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The management of pre-eclampsia and eclampsia with chlormethiazole is reviewed. Chlormethiazole, magnesium sulphate and benzodiazepines were found to be easy to administer, rapidly acting and effective in controlling convulsions. Respiratory depression in the fetus was found to be shorter lived when using chlormethiazole than the other two treatments.
UNLABELLED: It has been demonstrated that the concentrations of molecules related to endothelial cell dysfunction, coagulation and vasoconstriction are altered in preeclamptic patients, but they have not been evaluated in their relationship with the severity of preeclampsia. OBJECTIVE: To determine the relationship between the plasmatic concentrations of fibronectin ED1+, antithrombin III, prostacyclin and thromboxane, and the severity of preeclampsia. METHODS: Peripheral blood was collected from 215 women in the third trimester of pregnancy, admitted to the Luis Castelazo Ayala Gynecology and Obstetrics Hospital with mild preeclampsia (n = 103), severe preeclampsia (n = 71), HELLP syndrome (n = 25) or eclampsia (n = 16). Plasma aliquots were stored at -70 degrees C until analysis. Fibronectin ED1+ was measured by ELISA; antithrombin III activity was determined using an automated amidolytic technique, and the concentrations of the stable metabolites 6-keto-prostagiandin F1a and thromboxane B2 were measured by RIA. Statistical analysis included ANOVA and logistic regression. RESULTS: Maternal age was similar in all participants. Prematurity and low birth weight were present in the patients with severe preeclampsia, HELLP and eclampsia. The values for fibronectin were similar among the 4 groups of patients. Antithrombin III activity was significantly lower in the patients with HELLP. In patients with severe preeclampsia and HELLP syndrome, prostacyclin (Pc) and thromboxane (Tbx) concentrations were significantly higher, and the Pc/Tbx ratio was lower than in patients with mild preeclampsia. Those patients who had the highest thromboxane levels and the lowest Pc/Tbx ratio had a higher chance to develop severe preeclampsia or HELLP (5 times), as well as to have premature babies (12 times) than patients with mild preeclampsia. CONCLUSIONS: Our study demonstrates relationships among antithrombin III activity, prostacyclin and thromboxane concentrations, and the severity of preeclampsia. These compounds were significantly more altered in patients with HELLP syndrome, probably due to a higher organic and vascular dysfunction. Plasma determination of these compounds may be valuable as a tool in the screening of preeclampsia, and as an indicator of severity of the disease.
UNLABELLED: Preeclampsia and eclampsia are the primary causes of maternal mortality. In the state of Nuevo León, from 1990 to 1998, these conditions represented 44.1% of maternal deaths. The presence of thrombogenic substances (homocysteine, C protein, and anticardiolipin antibodies) in the mother's blood has been related to this problem. The C677T polymorphism of the enzyme methylene tetrahydrofolate reductase (MTHFR) favors the increase of homocysteine levels, while folic acid (FA) supplementation decreases its levels. OBJECTIVE: To establish the role of FA in the physiopathology of preeclampsia in our environment. KIND OF STUDY: Longitudinal, prospective and comparative. MATERIAL AND METHODS CASES: Women with severe preeclampsia and/or eclampsia (n-13). CONTROLS: Women in the third trimester of a normal pregnancy (n + 15). 20 mL Blood samples were taken during the first 24 hours of puerperium, and their AF, homocysteine and MTHFR polymorphism were measured. The t Student test and the Exact Fisher test were used to compare between both groups. RESULTS: The values obtained for homocysteine were (x + SD): CASES: 9.85 micromoles/L + 2.88, and controls: 7.61 micromoles/L + 1.32 (p < 0.04). The frequency (%) of the genetic polymorphism for MTHFR was: positive homozygotes (T/T): 38.46 vs. 20, heterozygotes (C/T): 38.46 vs. 26.6, negative homozygotes (C/C): 23 vs 53, for cases and controls, respectively. CONCLUSIONS: According to our study, the frequency of the homozygote state (T/T) of MTHFR and increased blood levels of homocysteine is greater in women suffering from preeclampsia.
OBJECTIVE: To assess the epidemiological aspects of the patient with preeclampsia assisted in the Centro Medico Nacional Torreón, of the IMSS. MATERIAL AND METHOD: We carried out a retrospective and descriptive survey of 138 consecutive admissions to the Department of Gynecology and Obstetrics, between January first to December 31, 1997 with diagnosis of preeclampsia according to the criteria of the ACOG. Maternal and perinatal secondary complications of this pathology were determined. Mortality and lethality rates were also estimated. Descriptive statistics were used for the analysis. RESULTS: The prevalence rate of preeclampsia was 2.1%. The age of the patients was 23.2 years (SD 3.05) and the gestational age at the moment of the diagnosis of preeclampsia of 36.4 weeks (SD 3.2). Only 41.3% of the patients received regular prenatal control. The prevalence rate of maternal complications was 29.0%. Mortality rate was 0.15 x 1,000, lethality rate was 0.72%. The weight average of the new born were 2.011 kg (SD 0.429), the Apgar to the first minute 7.72 (SD 0.98) and 8.66 (SD 1.10) to the fifth minute. The prevalence rate of perinatal complications was 35.5%. There were 15 neonatal deaths (10.9%) and one fetal lost. CONCLUSIONS: The preeclampsia-eclampsia is still a disorder with a great influence in the maternal and perinatal morbidity and mortality rates. It is necessary to continue working for find out the way of preventing their appearance or modifying their evolution avoiding the eclampsia or other serious forms of this illness.
UNLABELLED: Hypertension is the most important cause of disease in the expectant mother and the fetus, and it unfavorably affects the perinatal morbidity and mortality. AIM: To determine the method of delivery of a pregnant women with Praeeclampsia-Eclampsia (PE-E) depending upon the severity, continuity and term of appearance of hypertensive disease during pregnancy and its impact on perinatal morbidity and mortality. MATERIAL AND METHODS: The study covers a two year period (2002-2003), during which 84 pregnant women are treated and deliver with PE-E in the Ist and IInd Obstetrics clinics. Of them 64 (76.20%) are with mild form of PE, 10 (11.90%) with mid severe form and 10 (11.90%) severe form of which 3 had Eclampsia. The pregnancies were followed using echography and cardiotocographic monitoring. RESULTS AND DISCUSSIONS: With the severe forms of PE-E the disease started between 25-30 gestational weeks (60%), while with the mid severe the appearance was between 31-36 g.w. (50%). Persistence of PE > 4 g.w. was observed with severe PE, whereas in mild forms continuity of < 3 g.w. (73.44%) prevailed with its onset after 37 g.w. (57.81%). Normal delivery was attained with 41 pregnancies (48.81%), Caesarean section (CS) with 40 (47.62%), vacuum extraction with 1 (81.19%) and 2 (2.38%) had incomplete aborts. Frequency of CS with the severe forms of PE-E is 80%, with mid severe 50%, and with the mild forms is 42.19%. The most frequent indication of CS is fetal distress--11 (27.50%) and complicated obstetric anamnesis--9 (22.50%). With severe PE-E the most frequent indication is aggravation of symptoms and its non responsiveness to treatment. Born dead are 3 fetuses with severe retardation and body weight < 800 gm. Early gestational age hasn't given us the reason for premature delivery. Death of 1 child, born by CS with 750 gm weight is recorded. The higher rate of CS (3 times more than the median for the clinic--15.16%) can be explained to a degree by the fact that operative delivery by CS in pregnancies with PE-E reduces complications and has an aim to prevent complications to the fetus as well as the mother.
Quantitative analysis of placental pathology was carried out on 20 placentae from various grades of pre-eclampsia eclampsia syndrome and 20 placentae from control group. Placental weights were lower in the study group. The gross abnormalities noted were the placental infarcts, retroplacental haematoma and calcification. The striking villous lesions observed in the study group were cytotrophoblastic cell proliferation, thickening of villous basement membrane and paucity of vasculosyncytial membrane and these findings correlated well with the severity of maternal disease. These vascular villous lesions were considered secondary to uteroplacental ischaemia.
Haemodynamic function was assessed in twenty patients with severe pre-eclampsia or eclampsia. In front of the earlier well-known data hypercinetic circulatory status was found with vascular resistance almost unchanged. As some investigators found two levels placental blood flow, haemodynamic status may be different in some cases. Consequences on therapy are discussed especially beta-bloquers and potential deleterious effects of anti-hypertensive treatments.
The objective was to describe the epidemiology of preeclampsia-eclampsia (P-E) at the Hospital General O'Horán (HGOH) in Mérida, Yucatán, México, from 1995 to 1998. Patients with a discharge diagnosis of P-E were included. Their demographic and clinical data were ascertained. To analyze information, descriptive statistics were used. There were 143 patients. Preeclampsia was documented in 41% and eclampsia in 59%. The mean age of the group was 24.4 +/- 7.3 years. It was found that 76% came from rural area. In 79% schooling was no more than elementary education. Seventy five per cent were married. Sexual life began at a mean age of 18.8 +/- 4.3 years. There was no prenatal care in 27% of the cases. Fifty five per cent were primigravida and 43% multigravida. Nuliparity was documented in 52%. Two o more parities were documented in 48%. Complications were seen in 30%. Overall mortality rate was 5%, more frequent eclamptic patients. At the HGOH, P-E was frequently documented in women with both low socioeconomic status and fewer years of schooling. Prenatal care was also irregular. Clinical evolution was satisfactory in most of them, and the mortality rate was low, although it usually occurred in young eclamptic women.
In this study we tested the hypothesis of an association between consanguinity and pre-eclampsia/eclampsia. This is a case-control study conducted at Princess Badea Teaching Hospital, Irbid-Jordan during the period May 1997-April 1998. The study population were Jordanian women delivered at Princess Badea Teaching Hospital with or without hypertensive disorders of pregnancy. The total number was 208 pre-eclamptic/eclamptic women (76 primiparous and 132 multiparous) and 618 randomly selected non-hypertensive women. In primiparous as well as multiparous women, it was evident that neither consanguinity nor the degree of the relationship to the husband in consanguineous marriages had an impact on the incidence of preeclampsia/eclampsia. However, comparing the incidence of consanguinity between pre-eclamptic/eclamptic and non-hypertensive, multiparous women married to a relative other than first cousin, the P value was 0.0248, which we explained as chance incidence. When we compared the incidence of consanguineous marriages as a whole between pre-eclamptic/eclamptic and non-hypertensive, multiparous women, there was no evidence of any impact of consanguinity on the incidence of pre-eclampsia/eclampsia.
The possibility that the etiology of toxemia might be immunologic has been held for over 70 years. In the past decade, numerous studies have been instituted in attempts to verify the possible role of the immune system in this disease. The present study was undertaken as a probe to determine if a gross difference in the numbers of T and B cell lymphocyte populations might exist between pre-eclamptic and normally pregnant women. Twenty-five normally pregnant women in the third trimester were compared to 25 pre-eclamptic women, and significant differences were noted. If, indeed, there is an immunologic basis for pre-eclampsia, it is more subtle than the methodology used in this study is capable of detecting.
The mainstay of the management of severe pre-eclampsia is early referral, stabilization of the mother with antihypertensive therapy and anticonvulsants if required, full assessment of the mother and the baby, and delivery on the best day in the best way. It is to be remembered that delivery is the long-term cure, but most women get worse after delivery and most maternal deaths occur postpartum. It is important that doctors have the training to be aware of the dangers of this condition, guidelines to follow and senior support. Lowering blood pressure has been associated with a reduction in the mortality from cerebrovascular accident and early use of antihypertensive agents is beneficial to both mother and baby. The main cause of death is now pulmonary oedema, with renal failure a rare complication. It is important that, after delivery, vigilance is maintained and fluid replacement is given with care. It is better to 'run them dry' than to give fluid replacement that may encourage pulmonary oedema. Followup is required with counselling about what has happened and the prospects of recurrence.
Parenterally administered magnesium is a reliable and effective treatment to prevent and control convulsions associated with preeclampsia and eclampsia. Because of several side effects in the newborn, especially in the premature child, benzodiazepines are not recommended for prolonged medication. Clomethiazole has also been used with good acceptance, but clinical experience is limited. The anticonvulsive property of magnesium is not clearly understood. Beside a well known peripheral action by neuromuscular blockade through very high serum concentrations, a central mechanism is postulated already at lower levels. The two most widely used regimens of magnesium administration are the intravenous/intramuscular (i.v./i.m.) method popularized by Pritchard and the continuous intravenous (i.v.) route recommended by Zuspan. The concentrations of magnesium in the serum achieved with the i.v./i.m. regimen are significantly higher than those produced by the i.v. administration, especially in the first three hours after initiation of the treatment and if a maintenance dose of 1 g/h is chosen. Although therapeutic concentrations of magnesium effective to prevent seizures have been reported between 1.3 and 4.0 mmol/l, repeated convulsions are occasionally seen during i.v. regimen and at concentrations below 2 mmol/l. Because of this observation, a maintenance dose of 2 g/h and in some cases 3 g/h is required during the first hours of treatment. Side effects in mother and newborn are low, if there is no renal impairment and the treatment instructions are strictly followed. Respiration as well as urinary output have to be monitored at periodic intervals and the patellar reflex should be present. Calcium gluconate, 10 ml of a 10% solution, is an effective antidote in case of magnesium intoxication.
The study was retrospective, encompassing 2 years period of time (2000-2001), as it was carried out at the First and the Second Clinics of Obstetrics at the Higher Institute of Medicine-Pleven. Fifty pregnant women and women in-child-birth having Praeeclampsia-Eclampsia (PE-E) were treated during this period, as 26 of them were administered Cormagnesin (first group) and 24 (second group) were not treated with magnesium preparations. In the first group 6 pregnant women had severe PE and 4-E, total 10 (38.4%). All E pregnant women and the PE cases with RR > or = 180/120 were treated with Cormagnesin. In the second group there were 4 pregnant women with severe PE (16.67%) but proteinuria was predominant (> or = 5 g/l) as RR was not higher than 160/110, so we did not have the reason to administer them Cormagnesin. The highest total dose MgS was 100 g and it was applied only in 1 E case (20g /daily for the duration of 5 days). In the remaining E cases the total dose was 60, 48, 2 g, respectively, as the number of applications was from 1 to 4 times daily, and the duration from 1 to 4 days. Cormagnesin gave excellent results in 80% of the cases with severe PE-E. The frequency rate of s.c. in the first group was 57.69%, in the second group--25%. The authors made the conclusion that the severity of PE-E and mainly the high values of RR and the other accompanying symptoms determined treatment with MgSO4. Cormagnesin application scheme was strictly individual. MgSO4 application allowed the possibility for conducting the delivery under more favourable conditions when convulsions were under control and RR was stabilised.
1. From 1976 to 1980 858 patients with late gestoses were treated at the Department of Obstetrics and Gynecology of the Wilhelm-Pieck-University of Rostock (6,9% from 12.519 deliveries). 2. The principles of therapy with appropriate dosage of drugs are discussed in comparison to other countries. 3. The sedative-anticonvulsive therapy of severe preeclampsia is based mainly on magnesium sulfate used both in the USA and in our clinic, but seldom in Sweden. In England the basic principles of the sedative therapy are benzodiazepines. 4. In treatment of preeclampsia antihypertensive drugs are usually applied only above blood pressure values of 160/110 mmHg. 5. Hydralazine is preferred in our clinic like in the USA, in England methyldopa and beta-blocking agents. Diazoxide is said to be the drug of choice in acute hypertensive crisis. 6. Since many years in severe cases with hemoconcentration we prefer a short-term plasma volume expansion by hypertonic osmotically and oncotically active solutions. This osmoonco-therapy may be applied before or simultaneously with the administration of antihypertensive drugs. But there are controversies in this mode of treatment. 7. In our clinic the maternal mortality of 79 eclampsias was 2,25% from 1959 to 1980.
The preeclampsia-eclampsia syndrome is a vasospastic disorder and probably has a placental origin. Once the hypertensive syndrome is established the uteroplacental blood flow is reduced as well as the intervillous blood flow. Since 18-24 weeks of gestation and before the symptoms of preeclampsia become overt, changes in placental flow velocity can be detected with Doppler technics. The placental theories for the etiology of preeclampsia are focused on the hypoxic effect in the trophoblastic tissue of second trimester. The placental ischemic changes are evident and seen in the uteroplacental bed. They are interrelated with the stages of trophoblastic invasion of the spiral arteries during the 14 and 20 weeks. When the trophoblastic invasion is over, the spiral arteries become a high resistance system. The defect observed in preeclampsia is the lack of invasion of the trophoblast to the maternal arteries. The diminished placental perfusion probably creates endothelial damage. This damage has several effects: decreased prostaglandin production, activated coagulation cascade, stimulated fibrin aggregation, and increased vascular permeability. The ideal laboratory test for preeclampsia shall predict the onset of this entity. Recent findings seem promising. The fibronectin concentration increases 2-3 wks. prior to the clinical manifestation of preeclampsia. Severe hypertension shows an abnormal decrease in fibronectin levels. Hypocalciuria has been described as an early predictor in the development of preeclampsia. Other agents undergoing extensive evaluation as predictors are: uric acid, b-thromboglobin, prolactin and atrial natriuretic peptide. Recently high levels of b-HCG (human corionic gonadotrophin) have been linked to a lack of trophoblastic invasion during the second trimester, therefore this is a potential marker for those patients that will eventually develop preeclampsia.
Pre-eclampsia (PE) is the most severe pregnancy-related disease, leading to high maternal and fetal morbidity/mortality. Immunological imbalances associated with endothelial cell dysfunction have been hypothesized as a cause for the onset and perpetuation of PE. Valid and reliable animal models are urgently required to test this hypothesis and to better understand the mechanisms underlying PE. We developed a novel PE-model by adoptively transferring activated BALB/c Th1-like splenocytes into allogeneically pregnant BALB/c female mice during late gestation; the model mimicked the symptoms of PE, i.e. increased blood pressure and glomerulonephritis accompanied by proteinuria. Interestingly, these PE-like symptoms were not detectable in non-pregnant recipients of activated Th1-like cells. Adoptive cell transfer adversely affected the outcome of pregnancy by increasing fetal rejection, with uterine immune cells showing an inflammatory profile. In conclusion, we have established a valid and reliable PE mouse model, which opens vast opportunities for therapeutic interventions.
A case of pre-eclampsia/eclampsia appearing in three generations is presented combined with a review of literature. It is unknown whether the maternal genotype or the combination of the fetal and the maternal genotype is responsible for a disposition to this disease. Moreover the heredity as an autosomal-recessive or a dominant one with incomplete penetrance is in dispute. Further investigation will be convenient to improve the definition of groups at risk and a possible pharmacological prophylaxis.
The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.