New Onset Hypertension In Pregnancy Research Articles

Gestational Hypertension and Midlife Cognition: The CARDIA Study

AbstractBackgroundGestational hypertension (GH) increases the risk of cardiovascular diseases, which may contribute to worse cognitive outcomes, and yet little is known about the long‐term impact of GH on cognition. We investigated the association of GH with midlife cognitive performance and decline in the Coronary Artery Risk Development in Young Adults (CARDIA) Study.MethodsWe studied 1,273 parous Black and White women (106 with GH and 1167 without GH) aged 18‐30 years at baseline (1985‐86) who were followed up to Year 30 (mean age 55.2±3.6 years) when five cognitive tests measuring global cognition, memory, processing speed, executive function, and verbal fluency were administered. Accelerated decline over five years was defined as a decline ≥1.5 standard deviations from the mean change on each of the three tests available at year 25, measuring processing speed, memory, and executive function. GH, defined as having new onset hypertension in pregnancy without proteinuria, was self‐reported for each pregnancy since the previous visit up to 30 years. We conducted linear and logistic regression to assess the association of GH with cognitive performance and decline.ResultsCompared with women who did not develop GH during pregnancy, those with GH were more likely to be Black (62% vs 50%) and have obesity (22% vs 11%), and lower diet quality (CARDIA A Priori Diet Quality Scores) at baseline. After adjusting for age, race, education, number of pregnancies, and baseline cardiovascular and behavior risk factors (diabetes, obesity, smoking, alcohol use, physical activity, and diet quality), having GH was significantly associated with lower cognitive performance (z‐standardized) at year 30 in global cognition (‐0.27, 95% CI ‐0.44 to ‐0.11), processing speed (‐0.25, 95% CI ‐0.44 to ‐0.07), and verbal fluency (‐0.20, 95% CI ‐0.38 to ‐0.02). Additional adjustment for hypertension, diabetes, and obesity up to Year 30 did not change the results. GH was also associated with higher odds of experiencing an accelerated decline in processing speed over 5 years (9.2% vs. 4.5%, odds ratio 2.48, 95% CI 1.07 to 5.74), after adjustment for all covariates.ConclusionGH is independently associated with worse cognitive performance and accelerated decline in midlife.

A cross sectional study to assess the efficacy of glycosylated fibronectin (GlyFn) estimation in prediction of the severity of disease in new onset hypertension in pregnancy from 24 weeks to term

A cross sectional study to assess the efficacy of glycosylated fibronectin (GlyFn) estimation in prediction of the severity of disease in new onset hypertension in pregnancy from 24 weeks to term

Trends in County-Level Rates of New-Onset Hypertensive Disorders of Pregnancy in US, 2007-2019

Given that new-onset hypertension in pregnancy is a leading risk factor for adverse maternal and neonatal outcomes, we sought to define geographic variation in county-level rates and trends of new-onset hypertensive disorders of pregnancy (HDP) in the US.

Relation Between Labetalol and Methyldopa in Treatment of Pregnancy Induced Hypertension

Background: Hypertensive disorder is the most common medical problem encountered in pregnancy with a high perinatal and maternal mortality & morbidity. Worldwide about 76,000 pregnant women die each year from preeclampsia and related hypertensive disorders. Objective: To assess the relation between labetalol and methyldopa in treatment of pregnancy induced hypertension. Methods: This study was hospital based comparative prospective study was conducted at Dept. of Obstetrics & Gynaecology, Dhaka Medical College Hospital, Dhaka, Bangladesh from January to June 2021. The study consisted of 100 patients with pregnancy induced hypertension attending outpatient department and admitted in ANW, or who directly came to labour room. These patients were randomly selected on lottery basis after they fulfilled the inclusion criteria. Total patients were taken for the study and divided into 2 groups of 50 patients in each group. Results: A total 100 patients were included. The mean age in Group I was 24.4±4.55 years and in Group-II, 23.95±4.28 years. Maximum number of patients was between 19- 24 years in both the groups. In Group-I, 26 (52%) patients and in Group-II, 25 (50%) patients were in this age group. The maximum age in the Group I was 34 years and 35 years in the Group-II. The minimum age was 17 years in both the groups. The inter group difference was not statistically significant (p>0.05) thus the two groups were comparable by age. At baseline no significant difference was seen in SBP in both treatment groups. However after 8 days post testament SBP of women was significantly lower in Group-I patients as that of Group-II patients. i.e. Group-I: 123.41 vs. Group-II: 126.62, p- value=0.009. At baseline no significant difference was seen in DBP in both treatment groups. However at 8th day post treatment DBP of patients was significantly lower in Group-I patients. i.e. 77.18 vs. Group-II 79.64, p-value=0.005. For SBP more effective control was seen in women whose parity was 3-4 and for DBP notable difference was seen in women whose parity was 1-2. The control of systolic blood pressure was more effective in patients with normal body mass index and for Diastolic blood pressure (DBP) more effective control was seen in patients who were obese. On comparison methyldopa significantly causes more drowsiness, headache and nasal congestion and the incidence of Postural hypotension and dysponea in both groups were not significantly different. The patient who required additional drugs to control the uncontrolled hypertension. In Group I, 2 (4%) patients and in Group II, 3 (6%) patients did not respond with starting drug. The inter group difference was not statistically significant (p>0.05). Conclusion: Labetalol had less maternal adverse effect compared to methyldopa but fetal outcome was not observed in this study. Labetalol and methyldopa are equally efficacious in controlling blood pressure in new onset hypertension in pregnancy. This study is just a step in this long way. Therefore, labetalol can be considered positively in the treatment of pregnancy induced hypertension.

The Different Outcomes in Pregnant Women with Severe Features of Preeclampsia between New Onset Hypertension Group and Pre-Existing Hypertension Group

Background: There are extensive evidence that preeclampsia is the reason for many maternal and perinatal morbidities. However, there are no previous study on the different outcomes in severe preeclamptic women between new onset hypertension and chronic hypertension. Objective: To compare the rate of low Apgar score at 5 minutes and other adverse pregnancy outcomes of preeclamptic women with severe features between those who had new onset hypertension in pregnancy and those with chronic hypertension before pregnancy. Materials and Methods: A retrospective cohort study was conducted. The medical records of pregnant women diagnosed with preeclampsia with severe features and delivered at Chonburi Hospital between January 2017 and June 2020 were reviewed. The authors categorized these pregnant women into two groups, new onset hypertension and chronic hypertension. Descriptive statistics were used for the data analyses. Results: Of the 526 women diagnosed with preeclampsia with severe features, 290 met the inclusion and exclusion criteria. Eighty-nine had superimposed preeclampsia on chronic hypertension and 201 patients had new onset hypertension. The rate of low Apgar score at 5 minutes was not statistically different between the two groups (p=0.258). The incidence of impaired liver function and HELLP syndrome were increased in the new onset hypertension group at 18.9% versus 6.7% (p=0.008) and 9.5% versus 1.1% (p=0.010), respectively. Conclusion: There was no significant difference in the rate of low Apgar score between the two groups. Regarding the severity of maternal outcomes, new onset preeclampsia with severe features seems to be more severe than superimposed preeclampsia on chronic hypertension. Keywords: Low Apgar score; Preeclampsia with severe features; Chronic hypertension; Superimposed preeclampsia; Pregnancy outcomes

FC 012PRIMARY KIDNEY DISEASE IMPACTS OUTCOME IN CKD PREGNANCIES: COMPLICATIONS IN COL4A3-5 RELATED DISEASE (ALPORT SYNDROME) VS OTHER CKD PREGNANCIES

Abstract Background and Aims Chronic kidney disease (CKD) affects approximately 3% of pregnant women. CKD increases the risk of pregnancy complications such as prematurity, low birthweight and pre-eclampsia. Also, kidney function can deteriorate more quickly due to pregnancy. There is limited knowledge on pregnancy outcomes in specific kidney diseases. The aim of the ALPART network is to study pregnancy outcomes differentiated by CKD aetiology. We have started with COLA3-5 related disease (Alport syndrome), which is one of the most prevalent monogenic kidney diseases. Comparing outcomes in COLA3-5 related disease to pregnancies with other CKD aetiologies allows us to investigate whether this specific diagnosis impacts outcome in CKD pregnancies. Method The ALPART network is an international 15-center network, which aims to include ∼200 COLA3-5 related disease pregnancies. In this intermediary analysis, we present data on 109 pregnancies from 68 women with COLA3-5 related disease. We compared outcomes to a cohort of 457 CKD stage 1-2 patients (a similar CKD stage as our cohort) of diverse aetiology from a 2015 Italian study and 159,924 women from the general Dutch population. Results The main pregnancy and kidney outcomes are presented in Figure 1. Foetal outcomes were better in COLA3-5 pregnancies than in pregnancies of women with CKD stage 1-2 of diverse aetiology. We saw less prematurity (17% vs 36% respectively) and a higher mean birthweight of 3216 ± 663 gram compared to 2768 ± 680 in the Italian cohort. Maternal kidney outcomes should be interpreted with caution (>30% missing data): proteinuria (73%) and hypertension (30%) were more frequent in COLA3-5 pregnancies than the Italian cohort. In the ALPART cohort, 10% developed severe hypertension. Median eGFR was not impacted by pregnancy and decline of eGFR before and after pregnancy were not significantly different between groups. Conclusion Fetal outcomes in pregnancies with COLA3-5 related disease seem to be more favorable than in a cohort with mixed cause of CKD. In this intermediary analysis, proteinuria levels and frequency of new-onset hypertension in pregnancy are higher. There is no significant eGFR loss during pregnancy or increased eGFR deterioration in the long-term. The differences between COLA3-5 and general CKD pregnancies underscore the importance of investigating pregnancy outcomes in specific kidney disease phenotypes to ensure adequate (pre-) pregnancy counselling and care.

The Role of Mitochondrial Dysfunction in Preeclampsia: Causative Factor or Collateral Damage?

Preeclampsia, new onset hypertension in pregnancy, affects ~5%-10% of the world's population. Preeclampsia is the leading cause of morbidity and mortality for both the mother and fetus. As of today, there is no cure for this disease except for delivery of the fetal-placental unit. The exact causation and onset of the disease are unknown. However, recent studies have shown a strong correlation between mitochondrial dysfunction and preeclampsia. Circulating mitochondrial DNA, elevated reactive oxygen species, angiotensin II type 1 receptor agonistic autoantibodies (AT1-AA), activated natural killer cells, and upregulated inflammatory responses all contribute to mitochondrial dysfunction and the pathophysiology of preeclampsia. This review summarizes the current literature of both experimental and clinical observations that support the hypothesis that mitochondrial dysfunction contributes to the pathophysiology of preeclampsia and may be a precursor to the disease onset. This review will also address the use of therapies to improve mitochondrial dysfunction in preeclampsia.

Interactions between the complement and endothelin systems in normal pregnancy and following placental ischemia

Preeclampsia is characterized by new onset hypertension and fetal growth restriction and is associated with aberrant activation of the innate immune complement system and stressed or ischemic placenta. Previous studies have suggested a role for both endothelin and complement system activation products in new onset hypertension in pregnancy, but inter-relationships of the pathways are unclear. We hypothesized that complement activation following placental ischemia stimulates the endothelin pathway to cause hypertension and impair fetal growth. The Reduced Uterine Perfusion Pressure (RUPP) model results in hypertension and fetal growth restriction in a pregnant rat due to placental ischemia caused by mechanical obstruction of blood flow to uterus and placenta. The effect of inhibitor of complement activation soluble Complement Receptor 1 (sCR1) and endothelin A receptor (ETA) antagonist atrasentan on hypertension, fetal weight, complement activation (systemic circulating C3a and local C3 placental deposition) and endothelin [circulating endothelin and message for preproendothelin (PPE), ETA and endothelin B receptor (ETB) in placenta] in the RUPP rat model were determined. Following placental ischemia, sCR1 attenuated hypertension but increased message for PPE and ETA in placenta, suggesting complement activation causes hypertension via an endothelin independent pathway. With ETA antagonism the placental ischemia-induced increase in circulating C3a was unaffected despite inhibition of hypertension, indicating systemic C3a alone is not sufficient. In normal pregnancy, inhibiting complement activation increased plasma endothelin but not placental PPE message. Atrasentan treatment increased fetal weight, circulating endothelin and placental ETA message, and unexpectedly increased local complement activation in placenta (C3 deposition) but not C3a in circulation, suggesting endothelin controls local placental complement activation in normal pregnancy. Atrasentan also significantly decreased message for endogenous complement regulators Crry and CD55 in placenta and kidney in normal pregnancy. Results of our study indicate that complement/endothelin interactions differ in pregnancies complicated with placental ischemia vs normal pregnancy, as well as locally vs systemically. These data clearly illustrate the complex interplay between complement and endothelin indicating that perturbations of either pathway may affect pregnancy outcomes.

Abstract P265: Placental Ischemia Causes Renal Mitochondrial Impairment in Reduced Uterine Perfusion Pressure Rats

Introduction: Preeclampsia (PE) is characterized by new onset hypertension in pregnancy and is associated with renal dysfunction, proteinuria and is believed to be initiated by placental ischemia. Mitochondrial dysfunction is an important source of reactive oxygen species (ROS) generation. To better understand the role of mitochondrial dysfunction in hypertension during PE we examined renal mitochondrial expression in the kidney of RUPP rats. Methods: Female Sprague Dawley rats were dived into two groups; normal pregnant (NP) and RUPP rats. On gestational day (GD) 14, RUPP surgery was performed, GD18 carotid catheters were inserted, and GD19 conscious blood pressure (MAP) was measured, renal mitochondria were isolated for respiration and analysis. Respiration measurements were performed on intact isolated mitochondria under glutamate/malate as complex I substrate using Oroboros Oxygraph-2K. Oxidative phosphorylation was analyzed by western blot using total Oxphos cocktail antibody and VDAC. Results: MAP was elevated in RUPP (n=8) vs NP rats (n=10) (125±6 vs. 99±2 mmHg, p<0.05). RUPP (n=3) renal mitochondria show reduced expression of Complex I (0.5±0.02 vs 0.8±0.09, p<0.05) and Complex II (0.7±0.03 vs 1±0.08, p<0.05) compared to NP mitochondria. State 3 (624±112 vs 878±9 pmol/sec/mg, p=0.22) and maximal (496±87vs 748±75 pmol/sec/mg, p=0.14) respiration rates trended towards reduction in RUPPs (n=4) compared to NP (n=2). Conclusion: Reduced expression of Complex I and II expression with reduced respiratory rates indicate mitochondrial impairment in the RUPP kidneys. Although, renal mitochondrial mediated oxidative stress may be one mechanism of hypertension in the RUPP rat model of PE, further exploration of oxidative stress in the kidney is necessary to fully understand the contribution of mitochondrial mediated oxidative stress to pathology of PE.

Pre-gravid Determinants of New onset Hypertension in Pregnancy–Results from a Pre-conception Cohort Study in China

Pre-gravid Determinants of New onset Hypertension in Pregnancy–Results from a Pre-conception Cohort Study in China

Pre-gravid predictors of new onset hypertension in pregnancy − Results from a pre-conception cohort study in China

Pre-gravid predictors of new onset hypertension in pregnancy − Results from a pre-conception cohort study in China

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Objectives While obesity is a major risk factor for preeclampsia, which is new-onset hypertension in pregnancy, the mechanisms linking obesity and hypertension during preeclampsia are not understood. Hypertension in preeclampsia is associated with placental ischemia-induced release of factors such as anti-angiogenic sFlt-1 into the maternal circulation which antagonizes vascular endothelial growth factor (VEGF) and promotes endothelial dysfunction. The purpose of this study was to determine the effect of obesity on angiogenic factors and endothelial function in obese melanocortin 4 receptor (MC4R) knockout rats (MC4R+/−, n = 4–9) and lean control MC4R+/+ rats ( n = 4–8). Methods EchoMRI for measuring total body fat mass; carotid arterial catheters for measuring mean arterial blood pressure; ELISAs; wire myography. Results At gestational day (GD) 18, body weight (362 ± 6 vs. 336 ± 5 g) and total body fat mass (62 ± 6 vs. 45 ± 5 g) were greater ( P P P P Conclusions These data indicate that during normal pregnancy, obesity is associated with greater circulating VEGF levels and nitric oxide-dependent vasorelaxation in resistance arteries. Because soluble factors from the ischemic placental target reduce nitric oxide bioavailability, we propose that the hypertensive and endothelial dysfunction responses to reductions in uterine perfusion may be exaggerated in obese pregnant animals. Funding: HL105324, HL51971. Disclosures F.T. Spradley: None. A.C. Palei: None. J.P. Granger: None.

Maternal exposure to the production of fireworks and reduced rate of new onset hypertension in pregnancy

Background: Carbon monoxide (CO) is one of the main substances contained in fireworks. Previous studies suggested that CO may have protective effect on the development of hypertension of pregnancy. Method: The authors conducted a prospective cohort study in Liuyang, Hunan, China between January 2010 and December 2011. Demographic and life-style variables of the participating pregnant women were obtained through structured interview with the women and clinical data were retrieved from antenatal medical records. Density of fireworks factories was defined as the number of fireworks factories per 1000 residents in the township where the mothers resided during pregnancy. Multiple logistic regression analysis was used to analyze the independent association between maternal exposure to the production of fireworks and new onset hypertension in pregnancy. Results: A total of 5976 pregnant women were included in the final analysis. Density of fireworks factories was inversely correlated with incidence of new onset hypertension in pregnancy (Pearson correlation coefficient = −0.29, p < 0.001). Multiple logistic regression analysis showed that, compared with women who resided during pregnancy in a township with 0–0.25 fireworks factories per 1000 residents, the rates of new onset hypertension in pregnancy in women who resided in a township with 0.26–1.00 fireworks factories per 1000 residents (Odds Ratio = 0.66, 95% confidence interval: 0.46, 0.96) and >1.5 fireworks factories per 1000 residents (Odds Ratio = 0.65, 95% confidence interval: 0.44, 0.97) were reduced by more than 30%. Conclusion: Maternal exposure to the high density of fireworks factories is associated with reduced risk of developing new onset hypertension in pregnancy.

PMM.27 Unresolved proteinuria after pre-eclampsia: detecting renal disease

Abnormal proteinuria (a urinary protein creatinine ratio (PCR) >30 mg/mmol), combined with new onset hypertension in pregnancy, is the hallmark of pre-eclampsia. NICE guidelines1 recommend that a urine dipstick test...

Fetal sex and the circulating renin–angiotensin system during early gestation in women who later develop preeclampsia or gestational hypertension

There are fetal sex-specific differences in the balance between angiotensin (Ang) II and Ang-(1-7) in the maternal circulation during pregnancy. To determine whether at 15 weeks' gestation plasma levels of Ang II and Ang-(1-7), as well as levels of prorenin and Ang-converting enzyme (ACE), predicted the development of gestational hypertension (GH) or preeclampsia (PreE) and were associated with estimates of fetal and maternal health, women who later developed GH (n=50) or PreE (n=50) were compared with body mass index-matched controls (n=100). Women who subsequently developed PreE or GH had increased Ang-(1-7) levels at 15 weeks' gestation compared with women with normal pregnancies. When separated by fetal sex, this difference was seen only in women carrying a female fetus. Prorenin and ACE concentrations were not useful biomarkers for the prediction of either PreE or GH at 15 weeks' gestation. Women with a male fetus who developed PreE and women who subsequently developed GH had increased blood pressures at 15 weeks' gestation compared with women with normal pregnancies, suggesting that these women were on an early trajectory for the development of hypertension. We propose that measurement of Ang-(1-7) during early gestation could be useful in predicting, those women who will go on to develop new-onset hypertension in pregnancy.

OS102. Continuing pathology following a hypertensive pregnancy and the risk of future disease

New onset hypertension in pregnancy affects up to 6-8% of all pregnancies. For most women, hypertension and proteinuria settle following delivery. The National Institute for Health and Clinical Excellence (NICE) Hypertension in Pregnancy guideline recommends that this group of patients are reviewed by a medical professional postnatally [3]. However, studies have shown that blood pressure and urinalysis are often not checked in the postpartum period [4]. Women with a history of hypertension in pregnancy have a higher risk of future hypertension and cardiovascular disease (CVD) than women who have uncomplicated pregnancies [2]. Risk scores are available for assessing an individual's risk of CVD although they are not validated in women under 30. In UK, the most appropriate is QRISK2 score [1]. To determine the frequency of ongoing problems following a new onset hypertensive pregnancy and assess the risk of future cardiovascular disease. 351 women with new onset hypertension in pregnancy were reviewed 6 weeks postnatally. They were assessed for ongoing disease and cardiovascular risk. 10 year QRISK2 scores and heart age (the age at which a matched person has that score) were calculated. 211 women with pre-eclampsia (PE) and 140 with gestational hypertension (GH) were reviewed. 9% and 11% of women with previous PE and GH respectively still required antihypertensive agents at follow-up. Only 1 woman required more than one antihypertensive medication (PE group). 19 women with PE (9%) had ongoing proteinuria (PCR>30). 5% had an estimated GFR <60ml/min. In addition to those with a strong family history of hypertension, 23 patients (6.5%) required investigation for ongoing problems. Risk factors for CVD were common 6 weeks after delivery: Although the overall risk of CVD was low (median 10 year QRISK2 score 0.3, median relative risk 1.0), with 41% of women having the lowest possible heart age, 22% of women had a significantly elevated risk of CVD (QRISK2 heart age ⩾age+10). 16% of women had ongoing hypertension or proteinuria, evidence supporting the NICE guidance that all women with hypertension in pregnancy need follow-up after delivery. The overall risk of future CVD in women with previous hypertension in pregnancy is low but about one-fifth of women are at very high risk. A program of risk assessment is required to allow preventative measures to be implemented.

Editorial

Editorial

Knowledge of hypertensive disorders in pregnancy among obstetricians and midwives

BackgroundHypertension in pregnancy remains one of the leading causes of maternal deaths in the UK and is associated with an increased lifetime risk of cardiovascular disease.MethodsAn anonymous structured questionnaire, based...

False-Positive Amphetamine Toxicology Screen Results in Three Pregnant Women Using Labetalol

Labetalol is commonly used for control of hypertension in pregnancy. A component of the workup for new-onset hypertension in pregnancy often includes a urine drug screen. A labetalol metabolite is structurally similar to amphetamine and methamphetamine, thus causing potential cross-reactivity in drug immunoassays. We present one case of cocaine-induced hypertensive crisis superimposed on chronic hypertension and two cases of severe preeclampsia for which patients required escalating doses of labetalol for hypertension, with subsequent false-positive amphetamine urine drug screen results. In pregnant women requiring labetalol for treatment of hypertensive disease, a urine drug screen may be falsely positive for amphetamines and methamphetamines. Providers should be cognizant of this possibility when interpreting the results of urine drug screens.

Association Between Insulin Resistance, Glucose Intolerance, and Hypertension in Pregnancy

There is an association between insulin resistance, glucose intolerance, and essential hypertension, but the relation between insulin resistance, glucose intolerance, and hypertension diagnosed during pregnancy is not well understood. Transient hypertension of pregnancy, the new-onset nonproteinuric hypertension of late pregnancy, is associated with a high risk of later essential hypertension and glucose intolerance; thus, these conditions may have a similar pathophysiology. To assess the association between insulin resistance, glucose intolerance, essential hypertension, and subsequent development of proteinuric and nonproteinuric hypertension in pregnancy in women without underlying essential hypertension, we performed a prospective study comparing glucose (fasting, 1 and 2 hours postglucose load), insulin, glycosylated hemoglobin (HbA1c), high-density lipoprotein cholesterol (HDL-C), and triglycerides levels on routine screening for gestational diabetes mellitus. Women who developed hypertension in pregnancy (n = 37) had higher glycemic levels (fasting, 1 and 2 hours postglucose load) on a 100-gram oral glucose loading test, although only the fasting values showed a statistical significance (p < 0.05), and a significantly higher frequency of abnormal glucose loading tests, two hours after glucose load (>or=140 mg/dL) (p < 0.05) than women who remained normotensive (n = 180). Glucose intolerance was common in women who developed both subtypes of hypertension, particularly preeclampsia. Women who developed hypertension had greater prepregnancy body mass index (p < 0.0001), higher frequency and intensity of acanthosis nigricans (p < 0.0001), and higher baseline systolic and diastolic blood pressures (p <or= 0.0001 for both), although all subjects were normotensive at baseline by study design; they also presented lower levels of HDL-C (p < 0.05). However, after adjustment for these and other potential confounders, an abnormal glucose loading test remained a significant predictor of development of hypertension (p < 0.05) and, specifically, preeclampsia (p < 0.01). There was a trend toward higher insulin and homeostasis model assessment-insulin resistance (HOMA-IR) levels in women developing any type of hypertension. When comparing women that remained normotensive to term with those with transient hypertension and preeclampsia, the preeclamptic women were born with lower weight (p < 0.05) and shorter length (p < 0.005); at screening they were older (p < 0.005), showed higher frequency and intensity of acanthosis nigricans (p < 0.0001), had higher prepregnancy BMI (p < 0.0005), as well as higher baseline systolic and diastolic blood pressures (p <or= 0.0001 for both). They also showed higher HOMA-IR levels that did not show a statistical significance. When glucose tolerance status was taken in account, an association was found between increasing indexes of hypertension (p < 0.05) and of HOMA-IR (p < 0.05) with the worsening of glucose tolerance. These results suggest that insulin resistance and relative glucose intolerance are associated with an increased risk of new-onset hypertension in pregnancy, particularly preeclampsia, and support the hypothesis that insulin resistance may play a role in the pathogenesis of this disorder.