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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The presence of disseminated intravascular coagulation (DIC) in the syndrome of haemolysis, elevated liver enzymes and low platelets (HELLP) is debated. We assessed the occurrence of decompensated and compensated DIC (using predefined criteria) in 15 consecutive nulliparous pregnant patients with gestational hypertension combined with the HELLP syndrome and in 12 consecutive nulliparous controls with pregnancy induced hypertension (PIH) but without the HELLP syndrome. A combination of routine coagulation assays revealed the absence of decompensated DIC in all studied patients. However, using more specific and sensitive coagulation assays, compensated DIC was observed in all HELLP patients and in three patients in the control group. The mean values of antithrombin III, thrombin-antithrombin III complexes and protein C in the HELLP and the control group were 66 vs 87% (P = 0.0004), 21 vs 8 ng/ml (P = 0.0008) and 57 vs 90% (P = 0.0018) respectively. We conclude that HELLP patients show evidence of compensated DIC which may have pathophysiological significance for the observed organ damage.
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PMID:Coagulation studies in the syndrome of haemolysis, elevated liver enzymes and low platelets. 199 31

Plasma fibronectin (Fn) levels and activities of antithrombin III (AT-III) function were determined in 219 cases, including 61 cases of pregnancy-induced hypertension (PIH) and 127 normal pregnant women and 31 normal nonpregnant women as controls. The plasma Fn levels of PIH patients were significantly increases to 539.04 +/- 256.3 mg/L, while the plasma AT-III activities were significantly lowered to 76.1 + 13.9%. There was a negative correlation between plasma Fn and AT-III in PIH patients (r = -0.377, P less than 0.01). High plasma Fn and low plasma AT-III in PIH were related to proteinuria. Plasma AT-III decreased as PIH became more severe. The results suggested that the high plasma Fn with low AT-III levels may serve as an indicator of the severity of PIH.
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PMID:[Changes of plasma fibronectin and antithrombin III in pregnancy-induced hypertension]. 200 75

During pregnancy an increase of antithrombin III can be observed. In hypertensive pregnant women this increase may be smaller. This fact may be a sign of hypertension induced disseminated intravascular coagulation and important for prognosis and therapy of pregnancy-induced hypertension. We carried out estimations of antithrombin III by double determinations using radial immundiffusion. Antithrombin III levels were lower in patient with pregnancy-induced hypertension.
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PMID:[Antithrombin III level in normal pregnancy and patients with pregnancy-induced hypertension]. 237 98

Forty-five women with preeclampsia and 39 woman with chronic hypertension in pregnancy were studied by catheterization of the superior vena cava and by impedance cardiography before therapy was started. An initial hemorrheology and hemostaseologic protocol was prepared which included hematocrit, erythrocyte aggregation, erythrocyte deformability, plasma viscosity, colloid osmotic pressure, serum osmolality, uric acid, fibronectin, antithrombin III and fibrinogen. The hematocrit and the peripheral resistance were greater in preeclampsia than in essential hypertension. Moreover, preeclamptic patients showed a significantly lower cardiac output and central venous pressure than women with chronic hypertension. On the other hand, the plasma viscosity of women with essential hypertension increased, whereas patients with preeclampsia showed a lower erythrocyte deformability and a higher concentration of leukocytes. Finally, volume expansion with Hydroxyethyl-starch appears to be of therapeutic benefit for hypertensive patients with low cardiac output.
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PMID:[Hemodynamic and hemorheologic findings in patients with pregnancy-induced hypertension: comparison of pre-eclampsia and chronic hypertension]. 237 51

Plasma beta-thromboglobulin (beta TG) and platelet factor 4 (PF4) were significantly higher in a group of 116 hypertensive men than in a normotensive group of 142 men. They increased with the stage of hypertension but the level did not correlate with the age of the subjects. Platelet aggregation was similar in the two groups and positively correlated with the age of the subjects in the normotensive group but not in the hypertensive group. A strong positive correlation was observed between the levels of plasma beta TG and PF4 and between platelet aggregation to ADP and that to epinephrine in both the hypertensive and normotensive groups. However, there was no correlation between the level of plasma beta TG or PF4 and platelet aggregation. Plasma antithrombin III was lower in the hypertensive group than in the normotensive group. These studies suggest that plasma levels of beta TG and PF4 are closely related to the stage of hypertension and are better indicators than aggregation of in vivo platelet activation in hypertensive subjects. Enhanced platelet activation may be involved in the acceleration of hypertensive arteriovascular damage and atherosclerosis.
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PMID:Plasma concentrations of platelet-specific proteins in different stages of essential hypertension: interactions between platelet aggregation, blood lipids and age. 241 54

We studied parameters of hemostasis reported to be altered with "pure" preeclampsia in hypertensive disorders of pregnancy. Plasma fibronectin, antithrombin, and alpha-2 antiplasmin were measured in normal pregnancies (N = 26) and in pregnancies complicated by preeclampsia (N = 19), hypertension (N = 11), and chronic hypertension with superimposed preeclampsia (N = 11). Preeclampsia, both pure and superimposed, was associated with high fibronectin (P less than .001), low antithrombin III (P less than .001), and low alpha-2 antiplasmin (P less than .05) levels, suggesting endothelial injury, clotting, and fibrinolysis, respectively. Alpha-2 antiplasmin was increased with chronic hypertension (P less than .001), regardless of whether there was superimposed preeclampsia. Fibronectin appeared to be more closely linked with preeclampsia than antithrombin III or alpha-2 antiplasmin and may prove valuable in detecting preeclampsia when evaluating hypertension in pregnancy.
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PMID:Hemostasis in hypertensive disorders of pregnancy. 245 98

Vascular risk, mainly thromboembolitic risk, attributed to oral contraceptives (OCs) since 1962, has been primarily linked to ethinyl estradiol (EE). OCs which combine estrogen and have been associated with cerebral vascular accidents. A 1977 study showed a 40% increase of mortality due to cardiovascular complications in women taking OCs. There were of both an arterial and a venous character. The risk of myocardial infarction was 3 times more frequent among OC users. Deep venous thrombosis and pulmonary embolism were more numerous. Some other risk factors include smoking, hypertension, diabetes, and age 35. The risk of heart attack vanishes a few years after stopping OC use. The reduction of EE (and similarly progesterone) dosage from 100-50 mcg also lower the risk of hypertension, cerebral vascular accidents, and venous thrombosis. Prolonged use of OCs causes disorders of hemostasis affecting the walls of blood vessels, modifying the viscosity of blood flow (increase of hematocrits, reduction of venous tonus), modifying plasmatic coagulation (increase of platelets, increase of factors VII and X and plasma fibrinogen, and decrease of antithrombin III activity), and increased fibrinolysis. These anomalies are exclusively associated with high doses of estrogens. 5% of women using OCs develop moderate hypertension of 5-10 mm Hg of systolic pressure 5 years later, but after cessation it is reversed. OCs stimulate the renin-angiotensin-aldosterone system causing accelerated production of angiotensin II with the resultant forceful vasotension. 3 months after quitting OC use, high blood pressure returns to normal. EE can provoke diabetes; it increases very low density lipoprotein (VLDL) and high density lipoprotein (HDL) production, but total cholesterol is hardly affected. The androgenic property of progestogens reduces HDL. Combined OCs are contraindicated for women with hypertension, hyperlipidemia, diabetes, and a family history of vascular accidents.
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PMID:[Oral contraception and the vascular risk]. 251 20

We investigated the plasma levels of thrombin-antithrombin III complexes in women with uncomplicated pregnancy, patients with preeclampsia, gestational hypertension, and nonpregnant control subjects. In addition, we measured the coagulation inhibitors antithrombin III, protein C, and protein S. In normal pregnancy we observed a progressive increase in plasma thrombin-antithrombin III levels, and a decrease in protein S levels. In preeclampsia we observed increased thrombin-antithrombin III levels, reduced antithrombin III and protein C levels, and no further reduction of protein S compared with normal pregnancy. These new methods provide solid evidence for a prethrombotic state in normal pregnancy, especially in preeclampsia.
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PMID:Enhanced thrombin generation in normal and hypertensive pregnancy. 252 25

The arterial renal hypertension (170-180 mm Hg compared to the norm 100-120 mm Hg) developed in 2 months after one side nephrectomy and partial occlusion of the other renal artery. The level of high molecular weight plasma proteins was raised which led to the increase in the peripheral vessel resistance and hypertension degree. Fibrinolysis was depressed in the blood and in the cortical zone of the kidney. In early stages of hypertension fibrinolysis was sharply elevated, and high molecular weight compounds content was decreased. The antithrombin III and nonenzymatic fibrinolysis level were increased during the whole period (10-150 days).
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PMID:[Changes in the hemostasis and fibrinolysis system in rats with experimental renal hypertension]. 259 72

Preeclampsia, a major cause of fetal and maternal morbidity and mortality, may be difficult to distinguish clinically from other hypertensive disorders of pregnancy. Signs helpful in its diagnosis include presentation during late gestation in a nullipara with edema and proteinuria, and one or more of the following: hemoconcentration, hypoalbuminemia, liver function and/or coagulation abnormalities, and increased urate levels. Measures that may prove useful in differentiating preeclampsia from less dangerous forms of hypertension are decreased antithrombin III levels, increments in serum iron and carboxyhemoglobin, and decreases in urinary calcium. Major pathophysiological features of preeclampsia are decreased cardiac output, pulmonary capillary wedge pressure, and plasma volume; and marked increases in peripheral vascular resistance, as well as exaggerated pressor responses to endogenous angiotensin II and catecholamines. Renal hemodynamics decrease, in part as a result of a characteristic morphological lesion in glomeruli ("endotheliosis"), and there may be increased vascular permeability leading to albumin loss from the intravascular space. When gestation is advanced, termination is the treatment of choice; when temporization is required, several antihypertensive medications whose safety and efficacy have been tested in pregnant women are available. Magnesium sulfate remains the drug of choice for impending convulsions (the eclamptic phase of the disease). Finally, the etiology of preeclampsia remains unknown, but a popular theory suggests that alterations in prostaglandin metabolism may be responsible for the hypertension and coagulopathy in this disorder. In this respect, prophylactic treatment with low doses of aspirin, which decrease platelet thromboxane production but spare endothelial prostacyclin release, may decrease the incidence of preeclampsia in "high-risk" populations.
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PMID:Preeclampsia: pathophysiology, diagnosis, and management. 265 50


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