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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pre-eclampsia is a pregnancy specific syndrome that is a principal cause of maternal morbidity and mortality, accounting for almost 15% of pregnancy associated deaths, and is one of the major causes of iatrogenic prematurity among new born babies. The mild form of pre-eclampsia most commonly presents with the features of maternal hypertension and proteinuria, but can swiftly and unpredictably become severe with numerous multisystem complications involving the maternal liver, kidneys, lungs, blood and platelet coagulation and nervous systems. The diverse symptoms of pre-eclampsia have made it a difficult disease not only to define, but also to identify a causative agent for the symptoms. This review examines the complex endocrinological mechanisms believed to be responsible for the extensive complications of pre-eclampsia from the role of placental and endothelial dysfunction, to the causes of the oxidative stress and the ensuing general inflammation. It also highlights current endocrine findings that exhibit the potential for clinical application, as either potential markers or novel therapeutic targets, with the aim of either preventing or altering the course of this life-threatening disease of pregnancy.
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PMID:The endocrinology of pre-eclampsia. 1235 23

1. Pre-eclampsia is a human disease of pregnancy characterized by high blood pressure, proteinuria and end-organ damage, if severe. Pre-eclampsia is thought to be related to changes in early placental development, with the formation of a shallower than normal placental bed. 2. Transforming growth factor (TGF)-beta1 is a multifunctional fibrogenic growth factor involved in immune regulation that is elevated in some populations with a high risk of hypertensive end-organ disease related to increases in endothelin release. Transforming growth factor-beta1 is also an important factor in placental implantation. Alterations in TGF-beta1 may be related to abnormal placental development in early pregnancy and, thus, are a candidate for the development of hypertension in pre-eclampsia. 3. The aim of the present study was to examine the placental distribution and serum concentration of TGF-beta1 in patients with pre-eclampsia compared with normal pregnancy. 4. Patients with pre-eclampsia (n = 12) were compared with patients with normal pregnancy (n = 14). Transforming growth factor-beta1 was determined by TGF-beta1 Max ELISA (Promega, Madsion, WI, USA) after serum dilution (1/150) and acid activation. Placental distribution was determined by immunostaining with TGF-beta1 (Santa Cruz, Santa Cruz, CA, USA; 20 ng/mL) and the villi and decidual trophoblast were scored for intensity and extent of staining. 5. Patients with pre-eclampsia had a mean gestational age of 36 weeks, whereas those with a normal pregnancy had a mean gestational age of 39.0 +/- 0.4 weeks. There was no difference in TGF-beta1 concentration between the two groups (mean (+/-SEM) 27.1 +/- 1.0 vs 26.4 +/- 0.7 pg/mL for normal pregnancy and pre-eclampsia, respectively; P = 0.73, Mann-Whitney U-test). There was no correlation between systolic or diastolic blood pressure and TGF-beta1 concentration (regression analysis P = 0.4 and 0.2). Immunostaining was absent in the villous trophoblast cells and endovascular and extravillous trophoblast of term placentas. 6. Although TGF-beta1 is present in trophoblast cells in early pregnancy during placental development, TGF-beta1 concentrations were not increased in the placenta at term in pre-eclampsia and there was no correlation between blood pressure and serum TGF-beta1, suggesting that TGF-beta1 does not play a role in the development of late gestation pre-eclampsia and hypertension.
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PMID:Transforming growth factor-beta 1 does not relate to hypertension in pre-eclampsia. 1236 87

Pre-eclampsia (PE) is a pregnancy-specific syndrome that is a principal cause of maternal morbidity and mortality, accounting for almost 15% of pregnancy-associated deaths. It is also one of the major causes of iatrogenic prematurity among new born babies, placing a heavy burden on both prospective parents and on the health service. The mild form of PE most commonly presents with the features of maternal hypertension and proteinuria but can swiftly and unpredictably become severe with many extensive complications, which can involve the maternal liver, kidneys, lungs, blood and platelet coagulation and nervous systems. These clinical problems normally only become apparent in the second half of pregnancy but are believed to start during the first trimester. The diverse symptoms of PE have made it a difficult disease not only to define but also to identify a causative agent for the symptoms. It has therefore proved difficult to develop specific drugs that can be used to manage the condition in the clinic. Therapeutic intervention so far has been primarily aimed at combating the two main complications of PE - the hypertension and seizures. Current therapies are widely recognised as inadequate. This review examines the complex pathological mechanisms believed to be responsible for the multi-system complications of PE. It highlights current findings that exhibit the potential to target these effects with the aim of either preventing or altering the course of this life-threatening disease of pregnancy.
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PMID:Emerging molecular targets for the treatment of pre-eclampsia. 1254 Feb 73

At an incidence of 3.2-4% world-wide, pregnancy-induced hypertension (PIH) is the most common disease of pregnancy. Since this holds a risk, not only for the mother, but also for the child, the placenta should undergo pathological-anatomical examination in every case. Pathomorphological findings can be described in the feto-maternal border zone as well as in the fetal placenta. These are not, however, specific, nor do they offer diagnostic proof. Pathomorphological findings in the feto-maternal border zone: defective invasion of the extravillous cytotrophoblast, hyperplastic arterio-/arteriolopathy, acute atherosclerosis, and fibrinoid necrosis of endothelium. Disorders of the fetal part of placenta: infarctions/fibrin deposits, obliterative angiopathy, stromal fibrosis/fibrinoid degeneration, syncytiotrophoblastic nodes (Tenney-Parker-phenomenon), and disturbances of maturation of the villi. There is a general lack of correlation between the seriousness of the disease and the morphology. The only exception in this respect are the findings in the vessels both of the placental bed and of the chronic villi. These show a high correlation with doppler sonographic findings.
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PMID:[Placenta in gestational hypertension]. 1506 Jul 25

Preeclampsia is a pregnancy disorder of unknown origin, characterized by vasospasm, elevated blood pressure, and increased neuromuscular irritability, features common to syndromes of magnesium deficiency. Evidence of serum and ionized magnesium metabolism disturbances have been observed in women with preeclampsia. This and the therapeutic utility of magnesium in preeclampsia led us to investigate the extent to which an endogenous tissue magnesium deficiency might be present in and contribute to its pathophysiology. We used (31)P nuclear magnetic resonance spectroscopy to noninvasively measure in situ intracellular-free magnesium levels in brain and skeletal muscle of fasting nonpregnant women (n=12), and of third trimester women with uncomplicated pregnancies (n=11) and preeclampsia (n=7). Compared with nonpregnant controls (brain 519+/-59 micromol/L; muscle 604+/-34 micromol/L), brain and skeletal muscle intracellular magnesium levels were significantly lower in both normal pregnant (brain 342+/-23 micromol/L; muscle 482+/-40 micromol/L; P=0.05 for both tissues) and preeclamptic women (brain 229+/-17 micromol/L; muscle 433+/-46 micromol/L; P=0.05 for both tissues). Brain intracellular magnesium was further reduced in preeclamptics compared with normal pregnant subjects (P=0.05). For all pregnant subjects, blood pressure was significantly and inversely related to the concomitantly measured intracellular magnesium level in brain (systolic, r=-0.59, P=0.01; diastolic, r=-0.52, P=0.02) but not in muscle. Cellular magnesium depletion is characteristic of normal pregnancy and may be one factor contributing to the pathophysiology of preeclampsia. Furthermore, the influence of central nervous system factors on blood pressure may be mediated, at least in part, by ambient intracellular magnesium levels.
Hypertension 2004 Sep
PMID:Cellular-free magnesium depletion in brain and muscle of normal and preeclamptic pregnancy: a nuclear magnetic resonance spectroscopic study. 1526 10

Preeclampsia (PE) is a complication of the second half of the pregnancy whose clinical course is hypertension and proteinuria with or without edema. Its pathogenesis is characterized with generalized vasoconstriction and endothelial dysfunction. The aim of this study is to evaluate the diagnostic value of the Doppler ultrasound examination of the renal interlobar vessels in pregnancy complicated with preeclampsia in the context of the theory of the increased vessel resistance in this pregnancy disorder.
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PMID:[Diagnostic value of the Doppler ultrasound of kidney vessels in pregnancy complicated with preeclampsia]. 1551 79

Discrete hidden Markov models (HMMs) were applied to classify pregnancy disorders. The observation sequence was generated by transforming RR and systolic blood pressure time series using symbolic dynamics. Time series were recorded from 15 women with pregnancy-induced hypertension, 34 with preeclampsia and 41 controls beyond 30th gestational week. HMMs with five to ten hidden states were found to be sufficient to characterize different blood pressure variability, whereas significant classification in RR-based HMMs was found using fifteen hidden states. Pregnancy disorders preeclampsia and pregnancy induced hypertension revealed different patho-physiological autonomous regulation supposing different etiology of both disorders.
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PMID:Hidden Markov models based on symbolic dynamics for statistical modeling of cardiovascular control in hypertensive pregnancy disorders. 1640 14

Plasma ascorbic acid is decreased in women with the pregnancy disorder preeclampsia. We used a mutant strain of rats (Osteogenic Disorder Shionogi), dependent on dietary sources of vitamin C, to investigate whether reduced intake of the vitamin would differentially affect vascular function in late-pregnant (day 19) and age-matched virgin rats. The animals were given either 1 mg/mL of ascorbic acid ad libitum in drinking water [fully supplemented (FS)] or 0.25 mg/mL [marginally supplemented (MS)]. Fetal weights were 21% lower in MS than FS rats, whereas mean maternal weights and pup numbers did not differ. Small mesenteric arteries (diameter, 268+/-7 microm) were mounted in a pressurized arteriograph. Myogenic reactivity (contractile response to step increases in intraluminal pressure) was increased in arteries from MS pregnant compared with FS pregnant rats to levels observed in virgin rats. Ascorbic acid intake did not affect myogenic responses of arteries from virgin rats. Hence, the normal pregnancy-induced reduction in myogenic reactivity was abrogated in MS pregnant animals. Inhibition of nitric oxide synthase had no effect on the myogenicity of arteries from virgin or MS pregnant rats but increased myogenicity of FS pregnant rats to the level of MS pregnant rats. Free radical scavengers reversed the accentuated myogenicity of MS pregnant rats without affecting FS pregnant or virgin rat arteries. These data indicate that moderate ascorbate deprivation increases mesenteric artery myogenic responsiveness during pregnancy. This increase may result from a decrease in nitric oxide-mediated modulation of the myogenic contractile response.
Hypertension 2006 Mar
PMID:Moderate ascorbate deficiency increases myogenic tone of arteries from pregnant but not virgin ascorbate-dependent rats. 1643 38

Insulin resistance syndrome has been observed in women with hypertensive disease of pregnancy, but few studies evaluated the presence of the syndrome a few years after delivery. The objective of this study was to evaluate the presence of insulin resistance and its metabolic alterations in these women compared with those who had a normal pregnancy. We performed an observational study in 168 women with previous hypertensive disease of pregnancy and 168 control subjects with normal pregnancy contacted, on average, 7.8 years after their first delivery (mean age: 34.8 years). Complete blood lipid profile, insulin, glucose, homocysteine, adipokins, and markers of inflammation were measured. Also, an oral glucose tolerance test was performed in 146 case and 135 control subjects. Case subjects were more overweight compared with control subjects. We found significantly lower high-density lipoprotein cholesterol and adiponectin levels and higher apolipoprotein (apo) apoB/apoA1 ratio, homocysteine, leptin, and insulin levels among case subjects compared with control subjects (P<or=0.004). Also, case subjects were more insulin resistant in the basal state estimated by homeostasis assessment model 2, as well as in the nonbasal state as estimated by insulin sensitivity indices calculated from the oral glucose tolerance test. Finally, in a multivariate regression model, leptin, apoB/apoA1 ratio, waist circumference, adiponectin, and free fatty acids explained 40% of homeostasis assessment model 2 variance. Young women with previous hypertensive disease of pregnancy show signs of insulin resistance within the first decade after delivery. These findings suggest that insulin resistance may be the link between hypertensive disease of pregnancy and increased cardiovascular risk later in life.
Hypertension 2007 May
PMID:Previous hypertensive disease of pregnancy is associated with alterations of markers of insulin resistance. 1738 57

Pre-eclampsia, a disease of pregnancy, is a cause of maternal and fetal mortality worldwide and a major factor in preterm birth. Up to 10% of primipara suffer from this disorder, characterized by pregnancy-induced hypertension and proteinuria, usually in the third trimester when fetal demands on the placenta are greatly increased. The disease is thought to stem from an insufficiency in utero-placental blood flow triggering a cascade of events leading to the maternal syndrome, which may have been initiated by defective placentation early in pregnancy. Theories abound as to the primary cause of the placental pathologies associated with the disease, including those based on maternal immunity and the unique immune environment of the placental bed. Accumulating evidence from animal models, genetic studies, and isolated decidual leukocytes suggests that decidual natural killer (NK) cells supply factors necessary for development and arterial modification of the maternal-fetal interface. This beneficial role of NK cells to normal placentation may shed light on the cause of the placental pathologies observed in pre-eclampsia.
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PMID:NK cells and pre-eclampsia. 1828 77


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