On use of animal models.

Human pregnancy, critical for our species survival, is inefficient and prone to complications such as infertility, spontaneous miscarriages and preeclampsia (PE). Immunological factors may be important as the embryo is 50% paternal and foreign to the mother. Mouse pregnancy models, and in particular the murine CBA/J x DBA/2 mating combination, has been widely used to investigate mechanisms causing and preventing partner-specific recurrent miscarriages (RM) and PE. Occult losses can represent T cell-mediated rejection, and antigen-specific regulatory T cells (Tregs) with classical αß T cell receptors (TcR) activated by semen antigens at the time of mating are protective. If there is no occult loss, an inadequate Treg response can also predispose to RM. In RM, proinflammatory cytokines from natural killer (NK)-type cells and macrophages of the innate immune system are responsible and cells with γδ TcR protect via release of TGF-ß-type molecules. Immunization of abortion-prone female CBA/J mice or administration of cell-associated or soluble CD200, an immune check point inhibitor, can prevent abortions by augmenting uterine decidual suppressor cell activity. Human studies suggest that is also true in couples with RM. Environmental activators of the innate immune system, such as bacterial LPS and stress, can cause abortions as well as occult losses. The endogenous level of Tregs and activation of Tregs specific for the male H-Y antigen may determine success rates and alter the male:female birth ratio. Intralipid alters LPS clearance, prevents abortions in the CBAxDBA/2 model, and is effective in increasing live birth rates in couples undergoing IVF treatment.

Distribution of HLA-G extended haplotypes and one HLA-E polymorphism in a large-scale study of mother-child dyads with and without severe preeclampsia and eclampsia.

The etiological pathways and pathogenesis of preeclampsia have rendered difficult to disentangle. Accumulating evidence points toward a maladapted maternal immune system, which may involve aberrant placental expression of immunomodulatory human leukocyte antigen (HLA) class Ib molecules during pregnancy. Several studies have shown aberrant or reduced expression of HLA-G in the placenta and in maternal blood in cases of preeclampsia compared with controls. Unlike classical HLA class Ia loci, the nonclassical HLA-G has limited polymorphic variants. Most nucleotide variations are clustered in the 5'-upstream regulatory region (5'URR) and 3'-untranslated regulatory region (3'UTR) of HLA-G and reflect a stringent expressional control. Based on genotyping and full gene sequencing of HLA-G in a large number of cases and controls (n > 900), the present study, which to our knowledge is the largest and most comprehensive performed, investigated the association between the HLA-G 14-bp ins/del (rs66554220) and HLA-E polymorphisms in mother and newborn dyads from pregnancies complicated by severe preeclampsia/eclampsia and from uncomplicated pregnancies. Furthermore, results from extended HLA-G haplotyping in the newborns are presented in order to assess whether a combined contribution of nucleotide variations spanning the 5'URR, coding region, and 3'UTR of HLA-G describes the genetic association with severe preeclampsia more closely. In contrast to earlier findings, the HLA-G 14-bp ins/del polymorphism was not associated with severe preeclampsia. Furthermore, the polymorphism (rs1264457) defining the two nonsynonymous HLA-E alleles, HLA-E*01:01:xx:xx and HLA-E*01:03:xx:xx, were not associated with severe preeclampsia. Finally, no specific HLA-G haplotypes were significantly associated with increased risk of developing severe preeclampsia/eclampsia.

HLA class I expression in the human placenta.

Placental trophoblast cells of the semi-allogenic human conceptus invade deeply into maternal uterine tissue. From a classical immunoiogic point of view this invasion and the following growth and development of the fetus in the uterus have to be tolerated by a pregnant woman's immune system. Among the various possible protective mechanisms that may be involved, the unique expression pattern of HLA class I molecules seems to be relevant. Besides many other differences between placentation and organ transplantation, this extraordinary HLA class I expression on trophoblast explains why pregnancy should not be considered an immunologic paradox but rather a fascinating example of a very special challenge for the female immune system.

Activating autoantibodies to the angiotensin II type I receptor play an important role in mediating hypertension in response to adoptive transfer of CD4+ T lymphocytes from placental ischemic rats.

Hypertension in rats with chronic placental ischemia (reduced uterine perfusion pressure, RUPP) is associated with elevated inflammatory cytokines, agonistic autoantibodies to the angiotensin II type I receptor (AT1-AA) and CD4(+) T cells; all of which are elevated in preclamptic women. Additionally, we have shown that adoptive transfer of RUPP CD4(+) T cells increases blood pressure, inflammatory cytokines, and sFlt-1. The objective of this study was to determine the long-term effects of RUPP CD4(+) T cells on AT1-AA, renal and systemic hemodynamics in pregnant rats. To answer this question CD4(+) T splenocytes were magnetically isolated on day 19 of gestation from control RUPP and normal pregnant (NP) rats and injected into a new group of NP rats at day 13 of gestation. On day 19 of gestation mean arterial pressure (MAP) and renal function (glomerular filtration rates, GFR) were analyzed and serum collected for AT1-AA analysis. To determine a role for AT1-AA to mediate RUPP CD4(+) T cell-induced blood pressure increases, MAP was analyzed in a second group of rats treated with AT1 receptor blockade losartan (10 mg·kg(-1)·day(-1)) and in a third group of rats treated with rituximab, a B cell-depleting agent (250 mg/kg) we have shown previously to decrease AT1-AA production in RUPP rats. MAP increased from 101 ± 2 mmHg NP to 126 ± 2 mmHg in RUPP rats (P < 0.001) and to 123 ± 1 mmHg in NP rats injected with RUPP CD4(+) T cells (NP+RUPP CD4(+)T cells) (P < 0.001). Furthermore, GFR decreased from 2.2 ml/min (n = 7) in NP rats to 1.0 ml/min (n = 5) NP+RUPP CD4(+)T cell. Circulating AT1-AA increased from 0.22 ± 0.1 units in NP rats to 13 ± 0.7 (P < 0.001) units in NP+RUPP CD4(+)T cell-treated rats but decreased to 8.34 ± 1 beats/min in NP+RUPP CD4(+) T cells chronically treated with rituximab. Hypertension in NP+RUPP CD4(+)T cell group was attenuated by losartan (102 ± 4 mmHg) and with B cell depletion (101 ± 5 mmHg). Therefore, we conclude that one mechanism of hypertension in response to CD4(+) T lymphocytes activated during placental ischemia is via AT1 receptor activation, potentially via AT1-AA during pregnancy.

[Pregnancy and antiphospholipid syndrome]. / Grossesse et syndrome des antiphospholipides.

Antiphospholipid syndrome (APS) is associated with a risk of obstetrical complications, affecting both the mother and the fetus. Obstetrical APS is defined by a history of three consecutive spontaneous miscarriages before 10 weeks of gestation (WG), an intra-uterine fetal death after 10 WG, or a premature birth before 34 WG because of severe pre-eclampsia, eclampsia or placental adverse outcomes (intrauterine growth retardation, oligohydramnios). Pregnancy in women with a diagnosis of obstetric APS is at increased risk for placental abruption, HELLP (Hemolysis, Elevated Liver enzymes, Low Platelet count) syndrome and thrombosis that may be part of a catastrophic antiphospholipid syndrome (CAPS). A previous thrombosis and the presence of a lupus anticoagulant are risk factors for pregnancy failure. A multidisciplinary approach, associating the internist, the anesthesiologist and the obstetrician, is recommended for these high-risk pregnancies. Preconception counseling is proposed to identify pregnancy contraindications, and to define and adapt the treatment prior and during the upcoming pregnancy. Heparin and low-dose aspirin are the main treatments. The choice between therapeutic or prophylactic doses of heparin will depend on the patient's medical history. The anticoagulant therapeutic window for delivery should be as narrow as possible and adapted to maternal thrombotic risk. There is a persistent maternal risk in the postpartum period (thrombosis, HELLP syndrome, CAPS) justifying an antithrombotic coverage during this period. We suggest a monthly clinical and biological monitoring which can be more frequent towards the end of pregnancy. The persistence of notches at the Doppler-ultrasound evaluation seems to be the best predictor for a higher risk of placental vascular complications. Treatment optimization and multidisciplinary antenatal care improve the prognosis of pregnancies in women with obstetric APS, leading to a favorable outcome most of the time.

Hypertension in response to placental ischemia during pregnancy: role of B lymphocytes.

Preeclampsia is associated with innate inflammatory response resulting in elevated tumor necrosis factor-α, agonistic autoantibodies to the angiotensin II type I receptor, and activation of endothelin 1 (ET-1). This study was designed to determine the role of B-cell depletion, resulting in agonistic autoantibodies to the angiotensin II type I receptor suppression to mediate hypertension via activation of ET-1 in the placental ischemic reduced uterine perfusion pressure (RUPP) rat model of preeclampsia. To achieve this goal we examined the effect of RUPP on mean arterial pressure and ET-1 in the presence and absence of chronically infused rituximab (R; 250 mg/kg), a B-lymphocyte-suppressive agent used clinically to treat autoimmune diseases. Mean arterial pressure was 103±1 mm Hg in normal pregnant (NP) rats; 103±3 mm Hg in NP+R versus 133±2 mm Hg in RUPP rats, and 118±2 mm Hg in RUPP+R rats (P<0.001 vs RUPP controls). B lymphocytes decreased from 6.0±0.5% gated cells in RUPP to 3.7±0.8% gated cells in RUPP+R rats. Importantly, agonistic autoantibodies to the angiotensin II type I receptor decreased from 18±1 bpm in RUPP rats to 10±1 bpm in RUPP+R rats. ET-1 decreased 1.5-fold in kidneys and 4-fold in the placenta (P<0.01) of RUPP+R versus RUPP rats. Media ET-1 excretion from endothelial cells exposed to serum from NP, RUPP, NP+R, or RUPP+R rats was determined. ET-1 from endothelial cells treated with NP serum was 53+13 pg/mg and increased to 75+10 pg/mg with RUPP serum. In contrast, ET-1 secretion decreased in response to B-cell-depleted RUPP serum to 50±8 pg/mg and was unchanged in response to NP+R sera (46±12 pg/mg). These data demonstrate the important roles that B-lymphocyte activation and agonistic autoantibodies to the angiotensin II type I receptors play in the pathophysiology of hypertension in response to placental ischemia.

Elevated antiphospholipid antibody titers and adverse pregnancy outcomes: analysis of a population-based hospital dataset.

BACKGROUND: The primary objective of this study was to determine if elevated antiphospholipid antibody titers were correlated with the presence of preeclampsia/eclampsia, systemic lupus erythematosus (SLE), placental insufficiency, and a prolonged length of stay (PLOS), in women who delivered throughout Florida, USA. METHODS: Cross-sectional analyses were conducted using a statewide hospital database. Prevalence odds ratios (OR) were calculated to quantify the association between elevated antiphospholipid antibody titers and four outcomes in 141,286 women who delivered in Florida in 2001. The possibility that the relationship between elevated antiphospholipid antibody titers and the outcomes of preeclampsia/eclampsia, placental insufficiency, and PLOS, may have been modified by the presence of SLE was evaluated in a multiple logistic regression model by creating a composite interaction term. RESULTS: Women with elevated antiphospholipid antibody titers (n = 88) were older, more likely to be of white race and not on Medicaid than women who did not have elevated antiphospholipid antibody titers. Women who had elevated antiphospholipid antibody titers had an increased adjusted odds ratio for preeclampsia and eclampsia, (OR = 2.93 p = 0.0015), SLE (OR = 61.24 p < 0.0001), placental insufficiency (OR = 4.58 p = 0.0003), and PLOS (OR = 3.93 p < 0.0001). Patients who had both an elevated antiphospholipid antibody titer and SLE were significantly more likely than the comparison group (women without an elevated titer who did not have SLE) to have the outcomes of preeclampsia, placental insufficiency and PLOS. CONCLUSION: This exploratory epidemiologic investigation found moderate to very strong associations between elevated antiphospholipid antibody titers and four important outcomes in a large sample of women.

Relationship between erythrocyte catalase and serum adenosine deaminase activities in eclampsia.

OBJECTIVE: To examine the relationship between antioxidant status and T-cell activation in the pathogenesis of eclampsia by measuring the activities of erythrocyte catalase, an enzyme of antioxidant mechanism, and serum adenosine deaminase (ADA), regarded as a marker of T-cell activation. METHODS: A total of 60 patients [20 eclamptic (E) pregnant women, 20 healthy pregnant (HP) women and 20 non-pregnant (NP) women] were included in the study. Maternal venous blood samples were obtained from each patient during weeks 28-37 of gestation, and biochemical analyses of catalase activity in erythrocytes and ADA activity in serum were carried out. RESULTS: Erythrocyte catalase activity was significantly lower and serum ADA activity was significantly higher in the E pregnant women when compared with the HP women and NP women (P <0.001). No significant correlation was observed between erythrocyte catalase activity and serum ADA activity. CONCLUSIONS: Erythrocyte catalase and serum ADA activities may at least in part contribute to the pathogenesis of eclampsia. However, more studies are needed to verify and clarify the relationship between antioxidant status and T-cell activation in eclampsia.

C-reactive protein is elevated 30 years after eclamptic pregnancy.

Women with a history of preeclampsia or eclampsia (seizure during preeclamptic pregnancy) are at increased risk for cardiovascular disease after pregnancy for reasons that remain unclear. Prospective studies during pregnancy suggest that inflammation, dyslipidemia, and insulin resistance are associated with increased risk of preeclampsia. Elevated serum C-reactive protein (CRP >3 mg/L) is an indicator of inflammation and cardiovascular risk. We hypothesized that Icelandic postmenopausal women with a history of eclampsia would manifest higher concentrations of serum CRP than Icelandic postmenopausal controls with a history of uncomplicated pregnancies. We also asked whether elevated CRP is associated with the dyslipidemia and insulin resistance previously identified in this cohort. CRP, measured by high-sensitivity enzyme-linked immunoassay, was higher in women with prior eclampsia (n=25) than controls (n=28) (median mg/L [interquartile range]: 9.0 [0.9 to 13.2] versus 2.0 [0.3 to 5.1]; P<0.03). This difference remained significant after adjustment for body mass index, smoking, hormone replacement, and current age. Women with prior eclampsia clustered into either high CRP (range 8.97 to 40.6 mg/L, n=13) or lower CRP (median 1.0, range 0.05 to 3.77, n=12) subsets. The prior eclampsia/high CRP subset displayed significantly elevated systolic blood pressures, lower high-density lipoprotein (HDL) cholesterol, higher apolipoprotein B, and higher fasting insulin and homeostasis model of insulin resistance (HOMA) values compared to controls, whereas the prior eclampsia/low CRP subset differed from controls only by marginally increased apolipoprotein B. The triad of inflammation, low HDL, and insulin resistance may elevate risk for both preeclampsia/eclampsia and cardiovascular disease in later life.

Why much of the pathophysiology of preeclampsia-eclampsia must be of an autoimmune nature.

Preeclampsia-eclampsia (PE-E) is a poorly understood condition of human pregnancy, which can affect multiple organs and is a leading cause of maternal deaths worldwide. The etiology and pathophysiology remain enigmas, however, which hampers progress in prevention, diagnosis, and treatment of this condition. PE-E is characterized by many features typically seen in autoimmune diseases, or in association with autoimmune reactions. Although this does not mean that PE-E should be considered an autoimmune condition, it does suggest that abnormal autoimmune processes play an important part in the clinical presentation of PE-E. In that regard, PE-E mimics autoimmune responses also observed in situations of allograft rejection and graft-versus-host disease (GVHD). Indeed, PE-E shares many other clinical and laboratory characteristics with allograft rejection and GVHD. Recognizing PE-E as a clinical condition that is characterized by autoimmune abnormalities may facilitate earlier and more specific diagnosis, along with preventive and more specific therapies for women at risk.

[Preeclampsia-eclampsia: a change in utero-placental microcirculation. Immunologic, histologic, and biochemical features]. / Preeclampsia-eclampsia: una alteración en la microcirculación útero-placentaria. Aspectos inmunológicos, histológicos y bioquímicos.

BACKGROUND: To know the alterations in the microcirculation of the placenta, umbilical cord, as well as the immune and hemorrheologic disorders in preeclampsia-eclampsia. MATERIAL AND METHODS: Two groups were conformed, 30 patients each, all of them with pregnancy of more than 24-week gestation. Group A included patients with preeclampsia-eclampsia and group B (control group) included women with normal pregnancy. In all patients determinations of levels of platelets, fibrinogen, antinuclear antibodies, IgG and IgM anticardiolipin, VDRL were made; clotting times were determined, and histopathologic analyses (placenta, umbilical cord and uterus-placenta membranes) were performed. RESULTS: Platelet levels in the group A were normal in 40% and low in 60%. In group B they were normal in 83.3% and low in 16.7%. with p < 0.05. In group A fibrinogen was normal in 10% and high in 90%; in the group B it was normal in 62.1% and high 37.9%, with p < 0.05. In group A prothrombin time (PT) was normal in 40% and high in 60%; in group B it was normal in 76.7% and low in 23.3%, with p < 0.05. in group TPT was normal in 36.7% and high in 62.1%, with p > 0.05. VDRL was negative in the 100% of the women of group A and positive in the 3.3% of the controls with p > 0.05. The antinuclear antibodies were positive in 6.7% in group A, and in 23.3% in group B, p < 0.05. IgG anticardiolipin antibodies were negatives in the 100% in both groups and IgM antibodies were negative in 96.7% in the group B and 3.3% in group A, p > 0.05. Analysis of histopathologic and immune changes did not show statistic significance when comparing both groups. CONCLUSIONS: Statistical and clinical significance was observed only in the hemorrheologic changes (PT, TPT, fibrinogen and platelets) and in the newborn weight.

Antibodies to oxidised low-density lipoproteins and cardiolipin in pre-eclampsia and eclampsia.

The objective of this study was to test the hypothesis that autoantibodies to phospholipids and to oxidised low-density lipoprotein (ox-LDL) are increased in pre-eclamptic and eclamptic women compared with normal pregnancy. Serum concentrations of autoantibodies to ox-LDL and to cardiolipin were measured in 21 non-pregnant controls, 29 pregnant controls, 21 pre-eclamptic and six eclamptic women. Concentrations of IgG antibodies to ox-LDL and to cardiolipin were not significantly different in women with eclampsia as compared with the non-pregnant controls, pregnant controls and pre-eclampsia. Concentrations of IgM antibodies to cardiolipin were significantly lower in women with pre-eclampsia compared with non-pregnant controls and eclampsia. All three pregnant states differ markedly from the non-pregnant controls, of whom only 5% (1 of 21) had "high positive" IgG antibodies. These results suggest that ACAs rise as a result of the pregnant state rather than as a result of preeclampsia or eclampsia. According to these results, there is no evidence of increased production of serum autoantibodies against modified LDL in African women with pre-eclampsia, which may reflect reduced lipid peroxidation involving lipoproteins or no link at all. In addition, IgG and IgM anticardiolipin antibodies have no diagnostic value in preeclampsia and eclampsia.

Changes in lymphocyte subsets during pregnancy and post-partum in cases of beginning eclampsia.

AIMS: The goal of the present retrospective study was to examine the peripheral blood lymphocytes for expression of phenotypic and activation markers concerning the development of hypertension in pregnancy. METHODS: 16 women (aged 25-43 years; mean 35.1) developing hypertension in the third trimester (week 25-34) have had blood samples taken in the first (< 14 weeks), the second (week 14-23), the third trimester (week 24-35), in late pregnancy (week 36-termination of pregnancy) and within 1 week post-partum, The control group consisted of 16 age-matched pregnant healthy women, who underwent the same regime. All blood samples were taken in the morning, stored at room temperature and stained within 6 hours and measured within 24 hours. Kruskal-Wallis analysis of variance between both groups was done with multiple comparison according to Dunn. RESULTS: Comparing both groups, the total white cell count was significantly increased in all pregnancies and post-partum. In case of hypertension in pregnancy the cell numbers of suppressor/cytotoxic (CD 8+) and CD 56(+)-activated T cells showed a significant increase in the first trimester (< 14 weeks) [p < 0.05] and decreased thereafter to normal values. In the second trimester (week 14-23) helper/inducer lymphocytes and CD 56+/CD 3+ lymphocytes decreased in case of pre-ecclampsia and cytotoxic lymphocytes elevated [p < 0.05]. In the third trimester (week 24-35) there was no difference in both study groups and in late pregnancy (week 36-termination) there were only small differences without statistical significance. Within 1 week postnatal the value of Il-2 receptor T lymphocytes decreased in the group of pre-eclampsia in comparison to normal pregnancies [p < 0.05]. CONCLUSIONS: Regarding the major changes in activated T cells in both study groups no specific pattern of lymphocyte subsets in case of pre-eclampsia could be found in comparison to healthy pregnant women. Further investigations should focus on functional activation and/or suppression of the cellular immune system. Perhaps this could lead to a screening test for pre-eclampsia in future, which is non-invasive for the patient and economic for our social community because it might reduce medical costs.

Changing paternity and the risk of preeclampsia/eclampsia in the subsequent pregnancy.

To determine whether changing paternity affects the risk of preeclampsia or eclampsia in the subsequent pregnancy and whether the effect depends on a woman's history of preeclampsia/eclampsia with her previous partner, a cohort study was conducted based on 140,147 women with two consecutive births during 1989-1991 identified through linking of annual California birth certificate data. Among women without preeclampsia/eclampsia in the first birth, changing partners resulted in a 30% increase in the risk of preeclampsia/eclampsia in the subsequent pregnancy compared with those who did not change partners (95% confidence interval: 1.1, 1.6). On the other hand, among women with preeclampsia/eclampsia in the first birth, changing partners resulted in a 30% reduction in the risk of preeclampsia/eclampsia in the subsequent pregnancy (95% confidence interval: 0.4, 1.2). The difference of the effect of changing paternity on the risk of preeclampsia/eclampsia between women with and those without a history of this condition was significant (p < 0.05 for the interaction term). The above estimates were adjusted for potential confounders. These findings suggest that the effect of changing paternity depends on the history of preeclampsia/eclampsia with the previous partner and support the hypothesis that parental human leukocyte antigen sharing may play a role in the etiology of preeclampsia/eclampsia.

Anticardiolipin antibodies and the severity of preeclampsia-eclampsia.

OBJECTIVE: To identify and compare anticardiolipin antibodies (aCL) in patients with eclampsia, different grades of preeclampsia and women with normotensive pregnancy. METHODS: A cross-sectional study was conducted in 13 patients with eclampsia, 39 with preeclampsia (13 severe, 26 mild), and 52 normotensive pregnant women. All of them were studied in the 3rd trimester of pregnancy. The aCL were determined by an ELISA method. RESULTS: There were no significant differences in IgG aCL (F = 0.33, p = 0.80) and IgM aCL (F = 1.64, p = 0.18) between patients with eclampsia (6.9 +/- 3.9 U/GPL and 4.0 +/- 2.0 U/MPL), severe preeclampsia (5.7 +/- 3.5 U/GPL and 2.9 +/- 1. 3 U/MPL), mild preeclampsia (6.8 +/- 3.9 U/GPL and 2.8 +/- 1.0 U/MPL) and normotensive pregnant women (6.4 +/- 3.4 U/GPL and 3.0 +/- 1.8 U/MPL). None of the values of the aCL were considered as positive. CONCLUSION: Serum aCL levels were similar in patients with different grades of preeclampsia-eclampsia and women with normotensive pregnancy.

Antiphospholipid antibodies in eclamptic women.

Our purpose was to determine the prevalence of antiphospholipid antibodies (APA) in eclamptic women as well as the rates of intrauterine growth retardation (IUGR) and fetal death in APA-positive and -negative eclamptic women. Thirty-six eclamptic and 30 healthy pregnant women were enrolled in this study. APA in those groups were determined. The prevalences of IUGR and fetal death were determined in APA-positive and -negative eclamptic women. In the eclamptic group, APA were positive in 9 out of 36 patients (25%), where as only 2 out of 30 controls (6.7%) were positive (p < 0.05). Fetal death was encountered in 4 out of 9 (44.4%) APA-positive eclamptic women; this was a significantly larger proportion than that for APA-negative eclamptic women (1/27; p < 0.01). The rates of IUGR in APA-positive and -negative eclamptic women were not significantly different (p > 0.05). Similar conclusions about our results could also be made, when weakly positive anticardiolipin antibodies were regarded as negative in our study group and controls. Our study suggests that positive levels of APA in eclamptic women increase the risk for intrauterine fetal death.

Anticuerpos anticardiolipina en la preeclampsia/eclampsia / Anticardiolipine antibodies in preeclampsia/eclampsia

Introducción. Los anticuerpos antifosfolípidos se han encontrado elevados en pacientes con preeclampsia/eclamplsia. Objetivo. Determinar la presencia de anticuerpos anticardiolipina en pacientes con preeclampsia/eclampsia. Pacientes y métodos. Estudiamos prospectivamente 65 pacientes, 35 con preeclampsia/eclampsia (grupo problema, A) y 30 con embarazo normal (grupo control, B) en una UCI. Se efectuó determinación en sangre de IgM e IgG utilizando el método modificado de Harris al segundo y tercer trimestre de embarazo en los dos grupos. Resultados. Encontramos al 2o. y 3er. trimestre de embarazo: en el grupo A, lgG 1.3 ñ 0.9 U y 1.52 ñ 1.1, respectivamante (cuatro pacientes) y la lgM fue de 2.2 ñ 0.9 U y 2.06 ñ 0.81 U (nueve pacientes). En el grupo B (30 pacientes) la lgG fue 1.2 ñ 0.7 U y 0.2 ñ 0.1 U, y la lgM 2.1 ñ U y 1.7 ñ 1 U en los mismos periodos. Conclusión. Los anticuerpos anticardiolipinas se elevan frecuentemente en pacientes con preeclampsia/eclampsia

Coital rate and pregnancy-induced hypertension.

Previous workers have emphasized the possibility that pregnancy-induced hypertension (PIH) is associated with a change of sexual partner. It is noted here that any such association is far weaker than that between PIH and fecundability (the probability of conceiving in a month at risk). This latter association is so strong as to suggest its closeness to a true cause. Of the determinants of fecundability, coital rate seems the most promising to pursue as a possible cause of PIH.

Anti-beta 2 glycoprotein I antibodies in a general obstetric population: preliminary results on the prevalence and correlation with pregnancy outcome. Anti-beta2 glycoprotein I antibodies are associated with some obstetrical complications, mainly preeclampsia-eclampsia.

OBJECTIVE: To evaluate the prevalence in normal pregnancies of anti-32 glycoprotein I (anti-beta2GPI) antibodies, and their association with obstetrical complications. STUDY DESIGN: Prospective study of anti-beta2GPI and anticardiolipin (CL) antibodies in 510 healthy pregnant women at 15-18 weeks. According to the results, women were categorized into three groups: group I, negative for both antibodies; group II, positive for anti-beta2GPI antibodies; group III, positive for aCL only. The rates of fetal loss, abruptio placentae, preeclampsia-eclampsia, and fetal growth retardation were compared in the three groups. RESULTS: Anti-beta2GPI antibodies were found in 20 women (3.9%) and aCL in 8 patients (1.6%). Obstetrical complications were more frequent, even if not significantly different, in group II, 15%, than in group I, 4.1% (difference 10.9%; 95% confidence interval (CI): 1.6-20.2%; p=0.0575), while no complications were seen in group III. Preeclampsia-eclampsia were significantly more frequent in group II (10%) than in group I (0.8%; difference 9.2%; 95% CI: 4.4-14%; p=0.021). The prevalence of fetal growth retardation was not significantly different in the two groups (5% vs. 2%, respectively). COMMENT: Our findings indicate that anti-beta2GPI antibodies are associated with some obstetrical complications, mainly preeclampsia-eclampsia, even if more conventional antiphospholipid antibodies are not present. This observation suggests that these antibodies should be investigated in such cases, in order to improve the outcome of subsequent pregnancies, as well as in women with a history of early and/or recurrent severe preeclampsia in order to start a prophylactic treatment (i.e. low-dose aspirin or heparin).