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

The home health population is more seriously ill now than in the past. Patients with an illness previously treated in the hospital are being cared for in the home. Pregnancy-induced hypertension is one such process that is being treated by home care nurses. The purpose of this article is to assist the home healthcare nurse in the assessment and management of the patient who has pregnancy-induced hypertension.
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PMID:Home care of the patient who has pregnancy-induced hypertension. 796 Aug 70

Pregnancy-induced hypertension is no uniform disease with one cause and one pathophysiologic course. On the contrary it seems to be a multifactorial event with a very different symptomatology and a variable damage of various organs. Because of the heterogeneity of the disease and the difficulty of differentiation these various kinds of courses clinical studies, mostly retrospectively done, have to be criticized. The aim of this study is to examine vasoactive regulation systems by means of a standardized animal model, using wistar rats. A systemic hypertension could be achieved only in pregnant animals with aid a infrarenal aortic stenosis. Non pregnant and simulated operated pregnant animals are the control group. In the normotensive pregnant rats there was an elevation of all renal prostanoids: PGI2, TxB2 and PGE2. On the contrary hypertensive pregnant rats showed a decrease of all eicosanoids, prononcigated of PGE2.
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PMID:[Value of prostaglandins in a pre-eclampsia-equivalent animal model]. 802 20

Doppler assessment of umbilical artery waveforms using the peak systolic to end diastolic (S/D) ratio was used to determine if complications associated with impaired trophoblastic invasion of placental bed (i.e. pregnancy induced hypertension and intrauterine growth retardation) could be predicted. Values for S/D ratio of at least 4, 3.5 and 3 at 22-26, 30-32 and > or = 37 weeks gestation, respectively, were found to be better predictors of such complications. Pregnancy-induced hypertension could be predicted in 63% and growth retardation in 60% cases at 22-26 weeks of gestation.
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PMID:Doppler waveform patterns of the umbilical artery--screening test for high risk pregnancies. 809 79

Pregnancy-induced hypertension (PIH) is a frequent cause of maternal and neonatal morbidity and mortality. In the present study we focused on the pathophysiology of PIH, mainly on the role of mineralocorticoids, reversed blood pressure patterns, and the resulting necessity of continuous monitoring of the preeclamptic mother. Problems of antihypertensive therapy are discussed and the first results of a pilot study with Urapidil are presented. To examine the role of mineralocorticoids in the pathophysiology of PIH, we studied plasma aldosterone and 18-hydroxy-corticosterone (18-OH-B) levels in 25 women with PIH and in 25 healthy pregnant women. Furthermore, we evaluated the mineralocorticoid receptor (MR) count in mononuclear leukocytes in the 2 groups. The MR-count was significantly decreased in the PIH-group. The values of plasma aldosterone and 18-OH-B were also low. These results cannot be explained by receptor down-regulation due to higher level of mineralocorticoids of the zona glomerulosa. Perhaps deoxycorticosterone or a hitherto unknown mineralocorticoid is responsible for the hypertension and altered MR-status. The first results of continuous blood pressure measurements with a noninvasive, real-time blood pressure monitor (Finapres) are presented. The comparison of the obtained values with intraarterial measurements demonstrates a good correlation between the two methods. We also report on the first experiences with Urapidil in the treatment of hypertension in severe preeclampsia. The data show that hypertension in preeclamptic women can be treated by Urapidil without side effects or reflex-tachycardia. Further studies will have to prove if Urapidil is suited for prepartal treatment of PIH as well.
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PMID:Hypertension in pregnancy. 838 33

Pregnancy-induced hypertension (PIH) is a heterogeneous disorder which complicates 5-7% of all pregnancies and remains a leading cause of maternal, fetal and neonatal morbidity and mortality. Severe preeclampsia is the most distinctive and life-threatening form; a multi-system disorder more common in first pregnancies, it is characterized by high blood pressure and proteinuria. In a series of Caucasian women with pregnancy-induced hypertension, we have observed a significant association of preeclampsia with a molecular variant of angiotensinogen, T235, found previously to be associated with essential hypertension. This finding is corroborated in a sample ascertained in Japan. Together, these observations support a new pathophysiological interpretation of preeclampsia and of its relation to some forms of essential hypertension.
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PMID:A molecular variant of angiotensinogen associated with preeclampsia. 851 28

Pregnancy induced hypertension remains the largest cause of maternal death in the UK. This is often related to inadequate or incorrect care. Recent randomised studies have enabled evidenced based clinical practice to be directed to the management of this condition. This allows a logical stepwise management structure to be developed in each hospital to make sure all women at risk get the best care available. This starts with comprehensive antenatal care with close collaboration between all professionals involved, early referral to an outpatient daycare unit if hypertension develops or is suspected, early use of antihypertensive therapy to control blood pressure once the diastolic is persistently above 100 mmHg, the use of magnesium sulphate to control convulsions, delivery on the best day in the best way and careful fluid management after delivery. Postnatal care should also contain risk assessment to allow directed counseling to the women concerning subsequent pregnancies.
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PMID:Care of the patient with severe pregnancy induced hypertension. 870 45

Gestational hypertension is associated with insulin-resistance; insulin and insulin-like growth factor-1 (IGF-1), acting through their receptors, play a role in the growth of the feto-placental unit. Since both receptors are exposed to the maternal circulation, it has been suggested that maternal metabolic abnormalities might affect placental insulin (HIR) and IGF-1 (IGF-1R) receptors. To clarify this issue, we characterized HIR and IGF-1R in placenta at term from normal women, normoinsulinaemic women with gestational hypertension (NGH), and hyperinsulinaemic women with gestational hypertension (HGH). Insulin binding was decreased in HGH women (B/T 0.12 +/- 0.03) compared to control and NGH women (B/T 0.18 +/- 0.07, p < 0.036; and 0.22 +/- 0.5, p < 0.009 respectively). Receptor affinity was lower in HGH women (ED50 0.95 +/- 0.32 nmol/l) than control and NGH women (ED50 0.42 +/- 0.19 nmol/l, p < 0.01; and 0.40 +/- 0.1 nmol/l, p < 0.007, respectively), whereas low-affinity Ex11+ isoform was higher in HGH women (Ex11+ 50 +/- 7, %) than in control and NGH women (Ex11+ 34 +/- 9%, p < 0.001; and 39 +/- 4%, p < 0.01, respectively). Increased expression of Ex11+ isoform was correlated with ED50 (r = 0.71; p < 0.002) and insulinaemia (r = 0.70, p < 0.002). IGF-I binding was increased in HGH women (B/T 0.17 +/- 0.03) compared to control and NGH women (B/T 0.09 +/- 0.05, p < 0.002; and 0.11 +/- 0.03, p < 0.002, respectively). IGF-IR affinity was similar in the three groups. The percentage of insulin/IGF-I hybrid receptors was increased in HGH women (85 +/- 3%) compared to control and NGH women (68 +/- 7%, p < 0.001; and 63 +/- 9%, p < 0.001, respectively), and was positively correlated with insulinaemia (r = 0.62, p < 0.018), ED50 of insulin binding (r = 0.62, p < 0.05), and maximal IGF-I binding (r = 0.69, p < 0.004); whereas it was inversely correlated with maximal insulin binding (r = -0.69, p < 0.004). Results provide the first evidence for altered expression of insulin/IGF-I hybrids found in insulin-resistance states.
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PMID:Increased expression of low-affinity insulin receptor isoform and insulin/insulin-like growth factor-I hybrid receptors in term placenta from insulin-resistant women with gestational hypertension. 885 18

Pregnancy is accompanied by a physiological activation of intravascular coagulation; however without disorder. Normal markers of coagulation are unchanged despite activation. Special coagulation parameter--such as Thrombin-Antithrombin-III-complex (TAT) or D-Dimer are increased also in normal pregnant women. Pregnancy induced hypertension (SIH) and preeklampsia may be associated with a disorder of coagulation that precedes the well known clinical manifestation of hypertension. Therefore it was the aim of the study to distinguish both the pregnancy induced hypertension (15 patients) and preeklampsia (10 patients) as far as it is possible by coagulation parameters such as thrombin generation (by TAT), fibrinolysis (by D-Dimer), AT-III, platelets and others comparing them with 25 normotensive pregnancies. In preeklampsia, the results showed that clinical signs were associated with simultaneous coagulation abnormalities. TAT and D-Dimere are significant increased whereas a decrease of AT-III and platelets was observed. There are no significant differences between SIH and normal pregnancies. Three days after delivery there was an increase of D-Dimer, AT-III and platelets and a decrease of TAT-complex in all groups. For risk pregnancy, the parameters TAT and D-Dimer may be useful as screening test. They although may support confirming the diagnosis of preeklampsia.
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PMID:[Pre- and postpartum hemostatic characteristics in pregnancy-related hypertension and pre-eclampsia in comparison with normotensive pregnancies]. 896 81

The association between nulliparity and gestational hypertension was examined by analysis of the 1988 National Maternal and Infant Health Survey. Gestational hypertension was defined as the occurrence of two consecutive diastolic blood pressure readings > or = 90 mm Hg after 20 completed weeks gestation in the absence of proteinuria in subjects normotensive prior to pregnancy. Preeclampsia was defined as gestational hypertension in the presence of significant proteinuria. Using logistic regression, 110 subjects with gestational hypertension and 34 subjects with preeclampsia were compared with 4371 subjects free of all hypertensive disorders. Nulliparity was weakly associated with an increase in the risk of gestational hypertension among whites (odds ratio, 95% confidence interval: 1.58 [0.92-2.74]) and not associated with risk among blacks (1.09 [0.51-2.35]). Preeclampsia was strongly associated with increased risk among whites (2.86 [0.94-8.73]) and blacks (2.94 [0.94-9.18]). The small increase in risk of gestational hypertension associated with nulliparity in contrast with the large increase in risk of preeclampsia suggests that these disorders may have a different etiology.
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PMID:The association between nulliparity and gestational hypertension. 925 98

Pregnancy-induced hypertension may be regarded as a manifestation of endothelial-cell dysfunction. The role of the eNOS gene in the development of a familial pregnancy-induced hypertension was evaluated by analysis of linkage among affected sisters and in multiplex families (n = 50). Markers from a 4-cM region encoding the eNOS gene showed distortion from the expected allele sharing among affected sisters (P = .001-.05), and the statistic obtained from the multilocus application of the affected-pedigree-member method also showed distortion (T[f(P)=sqrt(P)] = 3.53; P < .001). A LOD score of 3.36 was obtained for D7S505 when a best-fitting model derived from genetic epidemiological data was used, and LOD scores of 2.54-4.03 were obtained when various other genetic models were used. Estimates of recombination rate, rather than maximum LOD-score values, were affected by changes in the genetic parameters. The transmission-disequilibrium test, a model-free estimate of linkage, showed strongest association and linkage with a microsatellite within intron 13 of the eNOS gene (P = .005). These results support the localization of a familial pregnancy-induced hypertension-susceptibility locus in the region of chromosome 7q36 encoding the eNOS gene.
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PMID:Evidence for a familial pregnancy-induced hypertension locus in the eNOS-gene region. 931 40


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