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Recurrent preeclampsia and perinatal outcome: a study of women with recurrent preeclampsia compared with women with preeclampsia who remained normotensive during their prior pregnancies.

OBJECTIVE: To evaluate the impact of preeclampsia recurrence on perinatal outcome. MATERIALS AND METHODS: A case-controlled study was performed in multiparous women who developed preeclampsia in index pregnancy (n = 64). Among these, women who had preeclampsia in previous pregnancies (n = 21) were compared to those who remained normotensive during their prior pregnancies (n = 43). Maternal and fetal variables were compared. Multivariate logistic analyses were performed to examine the impact of preeclampsia recurrence on fetal loss, preterm delivery, small for gestational age (SGA) occurrence and respiratory distress syndrome adjusted for confounding variables. RESULTS: No statistical significant difference was observed between the two groups in terms of age, delivery weeks, steroid use and laboratory markers. Fetal loss was higher in women with recurrent preeclampsia (19.0%) than in women with preeclampsia who had a normotensive pregnancy history (4.7%), with adjusted odds ratio (OR) of 5.77 [95% confidence interval (CI) 0.84-39.54]. CONCLUSION: Women with recurrent preeclampsia had a higher rate of perinatal loss compared to women with preeclampsia who were normotensive in their prior pregnancies.

Adult↗

Perinatal outcome in women with recurrent preeclampsia compared with women who develop preeclampsia as nulliparas.

OBJECTIVE: To compare the rates and perinatal outcome in women who experienced preeclampsia in a previous pregnancy to those in women who developed preeclampsia as nulliparas. STUDY DESIGN: This is a secondary analysis of data from 2 separate multi-center trials of aspirin for prevention of preeclampsia. Women who had preeclampsia in a previous pregnancy (n = 598) were compared with nulliparous women (n = 2934). Outcome variables were rates of preeclampsia, preterm delivery at <37 and <35 weeks of gestation, small-for-gestational-age infant, abruptio placentae, and perinatal death. Data were compared by using chi-square analysis and Wilcoxon rank sum test. RESULTS: The rates of preeclampsia and of severe preeclampsia were significantly higher in the previous preeclamptic group as compared to the nulliparous group (17.9% vs 5.3%, P <.0001, and 7.5% vs. 2.4%, P <.0001, respectively). Women who had recurrent preeclampsia experienced more preterm deliveries before 37 and 35 weeks of gestation than nulliparous women who developed preeclampsia. In addition, among women who developed severe preeclampsia, those with recurrent preeclampsia had higher rates of preterm delivery both before 37 weeks (67% vs 33%, P =.0004) and before 35 weeks of gestation (36% vs 19%, P =.041), and higher rates of abruptio placentae (6.7% vs 1.5%) and fetal death (6.7% vs 1.4%) than did nulliparous women. CONCLUSION: Compared to nulliparous women, women with preeclampsia in a previous pregnancy had significantly higher rates of preeclampsia and adverse perinatal outcomes associated with preterm delivery as a result of preeclampsia.

Abruptio Placentae↗

Risk factors associated with preeclampsia in healthy nulliparous women. The Calcium for Preeclampsia Prevention (CPEP) Study Group.

OBJECTIVE: Our goal was to identify risk factors for the development of preeclampsia in nulliparous women enrolled in a multicenter trial comparing calcium supplementation to a placebo. STUDY DESIGN: A total of 4589 women from five centers was studied. Analysis of risk factors for preeclampsia was performed in 4314 who carried the pregnancy to > 20 weeks. Baseline systolic and diastolic blood pressure, demographic characteristics, and findings after randomization were examined for the prediction of preeclampsia. Preeclampsia was defined as hypertension (diastolic blood pressure > or = 90 mm Hg on two occasions 4 hours to 1 week apart) and proteinuria (> or = 300 mg/24 hours, a protein/creatinine ratio > or = 0.35, one dipstick measurement > or = 2+ or two dipstick measurements > or = 1+ at an interval as specified for diastolic blood pressure). RESULTS: Preeclampsia developed in 326 women (7.6%). The first analysis treated each risk factor as a categoric variable in a univariate regression. Maternal age, blood group and Rh factor, alcohol use, previous abortion or miscarriage, private insurance, and calcium supplementation were not statistically significant. Risk factors initially found to be significant were body mass index, systolic blood pressure, diastolic blood pressure, non-white race (African-American and other), clinical center, and smoking. Adjusted odds ratios computed with a logistic regression model revealed that body mass index (odds ratio 3.22 for > or = 35 kg/m2 vs < 19.8 kg/m2), systolic blood pressure (odds ratio 2.66 for > or = 120 vs < 101 mm Hg), diastolic blood pressure (odds ratio 1.72 for > or = 61 mm Hg vs < 60 mm Hg), and clinical center (odds ratio 1.85 for Memphis vs the other clinical centers) were statistically significant predictors of preeclampsia. Results of the final model fit revealed that preeclampsia risk increases significantly (p < 0.0001) with increased body mass index at randomization, as well as with increased systolic and diastolic blood pressure at randomization. Calcium supplementation had no effect on the risks posed by body mass index and blood pressure. Among risk factors developing after randomization, an abnormal results of a glucose screen (plasma glucose > or = 140 mg/dl 1 hour after a 50 gm glucose challenge) was not found to be associated with a significant risk of preeclampsia. CONCLUSION: These risk factors should be of value in counseling women regarding preeclampsia and should aid in understanding the pathophysiologic characteristics of this syndrome.

Adolescent↗

Preeclampsia and cerebral palsy in low-birth-weight and preterm infants: implications for the current "ischemic model" of preeclampsia.

OBJECTIVE: One of the prevailing hypotheses for the pathogenesis of preeclampsia is the "ischemic model." It assumes that reduced uteroplacental perfusion is the primary step and the point of convergence of diverse pathogenic processes in the development of preeclampsia. One might expect a fetus under such "ischemic conditions" to be at an increased risk of later development of cerebral palsy (CP). The objective of this study was to test the hypothesis that maternal preeclampsia increases the risk of CP in preterm and low-birth-weight infants. METHODS: A meta-analysis was performed based on published articles identified by searching computerized databases (MEDLINE, EMBASE, CINAHL, Current Contents, Biological Abstracts, and Dissertation Abstracts) from 1966 through 1999. Ten observational studies on the association between preeclampsia and CP were identified based on prespecified inclusion criteria. Two independent reviewers extracted data and assessed the methodological quality of eligible articles. Odds ratios (OR) of CP for preeclampsia from individual studies were pooled. MAIN OUTCOME MEASURE: Cerebral palsy. RESULTS: In case-control studies, preeclampsia was associated with a statistically significant decreased risk of CP [pooled adjusted OR, 0.50; 95% confidence interval (CI), 0.33-0.81; p < 0.01). In cohort studies, preeclampsia was associated with a nonstatistically significant reduced risk of CP (pooled OR, 0.91; 95% CI, 0.35-2.41; p > 0.05). CONCLUSIONS: Preeclampsia may be associated with a decreased risk of CP in preterm and low-birth-weight infants. This challenges the currently held belief that reduced uteroplacental perfusion is the unique pathophysiological process in preeclampsia.

Cerebral Palsy↗

Critical pathways for the management of preeclampsia and severe preeclampsia in institutionalised health care settings.

BACKGROUND: Preeclampsia is a complex disease in which several providers should interact continuously and in a coordinated manner to provide proper health care. However, standardizing criteria to treat patients with preeclampsia is problematical and severe flaws have been observed in the management of the disease. This paper describes a set of critical pathways (CPs) designed to provide uniform criteria for clinical decision-making at different levels of care of pregnant patients with preeclampsia or severe preeclampsia. METHODS: Clinicians and researchers from different countries participated in the construction of the CPs. The CPs were developed using the following steps: a) Definition of the conceptual framework; b) Identification of potential users: primary care physicians and maternal and child health nurses in ambulatory settings; ob/gyn and intensive care physicians in secondary and tertiary care levels. c) Structural development. RESULTS: The CPs address the following care processes: 1. Screening for preeclampsia, risk assessment and classification according to the level of risk. 2. Management of preeclampsia at primary care clinics. 3. Evaluation and management of preeclampsia at secondary and tertiary care hospitals: 4. Criteria for clinical decision-making between conservative management and expedited delivery of patients with severe preeclampsia. CONCLUSION: Since preeclampsia continues to be one of the primary causes of maternal deaths and morbidity worldwide, the expected impact of these CPs is the contribution to improving health care quality in both developed and developing countries. The CPs are designed to be applied in a complex health care system, where different physicians and health providers at different levels of care should interact continuously and in a coordinated manner to provide care to all preeclamptic women. Although the CPs were developed using evidence-based criteria, they could require careful evaluation and remodelling according to each system's demands. Additionally, the CPs need to be tested in large-scale, multi-level studies in order to thoroughly examine and evaluate their efficacy and effectiveness.

Journal Article↗

What happens to women with preeclampsia? Microalbuminuria and hypertension following preeclampsia.

There is little published data on the incidence of remote hypertension, microalbuminuria (a possible marker of remote cardiovascular events) and diabetes following preeclampsia. This is of particular importance in Pacific Island populations as they have a high rate of preeclampsia, non-insulin dependent diabetes and cardiovascular related deaths. The aim of this study was to compare the rate of microalbuminuria and hypertension in 50 Samoan women with past preeclampsia (cases) with 50 Samoan women who did not have past preeclampsia (controls). Forty per cent of cases were hypertensive at follow-up compared to 2% in the control group (p < 0.0001). Microalbuminuria or proteinuria occurred in 40% of women with past preeclampsia and 18% of controls (p < 0.02). Half of the cases with microalbuminuria were hypertensive. No case or control had an elevated fructosamine, suggesting that current diabetes was an unlikely explanation for the microalbuminuria. We conclude that Samoan women with past preeclampsia are at increased risk of developing chronic hypertension and microalbuminuria. The significance of the microalbuminuria after preeclampsia is not known, but it may be a marker of either remote cardiovascular morbidity or non-insulin dependent diabetes. This study raises longterm health implications for women with preeclampsia.

Adult↗

Preeclampsia -- a state of prostaglandin deficiency? Urinary prostaglandin excretion, the renin-aldosterone system, and circulating catecholamines in preeclampsia.

Urinary excretion of prostaglandin E2 (PGE2) and F2 alpha (PGF2 alpha), plasma concentrations of renin, aldosterone, norepinephrine (NE) and epinephrine (E) were determined during pregnancy, 5 days, 3, and 6 months after delivery in preeclampsia, normotensive pregnant, and nonpregnant control subjects. The PGE2 was higher in normotensive pregnant control subjects than in nonpregnant subjects. In preeclampsia, PGE2 was reduced to nonpregnant level. PGF2 alpha was the same in preeclampsia and in normotensive pregnancy, but elevated when compared to the normotensive nonpregnant control group. Plasma concentrations of renin and aldosterone were increased during pregnancy, but considerably less in preeclampsia than during normotensive pregnancy. NE and E were the same as in nonpregnant subjects during both hypertensive and normotensive pregnancy. All parameters were normal 3 months after delivery. There were no correlations between PGE2, PGF2 alpha, plasma concentrations of renin, aldosterone, NE, or E and blood pressure level in third trimester either in preeclampsia or in normotensive pregnancy. PGE2 was positively correlated to plasma concentrations of renin. It is suggested that the lack of renal PGE2 in preeclampsia might be responsible for the decrease in renal blood flow and sodium excretion. It is hypothesized that preeclampsia is a state of prostaglandin deficiency. The changes in the renin-aldosterone system may be secondary to changes in prostaglandin concentration both in preeclampsia and normotensive pregnancy.

Aldosterone↗

[The role of plasma placental isoferritin in pathogenesis of preeclampsia and its predictive value for preeclampsia].

OBJECTIVE: To investigate the effect of placental isoferritin in pathogenesis of preeclampsia and its predictive value. METHODS: A prospective double-blinded study was performed. There were 120 initial normal pregnant women at earlier third trimester (from 24 to 34 weeks) in this study. Their plasma placental isoferritin and nitric oxide (NO) metabolites (nitrite/nitrate) (NO2-/NO3-) were examined by enzyme linked immunoabsorbent assay (ELISA) and Griess assay respectively. The outcomes of pregnancies were followed up. RESULTS: In 120 initial normal pregnant women, 19 pregnant women occurred preeclampsia (preeclampsia group), and 101 cases were normal (normal group) at follow up. The levels of plasma placental isoferritin (PLF) were significantly decreased in preeclampsia group (285.31 +/- 53.73 mg/L) than that of normal group (699.05 +/- 203.03) mg/L, P < 0.01. The levels of plasma NO were significantly increased in preeclampsia group (54.57 +/- 32.71 mumol/L) than that of normal group (38.89 +/- 30.00) mumol/L, P < 0.05. The significant negative correlation between the plasma placental isoferritin and NO levels was observed(r = 0.329, P < 0.01). At the cut point of 400 mg/L PLF level, the sensitivity, specificity, positive predictive value, negative predictive value and Kappa index of PLF level predicting on the outcomes of pregnancy with preeclampsia were 100%, 85.15%, 55.88%, 100%, 0.645. CONCLUSIONS: The decrease of plasma placental isoferritin levels is associated with preeclampsia, and the endothelial cell damage may be one of its mechanism. The PLF may be an earlier predictor of preeclampsia at 24-34 gestational weeks.

Adult↗

Expectant management of severe preeclampsia and preeclampsia superimposed on chronic hypertension between 24 and 34 weeks' gestation.

BACKGROUND: Timing of delivery is difficult to judge in preeclampsia. OBJECTIVE: To compare the differences of maternal and perinatal outcome of patients with severe preeclampsia and essential hypertension with superimposed preeclampsia, with expectant management at 24-34 weeks' gestation. STUDY DESIGN: A retrospective review of a conservative regime using intravenous magnesium sulfate, glucocorticoids and antihypertensive drugs, monitored by serial liver function tests, full blood count, coagulation profile, and renal function tests. Fetal status was assessed by daily non-stress test and ultrasound twice by week. RESULTS: A total number of 100 women had severe preeclampsia and 29 superimposed preeclampsia. The average pregnancy prolongation was 8.4 and 8.5 days, respectively. Oliguria, abruption placentae and HELLP syndrome were frequent complications similar in each group. There were no cases of eclampsia or disseminated coagulopathy in either group. The total neonatal survival rate was 93% in both groups. CONCLUSION: Expectant management is equally safe in both superimposed preeclampsia and severe preeclampsia of early onset.

Antihypertensive Agents↗

Preeclampsia and antioxidant nutrients: decreased plasma levels of reduced ascorbic acid, alpha-tocopherol, and beta-carotene in women with preeclampsia.

OBJECTIVE: Our purpose was to investigate the plasma levels of three potent antioxidant nutrients in women with preeclampsia. STUDY DESIGN: Fasting venous blood samples were collected from 30 women with preeclampsia and from 44 women with uncomplicated pregnancies. The criteria for recruitment included age 15 to 35 years, gestational age 28 to 42 weeks, singleton pregnancy, intact membranes, absence of labor contractions, and absence of any other medical complication concurrent with preeclampsia. Reduced ascorbic acid, alpha-tocopherol, and beta-carotene levels were assayed with high-pressure liquid chromatography. RESULTS: Plasma levels of reduced ascorbic acid were significantly decreased in patients with mild and severe preeclampsia (p < 0.01). Plasma alpha-tocopherol and beta-carotene levels were significantly decreased only in severe preeclampsia compared with controls (p < 0.05 and p < 0.05, respectively). CONCLUSION: In patients with preeclampsia antioxidant nutrients may be utilized to a greater extent to counteract free radical-mediated cell disturbances, resulting in a reduction in antioxidant plasma levels. Water-soluble antioxidant nutrients may initially be consumed, followed by lipid-soluble antioxidants.

Adolescent↗

Activation of endothelial cells in preeclampsia: increased neutrophil-endothelial adhesion correlates with up-regulation of adhesion molecule P-selectin in human umbilical vein endothelial cells isolated from preeclampsia.

OBJECTIVE: Increased endothelial activation has been suggested to be important in the pathophysiology for preeclampsia. Our objective was to examine whether in preeclampsia neutrophil adherence to endothelial cells is increased and whether endothelial cell-surface adhesion molecule expression is up-regulated. METHODS: Endothelial cells were isolated from normal (n = 10) and preeclamptic (n = 9) human umbilical veins (HUVECs). Neutrophils were isolated from normal, healthy, nonpregnant female volunteers. Freshly isolated neutrophils were labeled with 51Cr, and labeled neutrophils were coincubated with confluent normal and preeclamptic endothelial monolayers. Adhesion assays were then performed. To determine whether in preeclampsia endothelial cellular-surface adhesion molecules are responsible for increased neutrophil-endothelial adhesion, cellular adhesion molecule expression of P-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cellular adhesion molecule-1 (VCAM-1), and E-selectin were examined by an enzyme-linked binding assay. Furthermore, adhesion assays were also performed on HUVECs pretreated with antibodies against P-selectin, ICAM-1, VCAM-1, and E-selectin. RESULTS: Neutrophil adhesion to the HUVECs from preeclamptic pregnancies was significantly increased compared with neutrophil adhesion to the HUVECs from normal pregnancies (P < .01). Expression of cellular-surface adhesion molecule of P-selectin was significantly higher (P < .01) and ICAM-1 was significantly lower (P < .05) in HUVECs isolated from preeclampsia than from normal controls, whereas there was no difference for VCAM-1 and E-selectin expression between HUVECs from normal and preeclamptic pregnancies. No differences were found for neutrophil-endothelial adhesion on normal HUVECs pretreated with anti-P-selectin, anti-ICAM-1, anti-VCAM-1, and anti-E-selectin compared with the untreated cells. However, pretreatment of preeclampsia HUVECs with anti-P-selectin, anti-ICAM-1, anti-VCAM-1, and anti-E-selectin completely or partially blocked the neutrophil-endothelial adhesion compared to the untreated cells. CONCLUSION: There is a significant increase in neutrophil adhesion to HUVECs that are isolated from preeclamptic pregnancies compared with normal controls. This increase appears to be a result of up-regulation of the cell-surface adhesion molecule P-selectin. Elevated P-selectin expression may play a significant role in neutrophil-endothelial hyperadhesiveness and contribute to vascular complications associated with preeclampsia.

Antibodies↗

The predictive value of umbilical artery Doppler studies for preeclampsia or fetal growth retardation in a preeclampsia prevention trial.

OBJECTIVE: To determine the clinical utility of longitudinal Doppler umbilical artery systolic-diastolic ratios (S/D) to predict the occurrence of either preeclampsia or fetal growth retardation (FGR) in a low-risk population. METHODS: Healthy nulliparas with singleton gestations were enrolled in a double-blind trial of low-dose (60 mg) aspirin for preeclampsia prevention. Treatment was initiated at 24 weeks and continued until delivery. Continuous-wave Doppler studies were scheduled before assignment to treatment and at 27-31, 32-36, and 37-42 weeks. Preeclampsia was defined as a persistent diastolic blood pressure of at least 90 mmHg with proteinuria, and FGR was defined as birth weight below the tenth percentile. Doppler values were considered abnormal if they exceeded the 90th percentile for the gestational age range in the study population. Summary predictive values were computed for the abnormal S/D at each gestational age interval. To assess the potential effect of the administration of low-dose aspirin, logistic regression was used to model the relation between the Doppler indices, aspirin use, and these abnormal pregnancy outcomes. RESULTS: A total of 1665 Doppler examinations were performed on 565 women. Forty-four fetuses developed FGR and 21 women were diagnosed with preeclampsia. The positive predictive values of an abnormal S/D for the subsequent development of FGR were 13-17% across the gestational age ranges studied, and the positive predictive values for preeclampsia were 0-5%. Aspirin treatment did not affect the relation between the Doppler indices and these outcomes in the logistic regression model. CONCLUSION: Elevated umbilical artery S/D is not a clinically useful predictor of either FGR or preeclampsia in a low-risk population.

Adult↗

Tall or short? Twenty years after preeclampsia exposure in utero: comparisons of final height, body mass index, waist-to-hip ratio, and age at menarche among women, exposed and unexposed to preeclampsia during fetal life.

Women exposed to preeclampsia during fetal life have lower risk of breast cancer, compared with unexposed women, possibly through fetal programming. Hypothetically, preeclampsia exposure could affect well-known risk factors for breast cancer, such as pubertal development or adult anthropometry. Women born in a defined geographic area of Sweden from 1973 through 1978, with verified preeclampsia exposure (n = 230) and nonexposure (n = 359) during fetal life, answered questions about anthropometric measures, smoking, parity, and age at menarche in a telephone interview in early adulthood. Compared with unexposed offspring, female offspring of women who had preeclampsia were lighter and shorter for gestational age, but in young adulthood there were no differences in height, body mass index, waist-to-hip ratio, or age at menarche. When analyzing the effects of other maternal and fetal characteristics, the results indicate that approximately 50% of the variance in final height was explained by parental heights and birth length for gestational age. Young-adult body mass index was weakly associated with maternal body mass index, maternal smoking, and birth weight for gestational age, which together explained 12% of the variance. Neither of the assessed maternal or fetal characteristics were significantly associated with age at menarche or waist-to-hip ratio. These data indicate that neither adult anthropometry nor age at menarche is in the causal pathway between intrauterine preeclampsia exposure and the reduced risk of breast cancer.

Adolescent↗

Lipid profile in women with preeclampsia: relationship between plasma triglyceride levels and severity of preeclampsia.

It has been hypothesized that, in preeclampsia, hypertriglyceridemia may lead to increased endothelial triglyceride accumulation that, in turn, may result in endothelial cell damage. The purpose of our study was to determine whether hypertriglyceridemia is associated with the severity of preeclampsia. We studied 29 preeclamptic patients and 46 normal pregnant women, aged 15 to 35 years, with singleton pregnancies, at 28 to 37 weeks' gestation. Total cholesterol, low-density lipoprotein cholesterol, and triglyceride levels were measured enzymatically. High-density lipoprotein cholesterol was determined using a dextran sulfate-magnesium precipitation method. Patients with mild preeclampsia had a significant increase in plasma triglyceride levels (P < .001), while patients with severe preeclampsia had triglyceride levels comparable to controls. Our findings suggest that there is no direct relationship between triglyceride levels and severity of preeclampsia.

Adolescent↗

High sensitivity test for the early diagnosis of gestational hypertension and preeclampsia. IV. Early detection of gestational hypertension and preeclampsia by the computation of a hyperbaric index.

UNLABELLED: The aims of this study were to examine whether the combined approach of 1) establishing tolerance intervals for the circadian variability of blood pressure as a function of gestational age, and 2) computing the hyperbaric index by comparison of any patient's blood pressure profile (obtained by ambulatory monitoring) with the tolerance limits, provides a new highly sensitive test for the early detection of gestational hypertension and preeclampsia. We analyzed a total of 745 blood pressure series sampled by ambulatory monitoring for about 48 hours in each of several occasions in 189 women with uncomplicated pregnancies, 71 with gestational hypertension, and 29 with preeclampsia. After synchronization of all data by expressing times of sampling in hours from bed-time, circadian tolerance limits were first computed from the normotensive subjects as a function of trimester of pregnancy. The hyperbaric index and the percentage time of excess were then computed for each individual blood pressure series. The maximum hyperbaric index was below 15 mmHg X hour for normotensive pregnant women in all trimesters of pregnancy, and mostly above that value for women who subsequently developed gestational hypertension or preeclampsia. Sensitivity of the test based on the maximum hyperbaric index was 97% for women sampled during the first trimester of gestation, and increased up to 100% in the third trimester. The positive predictive value was 100% in all trimesters. Moreover, the computation of the hyperbaric index provided, on the average, an early identification of gestational hypertension or preeclampsia 20 weeks prior to the clinical confirmation of the disease. CONCLUSIONS: Ambulatory monitoring of blood pressure during gestation provides sensitive endpoints for use in early risk assessment and as a guide for establishing preventive interventions. The approach presented here represents a simple, reproducible, non-invasive, and highly sensitive test for the very early identification of gestational hypertension and preeclampsia.

Blood Pressure↗

Inositol phosphoglycans and signal transduction systems in pregnancy in preeclampsia and diabetes: evidence for a significant regulatory role in preeclampsia at placental and systemic levels.

Measurements have been made of the urinary content of inositol phosphoglycans IPG P-type and IPG A-type, putative insulin second messengers, in preeclampsia, in type I insulin-treated diabetic pregnant women and their matched control subjects, and nonpregnant women of child-bearing age. The content of IPG P-type and IPG A-type was also measured in the placenta from preeclamptic patients and from normal pregnancies. Pregnancy was associated with an increase, approximately twofold, in urinary output of IPG-P-type relative to nonpregnant controls (P<0.01). The 24-h output of IPG P-type in urine in preeclamptic women was significantly higher (2- to 3-fold) than in pregnant control subjects matched for age, parity, and stage of gestation (P<0.02). In contrast, insulin-dependent diabetic pregnant women did not show any significant change in urinary output of IPG P-type or IPG A-type relative to pregnant control subjects. Evidence for a possible relationship and correlation between the urinary excretion of IPG P-type and markers of preeclampsia, including proteinuria (r = 0.720, P<0.01), plasma aspartate transaminase (r = 0.658, P<0.05), and platelet counts (r = 0.613, P<0.05) is presented. A high yield of IPG P-type was extracted from human placenta, in preeclampsia some 3-fold higher (P = 0.03) than the normal value, whereas no IPG A-type (with lipogenic-stimulating activity) was found. Low concentrations of placental IPG A-type were detected relative to IPG P-type using assay systems dependent upon the effect of this mediator on cAMP-dependent protein kinase or on a proliferation assay using thymidine incorporation into DNA of EGFR T17 fibroblasts. It is postulated that the high urinary excretion IPG P-type in preeclampsia reflects high placental levels and relates to the accumulation of glycogen in the placenta. The paracrine effects of placental IPG P-type (stimulation off other endocrine glands and/or endothelial cells) could contribute to the pathogenesis of the maternal syndrome. A possible theoretical link between elevated placental IPG P-type and apoptosis is proposed.

Adult↗

Placental and decidual lipid peroxidation and antioxidant defenses in preeclampsia. Lipid peroxidation in preeclampsia.

We evaluated lipid peroxidation in serum, placenta and decidua basalis and antioxidant defenses in preeclampsia and normal pregnancy. The study group consisted of 70 women with preeclampsia and 72 healthy pregnant women. Lipid peroxides in serum, placenta and decidua basalis, and serum vitamin E and total carotene were measured by spectrophotometric methods. Unpaired Student's t-test, chi(2)-test and Pearson correlation test were used for the statistical analyses. Levels of lipid peroxides in serum, placenta and decidua basalis were markedly higher; and serum vitamin E, total carotene, bilirubin, albumin levels were markedly lower in preeclamptic pregnants compared with healthy pregnant women. Our findings demonstrated that both placenta and decidua basalis tissues may be a source of lipid peroxides in preeclamptic pregnancies. Prophylactic antioxidant therapy may abate the disease process. Further studies are needed to clarify the pathophysiology of preeclampsia and effectiveness of prophylactic antioxidant therapy in preeclampsia.

Journal Article↗

Plasma exchange for preeclampsia: II. Unsuccessful antepartum utilization for severe preeclampsia with or without HELLP syndrome.

OBJECTIVE: To explore the efficacy of plasmapheresis/plasma exchange as the primary therapy to arrest and reverse the progression of severe preeclampsia with or without HELLP syndrome in order to postpone delivery and improve perinatal outcome in very preterm pregnancies. STUDY DESIGN: In this case series of patients managed over a 4-year period from 1984 to 1987, seven gravidas with severe preterm preeclampsia underwent 1-2 plasmaphereses/plasma exchange procedures using the IBM 2997 Cell Separator with continuous electronic fetal heart rate monitoring (n = 7 patients) and central cardiovascular monitoring (n = 3 patients). RESULTS: The seven patients (one with HELLP syndrome, six without HELLP) presented between 24 and 30 weeks gestation and, despite plasmapheresis/plasma exchange, the severity of each study subject's preeclampsia persisted without clinically significant improvement. Maternal-fetal deterioration required cesarean delivery in all cases within 48 (in four patients within < 36) hours of therapy. No clinically significant adverse effect of plasma exchange therapy was recorded during cardiovascular and laboratory monitoring; two fetuses developed repetitive late decelerations during exchange despite adequate maternal fluid preload. The only patient with HELLP syndrome developed eclampsia as her third plasma exchange within 25 hours was being initiated. Significant problems with fluid retention and displacement (variable amounts of pulmonary edema, pleural effusions, large volume ascites) were encountered in all patients. Four neonates died (24-27 weeks/438-820 g) and three survived intact (740, 950, and 1,280 g). One mother (case 5) developed end-stage renal disease 21 months postpartum. CONCLUSIONS: The application of plasmapheresis/plasma exchange therapy as described in order to prolong very preterm pregnancies in the undelivered patient with severe preeclampsia/eclampsia with or without HELLP syndrome did not produced encouraging results. Patients in general were exposed to additional medical and surgical risk without a corresponding improvement in perinatal outcome.

Adolescent↗