnancy outcomes between the two groups were compared by using Student’s t test, chi-square test, and Fisher’s exact test, and logistic regression models were used to obtain adjusted odds ratios (aOR) with 95% confidence intervals (CI) for risk factors of early-onset preeclampsia.ResultsThe incidence of early-onset PE and growth discordance in dichorionic twin pregnancies with PE is significantly higher in IVF-PE group than in NC group (78.60% vs 43.80%, P < 0.001, 11.10% vs 25.00%, P = 0.015). We found that IVF (aOR = 4.635, 95% CI: 2.130–10.084, P < 0.001) and growth discordance (aOR = 3.288; 95% CI: 1.090–9.749, P < 0.05) increased the incidence of early-onset PE.ConclusionsIn preeclamptic dichorionic twin pregnancies, IVF and growth discordance were associated with the increased incidence of early-onset PE. The underlying mechanism for the relationship between IVF and early-onset PE or growth discordance may be placental dysfunction.

Aspirin Inhibits the Inflammatory Response of Protease-Activated Receptor 1 in Pregnancy Neutrophils: Implications for Treating Women with Preeclampsia.

Neutrophils expressing cyclooxygenase-2 (COX-2) extensively infiltrate maternal blood vessels in preeclampsia, associated with vascular inflammation. Because pregnancy neutrophils also express protease-activated receptor 1 (PAR-1, F2R thrombin receptor), which they do not in non-pregnant subjects, they can be activated by proteases. We tested the hypothesis that aspirin at a dose sufficient to inhibit COX-2 would reduce inflammatory responses in preeclampsia neutrophils. Neutrophils were isolated from normal pregnant and preeclamptic women at approximately 30 weeks' gestation. Normal pregnancy neutrophils were treated with elastase, a protease elevated in preeclampsia, or elastase plus aspirin to inhibit COX-2, or elastase plus pinane thromboxane, a biologically active structural analog of thromboxane and a thromboxane synthase inhibitor. Preeclamptic pregnancy neutrophils were treated with the same doses of aspirin or pinane thromboxane. Confocal microscopy with immunofluorescence staining was used to determine the cellular localization of the p65 subunit of nuclear factor-kappa B (NF-κB) and media concentrations of thromboxane were measured to evaluate the inflammatory response. In untreated neutrophils of normal pregnant women, p65 was localized to the cytosol. Upon stimulation with elastase, p65 translocated from the cytosol to the nucleus coincident with increased thromboxane production. When neutrophils were co-treated with aspirin or pinane thromboxane, elastase was not able to cause nuclear translocation of p65 or increase thromboxane. In untreated neutrophils of preeclamptic women, the p65 subunit was present in the nucleus and thromboxane production was elevated, but when preeclamptic neutrophils were treated with aspirin or pinane thromboxane, p65 was cleared from the nucleus and returned to the cytosol along with decreased thromboxane production. These findings suggest that COX-2 is a downstream mediator of PAR-1 and demonstrate that PAR-1- mediated inflammation can be inhibited by aspirin. Given the extensive and ubiquitous expression of PAR-1 and COX-2 in preeclamptic women, consideration should be given to treating women with preeclampsia using a dose of aspirin sufficient to inhibit COX-2.

Serum Collected from Preeclamptic Pregnancies Drives Vasoconstriction of Human Omental Arteries-A Novel Ex Vivo Model of Preeclampsia for Therapeutic Development.

New-onset maternal hypertension is a hallmark of preeclampsia, driven by widespread endothelial dysfunction and systemic vasoconstriction. Here, we set out to create a new ex vivo model using preeclamptic serum to cause injury to the endothelium, mimicking vascular dysfunction in preeclampsia and offering the potential to evaluate candidate therapeutic interventions. Human omental arteries were collected at caesarean section from normotensive pregnant patients at term (n = 9). Serum was collected from pregnancies complicated by preterm preeclampsia (birth < 34 weeks’ gestation, n = 16), term preeclampsia (birth > 37 weeks’ gestation, n = 5), and healthy gestation-matched controls (preterm n = 16, term n = 12). Using wire myography, we performed ex vivo whole vessel assessment where human omental arteries were treated with increasing doses of each serum treatment (2–20%) and vasoreactivity was assessed. All pregnant serum treatments successfully drove vasoconstriction; no significant difference was observed in the degree of vasoconstriction when exposed to preeclamptic or control serum. We further demonstrated the ability of esomeprazole (a candidate therapeutic for preeclampsia; 0.1–100 µM) to drive vasorelaxation of pre-constricted vessels (only with serum from preeclamptic patients). In summary, we describe a novel human physiological model of preeclamptic vascular constriction. We demonstrate its exciting potential to screen drugs for their therapeutic potential as treatment for vasoconstriction induced by preeclampsia.

Blood-brain barrier leakage years after pre-eclampsia: dynamic contrast-enhanced 7-Tesla MRI study.

Pre-eclampsia is a hypertensive complication of pregnancy that is associated with an increased risk of long-term cardiovascular and cerebrovascular disorders. Although the underlying mechanism of persistent susceptibility to cerebral complications after pre-eclampsia remains largely unclear, impaired blood-brain barrier (BBB) integrity has been suggested to precede several cerebrovascular diseases. In this study, we aimed to investigate the integrity of the BBB years after pre-eclampsia. This was an observational study of premenopausal formerly pre-eclamptic women and controls with a history of normotensive pregnancy who underwent cerebral magnetic resonance imaging (MRI) at ultra-high field (7Tesla) to assess the integrity of the BBB. Permeability of the BBB was determined by assessing leakage rate and fractional leakage volume of the contrast agent gadobutrol using dynamic contrast-enhanced MRI. BBB leakage measures were determined for the whole brain and lobar white and gray matter. Multivariable analyses were performed, and odds ratios were calculated to compare women with and those without a history of pre-eclampsia, adjusting for potential confounding effects of age, hypertension status at MRI and Fazekas score. Twenty-two formerly pre-eclamptic women (mean age, 37.8 ± 5.4 years) and 13 control women with a history of normotensive pregnancy (mean age, 40.8 ± 5.5 years) were included in the study. The time since the index pregnancy was 6.6 ± 3.2 years in the pre-eclamptic group and 9.0 ± 3.7 years in controls. The leakage rate and fractional leakage volume were significantly higher in formerly pre-eclamptic women than in controls in the global white (P = 0.001) and gray (P = 0.02) matter. Regionally, the frontal (P = 0.04) and parietal (P = 0.009) cortical gray matter, and the frontal (P = 0.001), temporal (P &lt; 0.05) and occipital (P = 0.007) white matter showed higher leakage rates in formerly pre-eclamptic women. The odds of a high leakage rate after pre-eclampsia were generally higher in white-matter regions than in gray-matter regions. This observational study demonstrates global impairment of the BBB years after a pre-eclamptic pregnancy, which could be an early marker of long-term cerebrovascular disorders. © 2022 The Authors. Ultrasound in Obstetrics &amp; Gynecology published by John Wiley &amp; Sons Ltd on behalf of International Society of Ultrasound in Obstetrics and Gynecology.

Serum neuregulin-4 levels in healthy and preeclamptic pregnancies: correspondence.

Serum neuregulin-4 levels in healthy and preeclamptic pregnancies: correspondence.

First trimester serum biomarker discovery study for early onset, preterm onset and preeclampsia at term

IntroductionPreeclampsia (PE) is a heterogeneous syndrome during pregnancy and postpartum and it is subdivided in this study into early onset (<34 weeks), preterm onset (34–37 weeks) and PE at term (>37 weeks). First trimester models currently lack a sufficient power to predict PE, but inclusion of biochemical markers shows an improvement of their predictive power. The aim of this study was to perform a biomarker discovery study in order to find possible novel first trimester biomarkers for each PE subtype. Further, our findings were related to available literature and the possible role of the proteins in the development of preeclampsia was discussed. MethodsIn this study, 9 early onset (<34 weeks), 8 preterm onset (34–37 weeks), 6 PE at term (>37 weeks) and 23 control samples were drawn between 11 and 14 weeks gestational age. Serum samples were prepared for liquid chromatography mass spectrometry analysis and protein data were exported for statistical analyses. All differentially expressed proteins were further evaluated by searching literature in MEDLINE, Embase and Web of science and differential expression of two proteins, which were not yet associated with PE, was verified through enzyme-linked immunosorbent assay (ELISA). ResultsAfter statistical analysis, six, four and eight proteins were differently expressed in early onset, preterm onset and PE at term, respectively. After exclusion of antibody fragments, only nine proteins remained. Seven out of these nine proteins were already in literature associated with preeclampsia and only three of them were described as differentially expressed in the first trimester or early second trimester of preeclamptic pregnancies. Differential expression of Apolipoprotein D (ApoD), which was not yet associated with PE, was confirmed by ELISA in both early and preterm onset PE in the first trimester. DiscussionIn this study, two main observations were made. First, some of the differentially expressed proteins have a role in the same biological pathway, such as the acute phase response or endometrium receptivity, and their differential expression was observed in all three PE subtypes. This observation supports the hypothesis that classification of PE could be more accurate when subtyping is based on the etiology and/or phenotype instead of the arbitrary parameter gestational age at onset or delivery. Second, seven differential expressed proteins were already associated in literature with preeclampsia, but this association was for only three of them observed in the first trimester. In addition, ApoD was not yet associated with PE in other studies and, moreover, its differential expression was confirmed by ELISA. Therefore the predictive power of these proteins in the first trimester is worth evaluating in a larger and more heterogeneous cohort.

Circulating levels of transforming growth factor beta-1, 2 and 3 in HIV associated preeclamptic pregnancies

The active role of transforming growth factor-beta in implantation, embryonic development and decidualization has driven our interest to evaluate circulating TGF-β(1–3) in the synergy of HIV associated pregnancy. Serum TGF-β(1–3) was quantified in normotensive (n = 38) and preeclamptic (n = 38) pregnant women, who were stratified by HIV status, HIV negative (n = 19) and HIV positive (n = 19), using a Bioplex immunoassay. Based on HIV status, we report no significant difference in TGF-β-1 (p = .95) and TGF-β2 (p = .80) however, TGF-β3 was significantly downregulated in HIV positive (p = .03) vs the HIV negative groups. A significant positive correlation (p < .05) was noted between TGF-β3 and gestational age (p = .03) (r = 0.51), birth weight (p = .04) (r = 0.53) and CD4 count (p = .02) (r = 0.53). Bivariate correlation between isoforms based on HIV status showed several significant positive associations. In the synergy of HIV infected PE, we demonstrate an association between TGF-β(1–3) with PE emanating from the hypoxic microenvironment that affects receptor-SMAD activity. Decreased TGF-β3 levels in HIV infected PE, may originate from ARV usage and/or the mutational/physiological dysregulation of SMAD expression. Impact Statement What is already known on this subject? TGF-β overexpression can convert its protective functions into pathogenic variants. It has a significant role in the oxidatively stressed and inflammatory condition of tissue fibrosis and hence may also be dysregulated in the microenvironment of PE. In HIV infection, TGF-β promotes viral replication and spreading through the induction of cellular proteins which induce TGF-β production. Also, mononuclear phagocytes infected with HIV also produce increased TGF-β mRNA and proteins. What do the results of the study add? Our results show no association of TGF-β isoforms (1–3) based on pregnancy type (PE vs normotensive pregnant) at term. The lack of association may be linked to TGF-βs dual promoter/suppresser nature or to gestational age. What are the implications of these findings for clinical practice and/or further research? Large-scale comprehensive clinical trials are warranted to elucidate the association and mechanistic role of TGF-β receptor-SMAD signalling, the effect of its inhibitors on cell invasion and angiogenesis as well as to deliver valuable data for the detection of novel therapeutic agents in pregnancies complicated by HIV infection.

Intrahepatic cholestasis of pregnancy: Green-top Guideline No. 43 June 2022.

Intrahepatic cholestasis of pregnancy: Green-top Guideline No. 43 June 2022.

Impact of preeclampsia on cardiovascular risk factors in mothers and newborns

Background and Aims : The increased risk of cardiovascular disease and mortality in later life of women with preeclamptic pregnancies is well-known. The impact of preeclampsia on the offspring is, however, still uncertain. The aim of the present study was to investigate the impact of preeclampsia on both mother and offspring.

Peripartum and Long-Term Maternal Cardiovascular Health After Preeclampsia.

There is widespread acceptance of the increased prevalence of cardiovascular diseases occurring within 1 to 2 decades in women following a preeclamptic pregnancy. More recent evidence suggests that the deranged biochemical and echocardiographic findings in women do not resolve in the majority of preeclamptic women following giving birth. Many women continue to be hypertensive in the immediate postnatal period with some exhibiting occult signs of cardiac dysfunction. There is now promising evidence that with close monitoring and effective control of blood pressure control in the immediate postnatal period, women may have persistently lower blood pressures many years after stopping their medication. This review highlights the evidence that delivering effective medical care in the fourth trimester of pregnancy can improve the long-term cardiovascular health after a preeclamptic birth.

Relationship between maternal serum uric acid level and preeclampsia with or without severe features

Hyperuricaemia is common in preeclampsia. Its relationship and the utility in predicting of preeclampsia must be evaluated. The objective was to determine the association between maternal serum uric acid level and preeclampsia with or without severe features, including maternal and neonatal outcomes. A retrospective study was conducted at Rajavithi Hospital between June 2015 and May 2019. Inferential analysis comparison using binary logistic regression analysis and correlation using Chi-Square test/Fisher’s exact test were used for analysis. Among the 400 participants, 331 (82.7%) women were preeclampsia with severe features. The mean uric acid level was significantly higher in women with preeclampsia with severe features compared to those without (6.44 ± 1.44 vs 5.87 ± 1.53 mg/dL, p-value = .016). Uric acid greater than 7 mg/dL was associated with renal involvement and preeclampsia with severe features. Uric acid 5–7 and greater than 7 mg/dL correlated with preterm birth (OR 2.67, 95% CI 1.59–4.49 and OR 4.89, 95% CI 2.75–8.68, respectively). Uric acid greater than 7 mg/dL also increased the risk of RDS and NICU admission. In conclusion, a high uric acid level is associated with preeclampsia with severe features and adverse pregnancy outcomes and may be the predictor of the severity of preeclampsia. Impact statement What is already known on this subject? Hyperuricaemia is a common finding in preeclamptic pregnancy due to reduction of uric acid clearance secondary to reduced glomerular filtration rate, increased reabsorption, and decreased secretion. The correlation of increase maternal uric acid level and preeclampsia including adverse pregnancy outcomes has been evaluated and supported the use of uric acid as a predictor for preeclampsia development. However, its clinical utility is still debateable. What the results of this study add? The present study demonstrated the association between higher maternal serum uric acid level and severity of preeclampsia. Particularly, serum uric acid greater than 7 mg/dL was associated with preeclampsia with severe features. Additionally, serum uric acid level 5–7 mg/dL and greater than 7 mg/dL had a positive correlation with adverse maternal and neonatal outcomes. What the implications are of these findings for clinical practice and/or further research? Maternal serum uric acid may be used as the predictor of severity of preeclampsia. However, the sensitivity and specificity and the precise clinical utility of uric acid related to preeclampsia need to be further evaluated in larger sample size.

Human leukocyte antigen HLA-C, HLA-G, HLA-F, and HLA-E placental profiles are altered in early severe preeclampsia and preterm birth with chorioamnionitis

The extravillous trophoblast expresses each of the nonclassical major histocompatibility complex class I antigens-human leukocyte antigens E, F, and G-and a single classical class I antigen, human leukocyte antigen C. We recently demonstrated dynamic expression patterns of human leukocyte antigens C, G, and F during early extravillous trophoblast invasion and placentation. This study aimed to investigate the hypothesis that the immune inflammatory mediated complications of pregnancy such as early preeclampsia and preterm labor may show altered expression profiles of nonclassical human leukocyte antigens. Real-time quantitative polymerase chain reaction, western blot, and immunohistochemistry were performed on placental villous tissues and basal plate sections from term nonlaboring deliveries, preterm deliveries, and severe early-onset preeclampsia, both with and without small-for-gestational-age neonates. Human leukocyte antigen G is strongly and exclusively expressed by the extravillous trophoblast within the placental basal plate, and its levels increase in pregnancies complicated by severe early-onset preeclampsia with small-for-gestational-age neonates relative to those of healthy term controls. Human leukocyte antigen C shows a similar profile in the extravillous trophoblast of preeclamptic pregnancies, but significantly decreases in the villous placenta. Human leukocyte antigen F protein levels are decreased in both extravillous trophoblast and villous placenta of severe early-onset preeclamptic pregnancies, both with and without small-for-gestational-age neonates, compared with those found in term and preterm birth deliveries. Human leukocyte antigen E decreases in blood vessels in placentas from preeclamptic pregnancies relative to its levels in term and preterm birth deliveries. Placental levels of human leukocyte antigens F and C are increased in cases of preterm birth with chorioamnionitis relative to those of cases of idiopathic preterm birth. Dysregulation of placental human leukocyte antigen expression at the maternal-fetal interface may contribute to compromised maternal tolerance in preterm birth with chorioamnionitis and excessive maternal systemic inflammation associated with severe early-onset preeclampsia.

Linking inflammatory adipose tissue to placental abnormalities in obese preeclamptic pregnancies.

Preeclampsia (PE), a pregnancy-specific disorder, is characterized by maternal hypertension and proteinuria or another accompanying sign/symptom of multiorgan dysfunction. Maternal symptoms resolve with delivery of the baby and, importantly, the placenta. Therefore, the placenta plays a causal role in PE. However, the precise cause of abnormal placental development and/or function is unknown. Women with obesity have an increased risk of developing PE that is potentially related to the increased inflammation that accompanies increased maternal adiposity. Furthermore, inflammatory adipokines, i.e., leptin, have been linked to the development of systemic inflammation, hypertension, and other adverse outcomes associated with PE. Rodent models that recapitulate key pathophysiological features of the maternal and fetal syndrome have been used translationally to study PE. This review covers inflammatory adipokines, immune cells, and impaired placental development associated with PE in women and in rodent models of PE that use functional genomics to test causation.

Searching for a paternal phenotype for preeclampsia

AbstractIntroductionPreeclampsia (PE) is a heterogeneous disorder and research to date has principally focused on maternal factors. In this study, however, we considered the associations between background factors and preeclampsia in men who fathered preeclamptic and non‐preeclamptic pregnancies.Material and methodsFrom 2008 to 2011, participants in the Finnish Genetics of Pre‐eclampsia Consortium (FINNPEC) cohort completed a questionnaire on their background information. Questionnaire data were available from 586 men who had fathered a preeclamptic pregnancy (PE fathers) and 660 control men who had fathered a non‐preeclamptic pregnancy. Two different control groups were established: Group 1: healthy controls (n = 457), which consisted of fathers whose current partners were healthy women with uncomplicated pregnancies; Group 2: other controls (n = 203), which also included fathers whose current partners had other pregnancy complications.ResultsThe PE fathers more often reported preeclampsia in a previously fathered pregnancy (p &lt; 0.05 for all). The PE and control fathers were similar in age, body mass index, smoking, and preexisting medical conditions. There were no differences in the socioeconomic background or health history of the PE and control fathers or their parents.ConclusionsIn the FINNPEC study cohort, the occurrence of preeclampsia in a previously fathered pregnancy was more common among the men who had fathered a preeclamptic pregnancy; other paternal phenotypic and lifestyle characteristics did not play a significant role in preeclampsia susceptibility of their partners.

Does HAART dysregulate angiogenesis in HIV infected preeclampsia?

A dysregulation of angiogenic mediators has been implicated in HIV infection. Inconsistent data exists on highly active antiretroviral therapy (HAART) usage in pregnancy and its association with PE development. In view of the high prevalence of HIV infection and PE in SA, this study was aimed at determining PlGF and sFlt-1 levels in HIV-infected normotensive and preeclamptic pregnancies treated with HAART. Both PlGF and sFlt-1 were quantified in serum from HIV positive [normotensive (N+) and preeclamptic (P+)]; and HIV negative [normotensive (N-) and preeclamptic (P-)] pregnancies, using a Milliplex Multiplex immunoassay. sFlt-1 was significantly upregulated in P+ vs the N+ groups. PlGF was significantly downregulated in PE vs normotensive groups, regardless of HIV status. sFlt-1/PlGF ratio was significantly increased in PE- vs the N- groups. We report an amplification of sFlt-1 in lieu of PlGF down-regulation in HIV-infected pregnancies receiving HAART .

Levels of blood pressure, cardiovascular biomarkers and their correlations in women with previous pre-eclamptic pregnancy within 7 years postpartum: a cross-sectional study in Thailand

ObjectiveTo assess the levels of blood pressure, cardiovascular biomarkers and their correlations measured within 7 years postpartum in women with previous pre-eclamptic pregnancies compared with women with previous normotensive pregnancies.DesignCross-sectional...

Downregulation of miR-1270 mediates endothelial progenitor cell function in preeclampsia: Role for ATM in the Src/VE-cadherin axis.

Preeclampsia, a pregnancy-related hypertensive disorder, is associated with endothelial dysfunction and increased cardiovascular risk of the offspring in adulthood. In preeclampsia, endothelial colony-forming cells (ECFC) are reduced in number and function. Recently, we have shown that miR-1270, which is involved in cancer in vitro proliferation, migration, and tumor progression, is downregulated in fetal ECFC from preeclamptic pregnancies. We now hypothesize that miR-1270 dysregulation contributes to vascular endothelial dysfunction occurring after preeclampsia via ATM (ataxia telangiectasia mutated) overexpression, the key kinase of DNA damage repair. Here, we show that miR-1270silencing in normal ECFC and downregulation in preeclamptic ECFC are accompanied by an increase in the expression levels of ATM. Furthermore, ATM activation correlates with upregulated tyrosine kinase Src leading to phosphorylation and internalization of VE-cadherin (vascular endothelial-cadherin) which subsequently compromises endothelial barrier permeability and morphodynamic cell parameters. Treatment with specific ATM inhibitors reveals a novel role of ATM upstream of tyrosine kinase Src activation. Subsequently, Src phosphorylation and internalization of VE-cadherin compromise endothelial barrier permeability. Our findings suggest that downregulation of miR-1270 contributes to impaired ECFC function via the associated ATM overexpression, which further identifies ATM as a novel and critical factor for ECFC defects in preeclampsia. Our study provides new insights into the understanding of ECFC impairment associated with cardiovascular risk in preeclamptic offspring and identifies potential novel therapeutic targets.

Level of Uric Acid in Women Suffering from Pre-Eclampsia and its Comparison with Normal Pregnancy

Objective: Current study is conducted to explore the variations in uric acid level in pre-eclamptic and normal healthy pregnancy in its third trimester in pregnant females. Methods: This descriptive cross sectional study was conducted to measure the serum uric acid level in mg/dl by kit method. The cutoff value was kept at 5mg/dl. The 10 ml of midstream urine was collected for estimation of urinary protein by dipstick method and graded from +1 to +3. For comparison between two groups in terms of levels of uric acid, independent sample t-test was used. Pearson Chi Square test was used to compare qualitative variables. Results: Raised levels of uric acid were obtained in 81.6% preeclampsia samples, and 13.1% found among normal samples, p&lt;0.01 showed that level of serum uric acid has a significant relationship with preeclampsia. Independent sample t-test showed a significant mean difference for SBP, DBP, and SUA between two groups, (p&lt;0.01) Conclusion: Significant high level of serum uric acid level was found in pre-eclamptic females than normotensive women. The findings suggest that measurement of serum uric acid may be a suitable marker in diagnosis of pre-eclampsia. Keywords: Pregnancy, Pre-eclampsia, Serum Uric Acid, Hypertension

Fetal out comes in Pre-Eclampsia with raised Maternal Serum Uric Acid

Aim: To compare adverse fetal outcome of hyperuricemic pre-eclamptic pregnancy with normouricemic pre-eclamptic pregnancy. Study design: A Cohort Study Methodology: In this study patients with serum uric acid level(SUA) &gt;5.5mg/dl were included in group A and patients with SUA level &lt;5.5mg/dl were included in group B. Patients with medical disorders like renal disease, hypertension, diabetes and currently using drugs affecting uric acid levels like thiazide diuretics were excluded. Both groups were followed until delivery. Intrauterine growth restriction, low birth weight was recorded. Results: A total of sixty patients were studied with age range from 18 to less than 40 years. The mean age in group A was 33.566± 4.19 years while 34.100± 3.46 years in group B. Mean Gestational age was 33.500±4.22 weeks in group A and 34.200±4.71 weeks in group B, while mean serum uric acid level was 7.416±1.04 in group A and 4.202±0.61 in group B. Intrauterine growth restriction was seen 93.3% in group A as compare to 60% in group B (P=0.002)(RRR=55.5%) while Low birth weight was 70% in group A and 10% in group B (P=0.000). Conclusion: The pregnancies with pre-eclampsia and raised serum uric acid levels result in adverse fetal outcome. Significant increased number of IUGR and LBW fetuses were observed in babies born to pre-eclamptic mothers with raised serum uric acid levels in comparison with babies born to normo-uricemic pre eclamptic mothers. Keywords: Pre-eclampsia, serum uric acid, fetal outcome

Sympathetic Responses to Isometric Handgrip Exercise in Women following Preeclamptic Pregnancies

Women who have had preeclamptic (PE) pregnancies are at increased risk for developing cardiovascular diseases later in life. One potential mechanism that may mediate this increased risk is sympathetic dysregulation. Indeed, there is evidence for elevated muscle sympathetic nerve activity (MSNA) both during and following PE pregnancies. Moreover, previously PE (PPE) women may demonstrate impaired MSNA responses during stress, although this has only been examined to a limited extent. Therefore, we tested the hypothesis that MSNA responses to isometric hand grip exercise (HG) would be greater in PPE women (n=6, age 31±6 years, BMI 29±5 kg/m2, 17±4 months postpartum) compared with women who had a healthy pregnancy (HP; n=8, age 29±2, BMI 25±4 kg/m2, 14±4 months postpartum). MSNA (peroneal nerve microneurography), mean arterial pressure (MAP; finger photoplethysmography), and total peripheral resistance (TPR; MAP/cardiac output), were assessed at baseline, during a 2‐min HG protocol, and during 2‐min post‐exercise circulatory occlusion (PECO). As previously reported, baseline MSNA was higher in PPE than HP (22±7 vs 13±5 bursts/min, P=0.01). Baseline MAP was not different between PPE and HP (94±11 vs 89±9 mmHg, P=0.23), nor was TPR (13±3 vs 13±2 mmHg/L/min, P=0.63). During HG, MSNA was greater in PPE than HP (24±8 vs 16±6 bursts/min, P=0.03), whereas MAP was not different between PPE and HP (95±12 vs 95±11 mmHg, P=0.99), nor was TPR (13±3 vs 14±2 mmHg/L/min, P=0.39). During PECO, no differences were observed between PPE and HP women in MSNA (26±8 vs 18±6 bursts/min, P=0.08), MAP (93±12 vs 96±12 mmHg, P=0.70), or TPR (12±3 vs 15±2 mmHg/L/min, P=0.18). These findings indicate that PPE women demonstrate exaggerated MSNA during isometric HG exercise relative to HP women, although the role of the metaboreflex in mediating this effect, as assessed using PECO, remains unclear. Importantly, these data also demonstrate that young PPE women were able to buffer the deleterious cardiovascular outcomes of elevated MSNA such that MAP and TPR outcomes were similar to age‐matched HP women during all conditions.