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Type 2 diabetes is a growing concern, with the number of new cases increasing and occurring at a younger age due to obesity. Consequently the number of cases arising in women of child-bearing age is increasing, and the condition will be encountered more frequently in the antenatal clinic. Type 2 diabetes is often perceived as a benign form of diabetes, but this is not the case when one examines pregnancy outcomes. Rates of perinatal mortality (25/1000) and congenital malformation (99/1000) are significantly greater than those in background populations and at least as poor as those in type 1 diabetes. The rates of hypertension, pre-eclampsia and postpartum haemorrhage are greater than the general maternity population, as is the rate of operative delivery. To improve outcomes we need to dispel the myth that type 2 diabetes is a benign condition. Educational programmes, population screening, and strategies to help vulnerable groups access the services available will increase our ability to identify and counsel women with type 2 diabetes early enough to make a difference.
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PMID:Type 2 diabetes and pregnancy. 1592 69

Obesity is a worldwide growing epidemic. The negative influence of obesity is huge and considered to be one of the major contributors to health problems in the western world. There is a significant association between obesity and diabetes mellitus, ischemic heart disease, some cancers and syndromes of sleep apnea. Furthermore, obesity was described to have a negative influence on fertility, pregnancy, labor and pregnancy outcomes. It was also discovered that obesity was significantly associated with gestational hypertension, preeclampsia, gestational diabetes mellitus and complications in cesarean delivery and anesthesia. This review aims to present updates on the relationship between obesity and pregnancy and labor outcomes, emphasizing the significance of obesity as a risk factor for adverse pregnancy outcome.
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PMID:[Maternal obesity as a risk factor for complications in pregnancy, labor and pregnancy outcomes]. 1612 15

Whether booking body mass index (BMI) in the UK is increasing is unknown but is of clinical interest since overweight or obese pregnant women face far greater risks of pregnancy complications including pre-eclampsia and gestational diabetes. We examined booking BMI in 1990 and 2002/2004, of women with singleton pregnancies. Our analyses indicate an increase of 1 U in mean BMI over this period despite lower parity in recent years. When the model was adjusted for maternal age, parity, smoking status and deprivation category the mean BMI was 1.37 U higher in 2002/2004 than in 1990. More striking was the significant increase in the proportion of women who were obese (BMI > or = 30 kg/m2) at booking--more than twofold higher in unadjusted analysis (18.9% vs 9.4%) rising to greater than threefold higher in multivariate analysis. These findings suggest that obesity-related pregnancy complications are likely to increase with implications for both mother and child.
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PMID:Changes in booking body mass index over a decade: retrospective analysis from a Glasgow Maternity Hospital. 1616 51

Hypertensive diseases in pregnancy are common and are associated with significant maternal and perinatal mortality and morbidity. Risk factors for pre-eclampsia include socio-demographical factors (extremes of reproductive age, socio-economic status, ethnic group), genetic factors, pregnancy factors (multiple pregnancies, primigravidae, previous pre-eclampsia) or personal medical history (obesity, chronic renal disease, chronic hypertension, diabetes mellitus, thrombophilia). These risk factors and Doppler screening can help target interventions such as aspirin and calcium that have been proven to reduce the incidence of pre-eclampsia in high risk women. Expectant management is the mainstay of treatment for pre-eclampsia. Hypertension should be controlled by oral or intravenous antihypertensive agents as necessary. Magnesium sulphate is the agent of choice for both the treatment and prevention of eclampsia. Fluid balance and thromboprophylaxis are also both important elements in the management of severe pre-eclampsia.
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PMID:Risk factors, prevention and treatment of hypertension in pregnancy. 1617 Feb 83

Leptin influences satiety, adiposity, and metabolism and is associated with mechanisms regulating puberty onset, fertility, and pregnancy in various species. Maternal hyperleptinemia is a hallmark of mammalian pregnancy, although both the roles of leptin and the mechanisms regulating its synthesis appear to be taxa specific. In pregnant humans and nonhuman primates, leptin is produced by both maternal and fetal adipose tissues, as well as by the placental trophoblast. Specific receptors in the uterine endometrium, trophoblast, and fetus facilitate direct effects of the polypeptide on implantation, placental endocrine function, and conceptus development. A soluble isoform of the receptor may be responsible for inducing maternal leptin resistance during pregnancy and/or may facilitate the transplacental passage of leptin for the purpose of directly regulating fetal development. The steroid hormones are linked to the regulation of leptin and the leptin receptor and probably interact with other pregnancy-specific, serum-borne factors to regulate leptin dynamics during pregnancy. In addition to its effects on normal conceptus development, leptin is linked to mechanisms affecting a diverse array of pregnancy-specific pathologies that include preeclampsia, gestational diabetes, and intrauterine growth restriction. Association with these anomalies and with mechanisms pointing to a fetal origin for a range of conditions affecting the individual's health in adult life, such as obesity, diabetes mellitus, and cardiovascular disease, reiterate the need for continued research dedicated to elucidating leptin's roles and regulation throughout gestation.
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PMID:Leptin in pregnancy: an update. 1626 10

We have recently proposed a common mechanistic pathway by which obesity and hypertension lead to increased renal cell cancer risk. Our hypothesis posits lipid peroxidation, which is a principal mechanism in rodent renal carcinogenesis, as an intermediate step that leads to a final common pathway shared by numerous observed risks (including obesity, hypertension, smoking, oophorectomy/hysterectomy, parity, preeclampsia, diabetes, and analgesics) or protective factors (including oral contraceptive use and alcohol) for renal cell cancer [Cancer Causes Control 2002;13:287-93]. During this exercise, we have noticed how certain risk factors for renal cell carcinoma are protective for breast cancer and how certain protective factors for renal cell carcinoma increase risk for breast cancer. Parity and oophorectomy, for example, are positively associated with renal cell carcinoma but are negatively associated with breast cancer. Similarly, obesity and hypertension are positively associated with renal cell carcinoma, but obesity is negatively associated with breast cancer in premenopausal women and hypertension during pregnancy is negatively associated with breast cancer. Furthermore, alcohol intake, negatively associated with renal cell carcinoma, is also positively associated with breast cancer. We propose here the possibility that lipid peroxidation may represent a protective mechanism in breast cancer. Although this runs counter to the conventional view that lipid peroxidation is a process that is harmful and carcinogenic, we present here the chemical and biological rationale, based on epidemiologic and biochemical data, which may deserve further consideration and investigation.
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PMID:Role of lipid peroxidation in the epidemiology and prevention of breast cancer. 1636 97

The prevalence of obesity continues to increase despite preventive strategies. Obese parturients are at increased risk of having either concurrent medical problems or superimposed antenatal diseases such as pre-eclampsia and gestational diabetes. Moreover, they have a tendency to labour abnormally contributing to increased instrumental delivery and Caesarean section. Obesity is a risk factor for anaesthesia related maternal mortality. Morbidly obese women must be considered as high-risk and deserve an anaesthetic consultation during their antenatal care. The significant difficulty in administering epidural analgesia should not preclude their use in labour. A more liberalised use of regional techniques may be a means to further reduce anaesthesia-related maternal mortality in the obese population. The mother's life should not be jeopardised to save a compromised fetus. Prophylactic placement of an epidural catheter when not contraindicated in labouring morbidly obese women would potentially decrease anaesthetic and perinatal complications associated with attempts at emergency provision of regional or general anaesthesia. Early mobilisation, aggressive chest physiotherapy and adequate pain control are essential components of effective postoperative care.
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PMID:Obesity and obstetric anaesthesia. 1697 43

We have recently proposed lipid peroxidation as a unifying mechanistic pathway by which several seemingly unrelated risk/protective factors (obesity, hypertension, diabetes, smoking, oophorectomy/hysterectomy, parity, antioxidants) affect renal cell carcinoma development. In experimental studies, increased lipid peroxidation is a principal mechanistic pathway in renal carcinogenesis induced by different chemicals. In this communication, we provide additional lines of evidence that further support a role for lipid peroxidation on renal cell cancer development. (1) Lipid peroxidation may explain the role of other risk (analgesic use, pre-eclampsia) or protective (alcohol intake, oral contraceptives) factors for renal cell carcinoma. (2) Additional experimental evidence supports lipid peroxidation as an important mechanism in renal carcinogenesis, and (3) Existing evidence support a cross-talk between the lipid peroxidation pathway and other pathways that are relevant to renal carcinogenesis, such as apoptosis, VHL, and possibly other pathways.
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PMID:Lipid peroxidation and renal cell carcinoma: further supportive evidence and new mechanistic insights. 1645 3

HDP (hypertensive diseases in pregnancy) are one of the leading causes of maternal and fetal mortality and morbidity. BMI (body mass index) is an established risk factor for pre-eclampsia, but its role in HELLP syndrome is unknown. We therefore investigated BMI as a risk factor in the development of HELLP syndrome. At the beginning of pregnancy, BMI was measured in 1067 women with a history of HDP and 1063 controls. Diagnoses of HDP were classified according to ISSHP (International Society for the Study of Hypertension in Pregnancy) and BMI according to WHO (World Health Organization) criteria. After verification of exclusion criteria and matching for confounders, 687 women with hypertensive diseases in pregnancy and 601 controls remained for statistical evaluation by chi(2) test and multiple logistic regressions. As a continuous variable, the increase in BMI was associated with an increase in the development of gestational hypertension {OR (odds ratio), 1.1 [95% CI (confidence interval) 1.062-1.197]} and pre-eclampsia [OR, 1.1 (95% CI, 1.055-1.144)]}, but not for HELLP syndrome. According to WHO definitions, overweight women (BMI > or =25 and <30 kg/m(2)) had a 2-fold (95% CI, 1.365-2.983) risk and obese women (BMI > or =30 kg/m(2)) had a 3.2-fold (95% CI, 1.7-5.909) risk of developing pre-eclampsia when compared with women of normal weight (BMI > or =15.5 and <25 kg/m(2)). Being overweight or having obesity had no effect on the risk of HELLP syndrome. As an increased BMI is correlated with the risk of developing pre-eclampsia but not HELLP syndrome, both diseases have a different risk profile. This finding supports that underlying physiological mechanisms in pre-eclampsia vary from those in HELLP syndrome.
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PMID:BMI: new aspects of a classical risk factor for hypertensive disorders in pregnancy. 1657 91

About one third of all pregnant women in the United States are obese. Maternal obesity at conception alters gestational metabolic adjustments and affects placental, embryonic, and fetal growth and development. Neural tube defects and other developmental anomalies are more common in infants born to obese women; these defects have been linked to poor glycemic control. Preeclampsia, a gestational disorder occurring more frequently in obese women, appears to be due to a subclinical inflammatory state that impairs early placentation and development of its blood supply. Fetal growth and development during the last half of pregnancy depends on maternal metabolic adjustments dictated by placental hormones and the subsequent oxygen and nutrient supply. Maternal obesity affects these metabolic adjustments as well. Basal metabolic rates are significantly higher in obese women, and maternal fat gain is lower, possibly in response to altered leptin function. The usual increase in insulin resistance seen in late pregnancy is enhanced in obese mothers, causing marked postprandial increases in glucose, lipids, and amino acids and excessive fetal exposure to fuel sources, which in turn increases fetal size, fat stores, and risk for disease postnatally. Impaired glucose tolerance, gestational diabetes, and hyperlipidemia are more common among obese mothers. To date, little attention has been given to the role of diet among obese women in preventing these problems. However, studies of women with impaired glucose tolerance show that replacing refined carbohydrates and saturated fat with complex, low-glycemic carbohydrates and polyunsaturated fatty acids improves metabolic homeostasis and pregnancy outcomes. Thus, current dietary guidelines regarding the amount and type of carbohydrates and fat for nonpregnant women seem appropriate for pregnant women as well.
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PMID:Maternal obesity, metabolism, and pregnancy outcomes. 1670 47


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