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The aim of the present study was to examine the use of maternal weight measurements during antenatal care throughout the United Kingdom. A postal questionnaire and follow-up letter were sent to 1500 midwives throughout the United Kingdom, selected at random from the UKCC register. The postal survey achieved a response rate of 44.8% (672/1500 questionnaires), and obtained responses from at least 10 midwives in all but the lowest grade. Respondents were representative of midwives practising throughout the country, in terms of their gender, working hours and grade, although there were fewer midwives in community settings than those in a contemporary representative English sample. The questionnaire obtained information on the background, training and experience of each midwife, together with their attitudes towards antenatal weighing. For those midwives currently involved in antenatal care, additional information was collected on the schedule of antenatal weight measurements, the criteria used to identify 'abnormal' weight gain, and the action taken in response to 'abnormal' weight gain. 61.8% of the midwives thought that the pattern of maternal weight gain was 'not important' in antenatal care, and only 51.5% of those who currently provided antenatal care weighted women at every antenatal visit. However, most midwives (86.1%) cited at least one clinical condition to explain why women are routinely weighed during pregnancy, and over a third of midwives thought that maternal weight gain could detect seven clinical conditions, including obesity, oedema, pre-eclampsia and polyhydramnios. Midwives with more advanced qualifications (degrees and teaching qualifications) and those working in educational or community settings were least likely to believe that weight gain was good at detecting clinical outcomes. Differences in the perceived utility of antenatal weighing influenced whether midwives would act in response to 'abnormal' maternal weight gain, and whether they advised women to gain or lose weight during pregnancy. However, the criteria that midwives used for identifying 'abnormal' weight gain were variable, and often inappropriate, so that different midwives are unlikely to intervene consistently or to give consistent advice on the basis of maternal weight gain. These differences in practice may lead to extensive and inappropriate variation in antenatal care. Clear guidelines are urgently required to ensure that, if maternal weight measurements are collected during antenatal care, they are collected and used consistently.
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PMID:The use of maternal weight measurements during antenatal care. A national survey of midwifery practice throughout the United Kingdom. 945 30

Several years ago the hypothesis was advanced that alterations of endothelial function could explain much of the pathophysiology of preeclampsia. Since that time, extensive data have been generated to support the hypothesis. Markers of endothelial activation can be demonstrated in women with overt preeclampsia. More importantly, many of these markers precede clinically evident disease and disappear with resolution of the disease. The original postulate was that materials produced by the poorly perfused placenta, which is characteristic of preeclampsia, entered the systemic circulation and altered endothelial cell activity. This was proposed to change vascular sensitivity to circulating pressors, activate coagulation, and reduce vascular integrity resulting in the pathophysiological changes of preeclampsia. As data have accumulated it has become increasingly evident that the insult to the endothelium is neither toxicity nor nonspecific injury but rather can better be characterized as endothelial activation. Candidate molecules have been suggested but not established. It seems likely that the responsible agent(s) will not be unique molecules but rather usual molecules present in excessive amounts. The hypothesis has been expanded to invoke involvement of the maternal constitution in the generation of endothelial injury and injurants. This concept is stimulated by the observation that reduced placental perfusion per se is not sufficient to generate the maternal syndrome. Women with growth-restricted fetuses frequently are not preeclamptic. Placental bed biopsies from not only growth-restricted but also prematurely born infants demonstrate failure of the physiological remodeling of decidual vessels responsible for the reduced placental perfusion of preeclampsia. This has led to the concept that preeclampsia is secondary to an interaction of reduced placental perfusion and maternal factors. Interestingly these maternal factors, obesity, insulin resistance, black race, hypertension, and elevated plasma homocysteine concentration are all risk factors for atherosclerosis in later life.
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PMID:Endothelial dysfunction in preeclampsia. 965 3

This review addresses the general hypothesis that the pathogenesis of preeclampsia is related to an imbalance of increased oxidative stress and lipid peroxidation coupled to a deficiency of antioxidant protection. Evidence will be presented that this imbalance is present in both the maternal compartment and the placental compartment and that interactions between these two compartments result in the clinical manifestations of this disorder. We suggest the following as a scenario for the development of preeclampsia: Oxidative stress in the maternal compartment affects the placenta in such a way as to bring about a decrease in placental antioxidant enzyme protection. The oxidative stress in the maternal compartment may be preexisting (e.g., obesity, diabetes, hyperlipidemia) or may be caused by placental secretion of lipid peroxides. Decreased placental antioxidant enzyme protection leads to a cascade of events in the placenta of uncontrolled lipid peroxidation with increased thromboxane production and increased tumor necrosis factor (TNF-alpha) production. Increased placental secretion of lipid peroxides and/or TNF-alpha results in activation of leukocytes as they circulate through the intervillous space. The activated leukocytes serve as circulating mediators that link the increased oxidative stress of the placenta with a widespread increase in oxidative stress and endothelial dysfunction in the mother. In the third trimester, when the placenta is growing rapidly, the mother's antioxidant capacity is no longer able to compensate, and the clinical symptoms of preeclampsia appear.
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PMID:Maternal-placental interactions of oxidative stress and antioxidants in preeclampsia. 965 11

Diabetes mellitus during pregnancy could result in severe or fatal complications to mother or the unborn product, like polyhydramnios, preeclampsia, abortion, neonatal asphyxia, macrosomia, stillbirth, and others, therefore is very important the early detection and treatment of diabetes. Gestacional Diabetes Mellitus (GDM) is the carbohydrate intolerance of variable severity first recognized during pregnancy. The screening test consist of 50 g of oral glucose and a plasma glucose measurement at one hour, regardless of the time of the last meal, and this may do in all pregnancies between 24 and 28 weeks of gestation. If plasma glucose level above 140 mg/dl results, a oral glucose tolerance test with 100 g must be done. This is the GDM diagnostic test. The risk factors for gestacional diabetes (older than 30 years of age, obesity, arterial hypertension, glucosury, previous GDM, family history of diabetes, family history of macrosomia) identify only 50% of pregnancies with gestacional diabetes, therefore, is necessary to screen all pregnancies who become pregnant, a strict control before pregnant is indispensable, with aim to slow congenital malformations probability and another complications. Gestacional diabetes prevalence in hispanic women in the U.S.A. is 12.3 percent. Diabetes mellitus prevalence in Mexico is about 2-6 percent. The goal of management of diabetes during pregnancy is the maintainance of fasting plasma glucose 105 mg/dl and 120 mg/dl two hours after meals. Treatment consist in diabetes education, diet with caloric needs calculation, exercise, and occasionally insulin. Is necessary the prenatal monitoring, the supervision of delivery or cesarean metabolic changes, and the postnatal monitoring of the mother and product.
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PMID:[Diabetes and pregnancy]. 967 96

Maternal pre-pregnancy obesity is a risk factor for pre-eclampsia (proteinuric hypertension in pregnancy) among North American and European women. We studied the relationship between maternal obesity and risk of pre-eclampsia among Zimbabwean women. A case-control study was conducted at Harare Maternity Hospital, Harare, Zimbabwe, between June 1995 and April 1996. Study participants were 144 women with pre-eclampsia and 194 normotensive women serving as controls. Maternal weight, height and mid-arm circumference were measured and recorded during study participants' postpartum hospital admission. Maternal mid-arm circumference, considered to be relatively stable during pregnancy among women of developing countries, was used as the primary indicator of maternal pre-pregnancy obesity. Logistic regression procedures were used to estimate odds ratios and 95% confidence intervals. There were linear trends in risk of pre-eclampsia with increasing mid-arm circumference, increasing weight and increasing body mass index. After adjusting for potential confounding factors, women in the highest quintile for mid-arm circumference (28-39 cm) were 4.4 times more likely to have had their pregnancy complicated by pre-eclampsia than women in the lowest quintile (21-23 cm). Odds ratios of similar magnitude were observed for the other anthropometric measures. To our knowledge, this is the first study to demonstrate a positive association between maternal obesity and pre-eclampsia risk in a black African population. Biological mechanisms thought to explain this relatively consistent epidemiological finding include endothelial cell injury, possibly resulting from hyperlipidaemia.
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PMID:Risk factors for pre-eclampsia among Zimbabwean women: maternal arm circumference and other anthropometric measures of obesity. 969 Feb 61

The currently accepted definition of gestational diabetes mellitus (GDM) is rather broad. One might expect that fetal and neonatal complications that may occur in GDM pregnancy would be similar to those in pregestational diabetic pregnancy. Comparative evaluation of reported data on morbidity in GDM are often hampered by confounding variables (maternal age, parity, obesity) as well as the influence of factors such as ethnic origin, diagnostic criteria, and intervention during pregnancy. Recent observations indicate that GDM may be associated with increased incidence of fetal malformation and perinatal mortality. Such poor outcome is likely confined to a subset of GDM patients in whom diabetes was present but unrecognized before pregnancy. The most frequent and significant morbidity is fetal macrosomia, which in turn is associated with increased risk of birth injuries and asphyxia. In a nationwide study in Sweden (1991-1993) of a large series (n = 3.322) of treated GDM pregnancies, perinatal mortality rate was not increased; but the rate of preeclampsia was doubled, and the rate of emergency cesarean section was 1.6 times higher than in the background population. The rates of fetal macrosomia (> or = 4,500 g), asphyxia, and transient tachypnea were two to three times higher than normal Erb's palsy was 0.7 and 5% in vaginally delivered infants weighing < 4,500 and > or = 4,500 g, respectively. There is a clear need to define the various levels of glucose intolerance in the mother that may have an adverse effect on the offspring. Of equal importance is to standardize and systematize the criteria used to assess the significance of any such impact.
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PMID:Neonatal morbidities in gestational diabetes mellitus. 970 32

Relationships between body mass index (BMI) and weight gain with perinatal outcome and birthweight were examined. BMI was calculated on 582 consecutive pregnant women who delivered at or >37 weeks gestational age. Statistical analysis was done using Chi-square tests, analysis of variance, and multiple logistic regression. Of those studied, 13% were underweight, 39% normal, 13% overweight, and 35% obese. Obesity was associated with increasing age (P < .01), multiparity (P < .01), previous cesarean delivery (P < .01), previous macrosomia (P = .01), previous fetal death (P = .03), hypertensive disorders (P < .01), gestational diabetes (P = .02), cesarean delivery (P = .03), and neonatal intensive care unit admission (NICU) (P = .01). The underweight group had the most low birthweight (LBW) infants and the lowest mean birthweight. Ideal weight gain occurred in 31%, inadequate weight gain in 34%, and excessive weight gain in 35%. Inadequate weight gain had increased asthma (P < .05), and hyperemesis (P = .03). Women with ideal weight gain had less smokers (P < .01), fetal distress (P < .05), cesarean delivery (P = .02), and preeclampsia (P < .001). The mean birthweight was highest in the excessive weight gain (P < .01). With multivariate analysis, previous LBW, BMI, and tobacco use were significant predictors of LBW. Normal BMI and ideal weight gain in pregnancy is associated with decreased perinatal complications and an optimum birthweight.
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PMID:Prepregnancy body mass index, weight gain during pregnancy, and perinatal outcome in a rural black population. 973 Apr 85

The ACS is a clinical entity that develops from progressive, acute increases in IAP and affects multiple organ systems in a graded fashion because of differential susceptibilities. The gut is the organ most sensitive to IAH, and it develops evidence of end-organ damage before the development of the classic renal, pulmonary, and cardiovascular signs. Intracranial derangements with ACS are now well described. Treatment involves expedient decompression of the abdomen, without which the syndrome of end-organ damage and reduced oxygen delivery may lead to the development of multiple organ failure and, ultimately, death. Multiple trauma, massive hemorrhage, or protracted operation with massive volume resuscitation are the situations in which the ACS is most frequently encountered. Knowledge of the ACS, however, is also essential for the management of critically ill pediatric patients (especially those with AWD) and in understanding the limitations of laparoscopy. The role of IAH in the pathogenesis of NEC, central obesity co-morbidities, and pre-eclampsia/eclampsia remains to be fully studied.
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PMID:Abdominal compartment syndrome. 975 58

We carried out a retrospective and prospective study between January 1995 and August 1996, of pregnant women with high blood pressure. The aim of this work was to determine the prevalence of each type of hypertension according to the classification of the American College of Obstetricians and Gynecologists (ACOG) and to evaluate the prognosis for the mother and child. The prevalence of hypertension in pregnancy was found to be 7.65%. A family history of hypertension, obesity and a personal history of hypertension in pregnancy were all risk factors. Severe hypertension (diastolic blood pressure (DBP) > 110 mm Hg) affected 59.4% of the women. Chronic hypertension occurred in 41.51% of cases, preeclampsia in 26.41% of cases, associated preeclampsia in 18.87% of cases and isolated hypertension in 13.21% of cases. Eclampsia (70.6%) was the principal maternal complication in this study population. Fifty-four of the women gave birth to normal babies, 21 to hypotrophic babies, 15 gave birth prematurely and 3 had miscarriages. Six of the seven deaths involved women with DBP above 110 mm Hg.
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PMID:[Types of hypertension in pregnant women of Benin admitted to the National University Hospital of Cotonou]. 985 12

The immune maladaptation hypothesis of preeclampsia is concordant with cytokine-mediated oxidative stress, chronology of endothelial activation, lipid changes, adverse effect of changing partners, and the protective effect of sperm exposure. Genetic factors may involve underlying hereditary thrombophilic disorders and hyperhomocysteinemia, essential hypertension and/or obesity, or control of the Th1/Th2 balance and thus affect the maternal response against fetal antigens. Placental ischemia and increased syncytiotrophoblast deportation are probably end-stage disease phenomena.
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PMID:The immunology of preeclampsia. 1010 68


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