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The aim of this study is to evaluate the diagnostic properties of waist circumference in the prediction of obesity-related gestational outcomes. Pregnant women 20 years or older were consecutively enrolled in six Brazilian State capitals from 1991 to 1995. Weight, height, and waist circumference were measured and an oral glucose tolerance test was performed. Patients were followed through childbirth by chart review. Diagnostic performance for the different outcomes, as measured by area under the receiver operating characteristic (ROC) curve, was estimated through logistic regression. Areas under the ROC curve (95%CI) for waist circumference were 0.621(0.589-0.652) for gestational diabetes, 0.640 (0.588-0.692) for preeclampsia, and 0.645(0.617-0.673) for macrosomia. These areas were similar to those for BMI (p > 0.05). A waist circumference of 82 cm jointly maximized sensitivity (63%) and specificity (57%). Cutoff points of 23 kg/m(2) for pre-pregnancy BMI and 26 kg/m(2) for BMI at enrollment produced similar diagnostic properties. In conclusion, waist circumference predicts obesity-related adverse pregnancy outcomes at least as well as BMI.
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PMID:Waist circumference in the prediction of obesity-related adverse pregnancy outcomes. 1722 Oct 88

Preeclampsia affects 3-5% of pregnancies and can have a significant impact on health for both mother and fetus. Risk factors include maternal co-morbidities such as obesity and chronic hypertension, paternal factors, and genetic factors. New hypertension and proteinuria during the second half of pregnancy are key diagnostic criteria, but the clinical features and associated prognostic implications are somewhat heterogeneous and may reflect different mechanisms of disease. Renal dysfunction and proteinuria correspond to the pathologic finding of glomerular endotheliosis, and generally resolve after cure of preeclampsia through fetal and placenta delivery. The molecular mechanisms behind this disease are being discovered and refined. The initial etiologic agents are currently unknown. Pathologic studies show abnormal development of an ischemic placenta with a high-resistance vasculature, which cannot deliver an adequate blood supply to the fetoplacental unit. Endothelial dysfunction plays a central role in the pathogenesis of the maternal syndrome. Dysfunctional endothelial cells produce altered quantities of vasoactive mediators, which lead to a tip in the balance towards vasoconstriction. An imbalance in circulating angiogenic factors is emerging as a prominent mechanism that mediates the endothelial dysfunction and the clinical signs and symptoms of preeclampsia. Soluble fms-like tyrosine kinase 1 (sFlt1), an endogenous anti-angiogenic factor that is a potent vascular endothelial growth factor (VEGF) antagonist, is highly elevated in preeclampsia. VEGF is not only important in angiogenesis, but also in maintaining endothelial health including the formation of endothelial fenestrae (a hallmark of the glomerular vascular endothelium). sFlt1 overexpression in animals induces glomerular endotheliosis with the loss of endothelial fenestrae that resembles the renal histological lesions of preeclampsia. More severe forms of preeclampsia, including the HELLP syndrome, may be explained by a concomitant elevation in both sFlt1 and soluble endoglin, another anti-angiogenic factor. Unraveling of the molecular mechanisms behind preeclampsia may help to expand our armamentarium to treat patients in a more directed fashion, as current management consists of supportive care and expedited delivery. Finally, long-term outcomes of women with preeclampsia include a significantly increased risk for hypertension and cardiovascular disease, including mortality, which may warrant more aggressive screening and treatment in this population.
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PMID:Pre-eclampsia: clinical manifestations and molecular mechanisms. 1757 Sep 33

The complexity of the several pathogenic pathways that cause hypertension and vascular disease and the prolonged interval that appears to predate clinical morbidity have hindered inquiry into the association between GDM and vascular disorders. As a forme fruste of later type 2 diabetes, GDM-affected gravidas are identified as at risk of diabetes-related atherosclerosis, glomerular disruption, and pathogenic retinal angio-genesis. That GDM is evidence for underlying chronic conditions such as dysregulation of innate immune response that, independent of the diabetic state, produces vascular disease is difficult state, produces vascular disease is difficult to assert with the present published literature. Cross-sectional studies of patients with established gestational hypertension or preeclampsia are ambiguous as to the possible pathogenic effect of insulin resistance. Cohort studies initiated in early and mid-pregnancy show evidence that both gestational hypertension and preeclampsia may be more prevalent in gravidas with greater insulin resistance. The association of gestational glucose intolerance with gestational hypertension appears to be independent of obesity and ambient glycemia but explained in part by insulin resistance. Late pregnancy preeclampsia is associated with elevated mid-pregnancy BMI, blood pressure, fasting glucose and insulin, urate, and C-reactive protein, suggestive of metabolic and immune dysregulation. GDM appears to be associated with overexpressed innate immune response, which, in turn, is associated with vascular dysfunction and vascular disease. Among women with GDM, markers of insulin resistance do not appear to correlate with hypertension in short-term cohort studies. However, when non-GDM subjects are compared with subjects with GDM, postpregnancy studies do show an associated with vascular dysfunction and vascular disease. Among women with GDM, markers of insulin resistance do not appear to correlate with hypertension in short-term cohort studies. However, when non-GDM subjects are compared with subjects with GDM, postpregnancy studies do show an association of insulin resistance with both inflammatory dysregulation and vascular dysfunction. Cohort studies that have used population-based pregnancy databases consistently identify a clinically significant association of both gestational hypertension and preeclampsia with later hypertensive disorders. Associations with coronary artery disease or stroke are less consistent, requiring further investigation. Preventing the evolution of diabetes and lipid and immune dysregulation of the metabolic syndrome has become a silent public health issue because of the epidemic of childhood and early adulthood obesity and the opportunity at hand to treat insulin resistance by behavioral and pharmacological interventions. However, limited available literature highlights the need for long-term cohort studies of women with well-characterized metabolic and vascular profiles during pregnancy and decades later. Our present knowledge suggests that screening for GDM provides an opportunity of pregnancy outcome improvement. Limited studies of diabetes prevention in at-risk patient groups suggest that we may have the opportunity to reduce the risk of later diabetes. Additional investigation is required to determine if interventions that prevent or postpone diabetes also delay the onset of vascular disease.
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PMID:Gestational diabetes, pregnancy hypertension, and late vascular disease. 1759 80

Adipose tissue secretes a wide range of hormones named adipokines, and these may play a role in obesity-related inflammation. Adiponectin is an exceptional adipokine because low plasma concentrations are associated with obesity, type 2 diabetes, and cardiovascular diseases. It has been observed that plasma adiponectin concentrations are elevated during inflammatory conditions like preeclampsia and arthritis. Nuclear factor-kappaB (NF-kappaB) is an essential transcription factor for expression of inflammation-related proteins. We have used U937 cells stably transfected to express luciferase under the control of NF-kappaB to examine if adiponectin may modulate NF-kappaB activity. Physiological concentrations of native adiponectin induced NF-kappaB activity. This effect was relatively strong compared with proinflammatory adipokines like leptin, resistin, and IL-6. The enhanced NF-kappaB activity was attributed to the high molecular weight adiponectin isoforms. NF-kappaB was not activated by mutated adiponectin that is unable to form high molecular weight complexes. Furthermore, the C-terminal fragment, globular adiponectin, markedly increased NF-kappaB reporter activity, cytokine release, and mRNA expression of inflammation marker genes, at higher levels than stimulation with TNF-alpha and lipopolysaccharide. NF-kappaB activation by globular adiponectin was not affected by antibody inhibition of toll-like receptor 4 or TNF receptors 1 and 2 but was attenuated by inhibitors of p38 MAPK, phosphatidylinositol 3-kinase, and protein kinase C. Analyses of the p65 subunit of NF-kappaB in different leukocyte cell lines showed activation of two monocytic cell lines (U937 and THP-1) by native and globular adiponectin. Our results indicate that adiponectin has proinflammatory properties in monocytic cells.
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PMID:Activation of nuclear factor-kappaB by high molecular weight and globular adiponectin. 1770 46

Cushing's syndrome (CS) during pregnancy is a rare nosology with only a few cases reported in the literature. Misdiagnosis is common, as the syndrome may be easily confused with preeclampsia or gestational diabetes. CS during pregnancy is usually associated with severe maternal and fetal complications. A high degree of clinical awareness is therefore required to avoid miscarriage or premature delivery. We report an 18-year old female referred to our institution with amenorrhea and truncal obesity. Physical examination revealed cushingoid characteristics, including mild hypertension (130/100 mmHg). She was also found to be 8 weeks pregnant. A provisional diagnosis of CS was made based on plasma cortisol and adrenocorticotropin hormone (ACTH) measurements but the patient did not receive any relevant therapy. She eventually gave birth to a healthy full-term infant via vaginal delivery. A right adrenal adenoma was diagnosed post-labor and was subsequently treated with surgical resection. The patient's condition remained stable and 19 months after the adrenalectomy she gave birth to a second healthy full-term infant. Hydrocortisone (30 mg/day) was administered throughout the second gestation. Six months post-labor the treatment was discontinued after a normal hypothalamic-pituitary-adrenal (HPA) axis was ascertained.
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PMID:Cushing's syndrome in pregnancy: report of a case and review of the literature. 1772 9

There is increasing epidemiological evidence that obesity increases the risk of asthma, atopic, and autoimmune diseases. We hypothesize that the increase in these diseases is caused, at least in part, by decreased immunological tolerance as a consequence of immunological changes induced by adipokines (e.g. leptin and adiponectin) and cytokines [e.g. interleukin 6 (IL6) and tumor necrosis factor alpha (TNFalpha)] secreted by white adipose tissue. The increasing body weight increases the levels of circulating IL6, leptin, and TNFalpha. IL6 and leptin down-regulate the activity of regulatory T-lymphocytes (Tregs). Additionally, adiponectin, which decreases with increasing obesity, down-regulates the secretion of IL10 from macrophages and adipocytes. These changes in IL6, leptin, and IL10 decrease the regulatory effect of Tregs resulting in decreased immunological tolerance to antigens. In pregnant women, these obesity-induced immunological changes might be transmitted to the fetus by epigenetic inheritance thereby increasing the risk of atopic disease. We propose that obesity results in immunological changes resulting in decreased immunological tolerance to antigens and skewing of the immune system towards a Th2 cytokine profile increasing the risk of allergy and other immune-mediated diseases. Furthermore, this hypothesis offers a unifying explanation for the observation that older siblings appear to confer protection against atopic diseases, preeclampsia, and certain autoimmune diseases. More studies are definitely needed to explore further the immunological effects of obesity and its possible effects on allergic disease.
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PMID:The link between the epidemics of obesity and allergic diseases: does obesity induce decreased immune tolerance? 1784 92

We evaluated the influence of maternal pre-pregnancy body mass index (BMI), based on reported pre-pregnancy weight and height, on blood pressure (BP) levels during pregnancy by using information from a prospective cohort of 1733 women recruited before 20 weeks' gestation. Maternal antenatal BP values were abstracted from medical records, and we evaluated the mean BP differences according to BMI group in regression models, using generalised estimating equations to account for repeated BP records within each pregnancy. In each trimester, mean systolic BP (SBP) and diastolic BP (DBP) values were positively associated with maternal pre-gestational BMI. This association persisted after adjustment for maternal age, parity, smoking, education, marital status and physical activity. Overweight women (25-29 kg/m(2)) had first-, second- and third-trimester mean SBPs that were 8.1, 7.7 and 8.2 mmHg, respectively, higher than values observed in lean women (<20 kg/m(2)). Mean DBP values were 4.5, 5.4 and 5.6 mmHg higher for each successive trimester in overweight vs. lean women. Obese (>30 kg/m(2)) women consistently had the highest mean SBP and DBP values. Trimester-specific mean SBP values were 10.7-12.0 mmHg higher among obese women vs. lean women. Corresponding trimester-specific mean DBP values were 6.9-7.4 mmHg higher in obese vs. lean women. Similar patterns were observed when trimester-specific average mean arterial pressures were evaluated. Elevated pregnancy BPs associated with maternal pre-gestational BMI are consistent with a large body of literature that documents increased pre-eclampsia risk among overweight and obese women.
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PMID:Trimester-specific blood pressure levels in relation to maternal pre-pregnancy body mass index. 1793 33

Increasing evidence indicates that hypertension in pregnancy is an under-recognized risk factor for cardiovascular disease (CVD). Compared with women who have had normotensive pregnancies, those who are hypertensive during pregnancy are at greater risk of cardiovascular and cerebrovascular events and have a less favorable overall risk profile for CVD years after the affected pregnancies. One factor that might underlie this relationship is that hypertensive disorders of pregnancy (pre-eclampsia, in particular) and CVD share several common risk factors (e.g. obesity, diabetes mellitus and renal disease). Alternatively, hypertension in pregnancy could induce long-term metabolic and vascular abnormalities that might increase the overall risk of CVD later in life. In both cases, evidence regarding risk-reduction interventions specific to women who have had hypertensive pregnancies is lacking. While awaiting results of large-scale studies, hypertensive disorders of pregnancy should be screened for during assessment of a woman's overall risk profile for CVD. Women at high risk must be monitored closely for conventional risk factors that are common to both CVD and hypertensive disorders of pregnancy and treated according to current evidence-based national guidelines.
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PMID:Hypertension in pregnancy: an emerging risk factor for cardiovascular disease. 1795 98

Obese women who become pregnant face many health risks, including gestational diabetes, pregnancy-induced hypertension, and pre-eclampsia. These women also have a greater incidence of preterm labor, cesarean sections, and perioperative morbidity. Infants born to obese women have increased rates of macrosomia and congenital anomalies, as well as life-long complications such as obesity and its associated morbidities. With the increase in numbers of weight loss operations being performed in women of child-bearing age, physicians will have to address patient concerns regarding the safety of pregnancy after surgery. Many of the proposed health benefits of weight loss after surgery could translate to decreased rates of complications experienced by obese pregnant women. Case reports and small series have emerged documenting pregnancy courses after bariatric surgery. We reviewed the studies that reported pregnancy outcomes compiled from PubMed and Ovid databases to help draw conclusions regarding the maternal, fetal, and infant safety in women after bariatric surgery. The observations from these studies have shown that the health risks experienced by obese women during pregnancy are reduced after weight loss surgery. Additionally, there does not appear to be any increased risk regarding fetal or infant outcome.
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PMID:Pregnancy outcomes after bariatric surgery: maternal, fetal, and infant implications. 1797 1

Developed countries represent 20% of the population in the world, but only 12% of human births annually, while 98% of medical publications are issued from these areas. What we can read on preeclampsia is correct, but only for 12% of human pregnancies! In addition, reproductive patterns in the developed world, but only for the last three decades, are different from elsewhere and during the first 70 years of the 20th century. A major difference is in the number of children in families but also, and mainly, in the ages at first pregnancies in primiparae (approaching now 30 years in many developed countries). This is probably why current epidemiological data seem different than that of the 20th century. The purpose of this article is to analyse to what extent the 'primipaternity model' may give clues for the comprehension of epidemiological descriptions past and present--and, indeed, it works in many respects. However, it is evident also that a proportion of preeclampsia cases cannot be explained by paternity patterns, and vascular disease predisposition in women (diabetes, obesity, thrombophilias, etc.) evidently comes into play. For these latter, maternal age is also strongly associated with these complications. Here, we reflect on what can be respective parts of the disease in preeclamptic couples, and on preeclampsia as a marker of subjects susceptible to vascular disease.
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PMID:Etiology of preeclampsia: maternal vascular predisposition and couple disease--mutual exclusion or complementarity? 1799 64


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