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

At present, magnesium treatment is employed routinely in the treatment of hypertension induced by pregnancy (PIH) and preeclampsia in USA with the object of preventing seizures. In USA the treatment of election consists of intravenous infusion of large doses of magnesium sulphate in order to obtain a therapeutic concentration. The anticonvulsive mode of action of magnesium is only partially understood. Magnesium is presumed to block the neuromuscular transmission but a central effect cannot be excluded. Treatment with magnesium has, in addition, an antihypertensive effect. The effect of magnesium on the blood pressure is probably a direct vasodilatory effect which explains the ability of magnesium to reduce the maternal blood pressure. Probably the same mode of action is responsible for the relaxing effect of magnesium on the vascular tone in the umbilical and placental vessels. This can probably explain the favourable effect of magnesium on the birth weight. Even if magnesium treatment implies a potential risk for neonatal hypermagnesemia and hypocalcaemia, only few side effects have been reported.
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PMID:[Magnesium therapy in pregnancy-induced hypertension and pre-eclampsia]. 846 49

This review on hypertension in pregnancy focuses mainly on the pathophysiology and prevention of pregnancy induced hypertension which, when associated with proteinuria, is usually called preeclampsia. Rather than a genuine hypertensive disease, preeclampsia is mainly a systemic endothelial disease causing activation of platelets and diffuse ischemic disorders whose most obvious clinical manifestations involve the kidney (hence the proteinuria, edema and hyperuricemia), the liver (hence the hemolytic elevated liver enzymes and low platelets, or HELLP syndrome), and the brain (hence eclamptic convulsions). Hypertension is explained by increased vascular reactivity rather than by an imbalance between vasoconstrictive and vasodilating circulating hormones. This increased reactivity is due to endothelial dysfunction with imbalance between prostacyclin and thromboxane A2 and possibly dysfunction of NO and endothelin synthesis. The aggressive substances for endothelium are thought to be of placentar origin and the cause of their release is explained by placentar ischemia related to a defect of trophoblastic invasion of the spiral arteries. The etiology of this latter defect is unknown but involves immunologic mechanisms with genetic predisposition. The only effective treatment for PIH is extraction of the baby with the whole placenta. The decision for extraction is often a very delicate obstetric problem. Antihypertensive drugs are mainly indicated in severe hypertension (> 160-100 mm Hg), with the aim of preventing cerebral hemorrhage in the mother, but have not been shown to improve fetal morbidity or mortality. Eclamptic seizures can be prevented and treated more effectively with magnesium sulfate than with diazepam or phenytoin. Prevention of preeclampsia remains the main challenge. Whereas antihypertensive drugs are ineffective, calcium supplementation and low dose aspirin have proven effective but mainly in selected populations with a relatively high incidence of preeclampsia (> 8-10%). In multiparas the selection of such a high risk population is relatively easy when at least 2 (or 1?) previous pregnancies were complicated with early preeclampsia and/or intrauterine growth retardation. In nulliparas the selection of the high-risk population is still a subject of research. The 2 most promising criteria are abnormal Doppler velocimetry of the uterine arteries at around 20 weeks of amenorrhea, and abnormally high plasma levels of beta HCG at 17 weeks of amenorrhea.
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PMID:[Hypertension and pregnancy. Diagnosis, physiopathology and treatment]. 853 76

The tests have been carried out on 64 women in 3rd trimester of pregnancy. 30 of them were the women with a normal course of pregnancy, and 34 were the ones with hypertension induced pregnancy (PIH). Their blood serum has been tested for the concentration of TG, phospholipids, total cholesterol, HDL- and LDL-cholesterol, alpha, beta and pre-beta lipoprotein fractions. The results have been calculated statistically. It has been found that the increase in the concentration of TG (p < 0.001), phospholipids (p < 0.02), total cholesterol (p < 0.01), the beta lipoprotein fraction (p < 0.001) was essentially higher in the women with PIH, in 3rd trimester of pregnancy, in comparison to those values observed in the healthy pregnant women. At the same time a lower concentration of alpha lipoproteins (p < 0.01) has been observed in the group of the pregnant with pregnancy induced hypertension.
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PMID:[Concentration of lipids and lipoproteins in serum of women with pregnancy induced hypertension]. 857 78

Multifetal pregnancy reduction (MFPR) appears to be an efficacious method for improving the perinatal outcome of 'high order' multifetal gestations. The present study was undertaken to evaluate pregnancy outcomes after MFPR to twins in comparison with spontaneously conceived twins. In all, 10 patients with quadruplet gestation (group 1) and 30 patients with triplet gestation (group 2), who underwent MFPR to twins, were prospectively enrolled. Pregnancy complications, gestational age at delivery, mode of delivery and birthweights were compared with 30 consecutive spontaneous twin gestations (group 3) matched by maternal age and parity. Mean gestational age at delivery and mean birthweights were significantly lower in group 1, compared with groups 2 and 3 (33.2, 35.9, 36.9 weeks, and 1843, 2209, 2361 g respectively). The incidence of pregnancy complications was significantly higher in group 1 compared with group 3. There was also a clear trend of increased incidence of specific pregnancy complications in group 1 compared with groups 2 and 3, especially premature contractions (PMC; 50, 27 and 13% respectively), and pregnancy-induced hypertension (PIH; 40, 23 and 7% respectively). In conclusion, the initial number of fetuses before reduction was inversely correlated with gestational age at delivery and birthweight, and positively correlated with pregnancy complications. Contrary to previous studies, we found a higher incidence of pregnancy complications after MFPR compared with spontaneous twins, especially PMC and PIH.
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PMID:Pregnancy outcome after multifetal pregnancy reduction to twins compared with spontaneously conceived twins. 867 50

This study was undertaken to determine the coagulation profile of women with pregnancy induced hypertension and to evaluate the changes in the level of AT-III in pre-eclampsia and eclampsia and its correlation with severity of disease in order to evaluate if it can be used as a marker for severity of PIH. 119 women with PIH in the third trimester of pregnancy constituted the study group. Age and parity matched 25 normal pregnant and 25 non-pregnant women were taken as control group. No significant difference between the coagulation profile of non-pregnant and normal pregnant women was seen. There is evidence of consumption coagulopathy in PIH patients and AT-III activity shows a gradual and almost linear reduction in various groups ranging from normal pregnant women to eclampsia. Reduction in AT-III activity has positive correlation with PIH and it can be a useful marker for severity of PIH.
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PMID:Pregnancy induced hypertension and antithrombin-III. 881 56

The purpose of the present study was to examine the relationship between severe pre-eclampsia/eclampsia (toxaemia) and obesity. We collected sociodemographic, anthropometric, medical and pregnancy outcome data from the hospital records of 248 Israeli women diagnosed with either pregnancy-induced or chronic hypertension, and compared these data to a control group of 236 women. Univariate analysis showed that while there exists a statistically significant positive association between obesity and hypertension (both pregnancy-induced and chronic) obesity presents no added risk to the development of toxaemia. Furthermore, we found a significant decrease in the rate of obesity among primigravid versus multigravid mothers with toxaemia superimposed on pregnancy-induced hypertension. On the other hand, primigravid mothers with PIH were at an increased risk of developing toxaemia as compared to multigravid women. These results suggest that obesity is not a significant factor in the development of toxaemia.
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PMID:Obesity and the risk of toxaemia of pregnancy. 888 43

Pulsed Doppler ultrasonography was used to asses the pulsatility index (PI) on flow velocity waveforms in uterine, umbilical and fetal middle cerebral arteries from a total of 659 pregnancies and the standard curves of each PI in relation with the gestational age were obtained from a total of 472 normal pregnancies. Cordocentesis was performed on 20 patients (centesis group) of PIH (pregnancy-induced hypertension) complicated with intrauterine growth retardation (IUGR) and fetal blood from the umbilical vein was sampled for blood gas analysis. Fetuses in the centesis group were acidemic (pH < 7.25) in 10 cases (50%), hypercapnemic (pCO2 > or = 50 mmHg) in 8 cases (40%), and hypoxemic (pO2 < 20 mmHg) in 6 cases (30%). In 13 cases (65%) in the centesis group, PI of the uterine artery (UTPI) was higher than +1.5 SD (standard division) of the standard curve (high UTPI), in 9 cases (45%) PI of the umbilical artery (UAPI) was higher than +1.5 SD of the standard curve (high UAPI), and in 10 cases (50%) PI of the middle cerebral artery (MCAPI) was lower than -1.5 SD of the standard curve (low MCAPI). All acidemic fetuses (100%) had high UTPI, 9 (90%) had high UAPI, and 8 (80%) had low MCAPI. All hypercapnemic fetuses had high UTPI, high UAPI and low MCAPI. All hypoxemic fetuses had high UTPI, high UAPI and low MCAPI. In the centesis group, the sensitivity, specificity, positive predictive value and negative predictive value of high UTPI to fetal acidosis was 100%, 70%, 76.9% and 100%, respectively. The sensitivity and the specificity of high UAPI and low MCAPI to fetal acidosis was 80% and 100%, respectively. The positive predictive value was 100% and negative predictive value was 83.3%. From this study, we conclude that measurement of uterine and fetal blood flow waveforms by pulsed Doppler ultrasonography is useful to assess fetal well-being in IUGR caused by hypertension during pregnancy.
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PMID:[The standard curves of pulsatility index from uterine and fetal blood flow, and their efficacy in clinical management of intrauterine growth retardation. A comparison with fetal blood gas analysis]. 893 19

Serum uric acid estimation was done in forty primigravidae with pregnancy induced hypertension and twenty normotensive primigravida in the third trimester of pregnancy, at delivery and six weeks postpartum. The mean serum uric acid levels in normotensive women in the antenatal period and at delivery were 4.65 +/- 0.33 and 4.88 +/- 0.23 mg% and in mild PIH were 5.42 +/- 0.55, 6.14 +/- 0.76 mg%, respectively. Level of serum uric acid in mild PIH was significantly higher than normotensive women (P). In severe PIH, the mean serum uric acid levels were 6.65 +/- 0.60, 8.24 +/- 1.09 mg% in antepartum and at delivery respectively which was significantly more than control group and mild PIH group women (P). However, no differences was observed, in the serum uric levels between these groups during the postpartum period. Serum uric acid level of 5.5 mg or more was observed to be an indicator of PIH. Levels of serum uric acid did show a high positive correlation with the severity of PIH in relation to hypertension and proteinuria. Hyper uricemia (more than 5.5 mg% is associated with increased perinatal morbidity and mortality.
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PMID:Hyperuricemia and pregnancy induced hypertension--reappraisal. 897 21

This paper discusses the spectrum of pregnancy-induced hypertension and presents a theory for its etiology. Endothelial injury is the purported precursor to pregnancy-induced hypertensive disorders, and this discussion expands on a possible mechanism by which injury could occur as a result of incomplete trophoblastic invasion. We review endothelin physiology and compare and contrast the evidence surrounding endothelin 1 as a putative mediator of PIH. An approach to treatment utilizing antagonists to the endothelin 1 receptor is introduced.
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PMID:Pregnancy-induced hypertension: genesis of and response to endothelial injury and the role of endothelin 1. 940 27

Mounting evidence clearly indicates an immunologic basis for PIH, parity being the most convincing factor. Genetic susceptibility, physiologic change, and environmental influence may also modulate an individual's risk of developing PIH. Pathologic and follow-up studies further suggests further suggest that currently diagnosed PIH may actually be a heterogeneous entity comprising several disorders of different etiologies (150), such as chronic renal disease, borderline chronic hypertension, genetic susceptibility to hypertension, and genuine PIH. For many diseases, etiologic research and clinical management often go hand in hand. Unfortunately, in the case of PIH, etiologic research may have followed clinical steps too closely and have been misled. For clinical management, genuine preeclampsia and preeclampsia superimposed on chronic hypertension are treated as virtually the same: The ultimate goal is to prevent eclampsia. Because a sizable portion of PIH is probably due to chronic renal disease or latent chronic hypertension (33), and late-onset gestational hypertension is of less concern than preeclampsia, one could argue that it may not be clinically important to separate the subtypes of PIH. In etiologic research, however, by focusing on a heterogeneous outcome we have confused ourselves and hampered our progress. On the other hand, one should also realize that currently available techniques are unlikely to substantially improve our proficiency in differential diagnosis. Besides renal biopsy, which is impractical, especially in epidemiologic research, there are virtually no measures available that can distinguish genuine PIH from hypertension due to latent renal disorder, chronic hypertension, or genetic susceptibility. Until noninvasive measures with acceptable-sensitivity and specificity are available for differential diagnosis, frustration in etiologic research on PIH is likely to continue. One clue that may potentially advance our knowledge of the pathogenesis and future prevention of PIH is the finding that smoking reduces risk of PIH. Epidemiologists should transfer this knowledge to laboratory scientists.
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PMID:Epidemiology of pregnancy-induced hypertension. 949 84


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