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The preeclampsia-eclampsia syndrome is a severe complication of the third trimester of pregnancy and represents the first cause of maternal death. It is mainly characterized by: weight increase, proteinuria and hypertension and can evolve with convulsions and maternal death. The etiology still remains unknown although a series of events have been identified, starting with endothelial damage and local vasoconstriction leading to hypertension. These events occur at first locally in the placental district and become generalized. This paper reports experimental and clinical data in order to demonstrate: 1) the presence of a substance that could evoke experimentally the damage present in this syndrome, 2) a mechanism that delivers such a substance to its primary action site, the placenta, and 3) the possibility to inhibit either the substance or the delivery mechanism in order to prevent this disease. Serotonin appears to play an important role in the chain of events leading to preeclampsia. Certain histological aspects, present in pregnant women with this type of hypertension, have been observed in experimental animals after the administration of serotonin. Platelet derived serotonin could be sufficient, in the case of endothelial damage, to determine vasospasm. In a condition of hypercoagulability, such as pregnancy, this situation can trigger a chain of mechanisms ending with renal damage. Low dose aspirin seems a valid therapeutic approach reducing thromboxane concentrations and therefore preventing vasospasm. In this way the pathogenetic sequence culminating in the preeclampsia-eclampsia syndrome is interrupted. Ketanserin inhibits the hypertensive potential of serotonin by selectively acting on S2 serotonin receptors and appears to be an effective treatment in this type of pregnancy induced hypertension.
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PMID:[Serotonin and hypertension in preeclampsia-eclampsia syndrome]. 210 37

A 26 year old primiparous woman in the 30th gestational week presented with upper right abdominal pain. Clinical examination revealed direct tenderness under the right curverture, oedema, hypertension and proteinuria. Ultrasound scanning showed a normal gallbladder. Laboratory findings revealed Hemolysis, Elevated Liver enzymes and Low Platelet count. On account of suspected HELLP-syndrome cesarean section was performed. We suggest screening of all pregnant with upper abdominal symptoms suspected for preeclampsia by measuring platelet count and liver enzymes.
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PMID:[Upper abdominal pain and pre-eclampsia--HELLP syndrome]. 221 34

A preventive effect of dietary marine n-3 fatty acids on early delivery and toxaemia has recently been hypothesized. In only one published controlled trial fish oil has been given to pregnant women, namely in that conducted during 1938-9 in London by the People's League of Health with a dietary supplement containing vitamins, minerals, and halibut liver oil. Although it was of high quality and its findings are hitherto unexplained, neglect and misinterpretation of the trial seem to occur commonly in reviews. Of the 5644 women who were enrolled the 622 withdrawals were independent of treatment. Alternate allocation to treatment was used, producing two groups that were well balanced as to age and parity. The supplement was given from about week 20. The control group did not receive any supplement. Reductions of 20.4% (95% confidence interval 9-30%, P = 0.00083) and 31.5% (95% confidence interval 11-47%, P = 0.0047) were seen in odds of delivering before 40 weeks of gestation and pre-eclampsia respectively. No significant effects were seen on perinatal mortality, average birth weight, deliveries after 40 weeks, hypertension in the absence of oedema and proteinuria, duration of labour, sepsis or breast-feeding occurrence. Later controlled trials with vitamins or minerals given in the same amounts as in this trial have largely failed to show convincing effects as seen here. A controlled trial assessing the isolated effects of fish oil in pregnancy is warranted.
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PMID:A possible preventive effect of low-dose fish oil on early delivery and pre-eclampsia: indications from a 50-year-old controlled trial. 226 75

In addition to hypertension and proteinuria, generalized edema is seen commonly in women with severe preeclampsia. A patient presented to us at term with the complaint of dysphonia. Upon examination she appeared to be clearly preeclamptic and had a grossly edemetous uvula, which we think occurred secondary to generalized edema. This case might be the first reported one of preeclampsia presenting as dysphonia and of uvular edema in association with preeclampsia.
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PMID:Severe preeclampsia presenting as dysphonia secondary to uvular edema. A case report. 227 70

The question of whether the HELLP syndrome exists as a distinct entity or is part of a spectrum of pregnancy complications, which have in common hemolysis, elevated liver enzymes, and thrombocytopenia, has long been a source of speculation and debate among obstetricians and internists. A review of the literature indicates a definite need for a uniform definition, diagnosis, and management of this syndrome. Patients manifesting this syndrome usually are seen before term (less than 36 weeks' gestation) complaining of malaise (90%), epigastric or right upper-quadrant pain (90%), and nausea or vomiting (50%), and some will have nonspecific viral-syndrome-like symptoms. Hypertension and proteinuria may be absent or slight. Thus some of these patients may have a variety of signs and symptoms, none of which are diagnostic of classic preeclampsia. In consideration of the high maternal and perinatal mortality and morbidity reported with the presence of this syndrome, I recommend that all pregnant women having any of these symptoms should have a complete blood cell count with platelet and liver enzyme determinations irrespective of maternal blood pressure.
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PMID:The HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets): much ado about nothing? 240 34

The purpose of this study was to determine the role of proteinuria on pregnancy outcome in 444 hypertensive women with singleton pregnancies. The patients were divided into three hypertensive groups: 98 with chronic hypertension, 199 with nonproteinuric gestational hypertension, and 147 with proteinuric preeclampsia and chronic hypertension with superimposed proteinuric preeclampsia. The presence of increased proteinuria (greater than 0.3 gm/L) predicted an adverse pregnancy outcome. Furthermore, the majority of small-for-gestational-age infants occurred in the group with proteinuric preeclampsia (52%), whereas the rate of small-for-gestational-age infants was 18% and 12% in the group with nonproteinuric gestational hypertension and chronic hypertension, respectively. The group with chronic hypertension did not show any increased risk for fetal outcome. Perinatal mortality rate was extremely poor in the group with proteinuric preeclampsia at 129 per 1000, four times higher than those of the other two groups.
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PMID:Proteinuria and outcome of 444 pregnancies complicated by hypertension. 230 16

Protein/creatinine ratio (mg/g) in random urine samples was measured in 35 preeclamptic patients and 70 healthy pregnant women. We found a close correlation between the protein/creatinine ratio in random urine samples and both the 24-hour protein excretion and the 24-hour protein/creatinine ratio in the preeclamptic patients. The ratio did not exceed 200 mg/g in any of the 70 healthy pregnant women; therefore, ratios below this value can be considered normal. We conclude that determination of the protein/creatinine ratio in random urine specimens may be a simple method for quantitation of proteinuria in preeclampsia.
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PMID:Protein/creatinine ratio in random urine specimens for quantitation of proteinuria in preeclampsia. 231 78

Antithrombin III (AT-III) activity was measured and compared in 29 patients with preeclampsia and 31 women with normal pregnancies. AT-III levels were 83 +/- 25% in preeclamptic patients with greater than 5 g/l proteinuria compared with 102 +/- 11% in the controls. Less severe proteinuria was not associated with decreased AT-III levels. Multivariate analysis revealed that the duration of pregnancy and the degree of proteinuria had an independent negative effect on AT-III levels. AT-III activity correlated poorly with platelet counts and blood pressure measurements. We conclude that urinary loss appears to be the major mechanisms of lower AT-III levels observed in our patients with preeclampsia.
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PMID:Antithrombin III levels in preeclampsia. 232 33

We report the case of a 32-year-old multipara who presented preeclampsia on the fourth day after childbirth without receiving proper treatment that progressed to eclampsia 4 days later. Pregnancy and delivery had been uneventful. The patient presented proteinuria (30 mg/dl), serum total proteins 5.3 g/dl and serum albumin 3.3 g/dl. Blood pressure was controlled with methyldopa, 500 mg at six-hour intervals by intravenous route. The patient presented hypoxemia secondary to bilateral pleural effusion and aspirative pneumonia requiring mechanical ventilation and invasive hemodynamic monitoring. Treatment with cefotaxime, 1 g at six-hour intervals by intravenous route and clindamycin, 600 mg at six-hour intervals by intravenous route was initiated. Sedation was maintained with thiopental sodium, 3 mg/kg/hour in continuous infusion. At dismission, the patient was completely recovered from her clinical picture and needed no antihypertensive therapy. Physiopathologic features and the aforementioned complications are discussed with particular reference to differential diagnosis.
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PMID:[Late postpartum eclampsia. Apropos of a case]. 233 15

Etiology and pathogenesis of focal and segmental glomerulosclerosis (FSGS) in patients with toxemia of pregnancy remain controversial. We examined 15 preeclamptic patients presenting with nephrotic syndrome. None of the patients had urinary abnormalities and hypertension before pregnancy. Clinically, proteinuria first developed during pregnancy and disappeared completely in all but one patient lost to follow-up after 1-30 months from delivery. Renal dysfunction, hypertension and edema rapidly resolved in the postpartum period. None of the patients had a progressive clinical course. Renal biopsy specimens obtained postpartum revealed typical features of preeclamptic nephropathy. In addition, findings compatible with FSGS were observed in 13 patients including 4 in which such lesions were unearthed by additional serial sectioning. These results indicate that FSGS may not only be induced by preeclampsia but also be one of the representative glomerular changes in preeclamptic patients with nephrotic syndrome. A favorable clinical course ensues in a manner similar to that of patients with the garden - variety of preeclampsia.
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PMID:Focal and segmental glomerulosclerosis in preeclamptic patients with nephrotic syndrome. 238 82


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