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Hypertension in pregnancy is one of the main causes of maternal, fetal and newborn morbidity and mortality in civilised countries. Current recommendations of the European Society for Hypertension prefer definition of hypertension in pregnancy based on absolute values of blood pressure, i.e. systolic blood pressure > or = 140 mm Hg or diastolic blood pressure > or = 90 mm Hg. The most important task of classification of hypertension in pregnancy is to distinguish whether hypertension comes before pregnancy (the so called pre-existing hypertension) or whether it is a pregnancy-induced condition (the so called gestational hypertension). Pre-existing hypertension is diagnosed either before pregnancy or within the first 20 weeks of pregnancy. Gestational hypertension is characterised with poor blood circulation in many body organs, higher value of blood pressure usually being just one of the characteristic features. Non-pharmacological treatment of hypertension must be considered in pregnant women with systolic blood pressure 140-150 mm Hg or diastolic blood pressure 90-99 mm Hg. Salt restriction is not recommended, as well as weight reduction in obese women. Systolic blood pressure > or = 170 mm Hg or diastolic blood pressure > or = 110 mm Hg in pregnant women must be considered serious condition necessitating hospitalisation. Pharmacological therapy should include labetalol i.v. or metyldopa or nifedipin administered orally. Intravenous administration of dihydralazine is no longer a therapy of choice, for its use is connected with increased occurrence of adverse effects. The threshold values for commencement of anti-hypertension therapy are systolic blood pressure 140 mm Hg or diastolic blood pressure 90 mm Hg in females with gestational hypertension without proteinuria or with pre-existing hypertension before commencement of 28th week of pregnancy. Drug administration to reduce hypertension is instituted after reaching the same threshold values in females with gestational hypertension and proteinuria or after occurrence of the symptoms any time during pregnancy, with the same threshold values of blood pressure in the case of pre-existing hypertension at the presence of accompanying diseases or organ malfunction and further in the case of pre-existing hypertension and gestational hypertension. In other cases drug treatment of hypertension is recommended at systolic blood pressure values of 150 mm Hg or diastolic blood pressure values of 95 mm Hg. Unless serious hypertension is involved, the drugs of choice include metyldope, labetalol, calcium channel blockers and beta-blockers. Calcium channel blockers are considered safe, unless administered concurrently with magnesium sulphate (risk of hypotension in the case of potential synergism). ACE inhibitors and angiotensine blockers II (AT1-blockers) are contraindicated in pregnancy. Treatment with diuretics is not substantiated, unless oliguria is present. I.v. magnesium sulphate is recommended for prevention of eclampsia and spasm treatment.
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PMID:[Hypertension in pregnancy]. 1672 58

Hypertensive disorders of pregnancy are the most common medical disorders of pregnancy and are associated with increased maternal and perinatal risks. The pathophysiology, diagnosis, and treatment are herein reviewed for chronic hypertension, preeclampsia, gestational hypertension, and severe hypertension. The benefits and risks of treating mild, moderate, and severe hypertension are discussed. A variety of oral and parenteral therapies are approved for the treatment of hypertension in pregnancy; methyldopa, labetalol, and nifedipine have been used safely in pregnancy, as has hydrochlorothiazide in those already taking this medication before conception. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are contraindicated in pregnancy because of adverse fetal effects, and atenolol should be avoided due to concerns with fetal growth. Severe hypertension >160/110 mmHg may require parenteral therapy, and treatment with intravenous labetalol now supplants the use of hydralazine. Women may remain hypertensive for a period postpartum and require treatment for a short interval. Early or severe preeclampsia warrants workup postpartum for secondary causes. Pregnancy induced hypertension or preeclampsia are emerging as risk factors for future cardiovascular risk.
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PMID:Hypertension in pregnancy. 1739 20

The National High Blood Pressure Education Program Working Group on High Blood Pressure in Pregnancy has defined four categories of hypertension in pregnancy: chronic hypertension, gestational hypertension, preeclampsia, and preeclampsia superimposed on chronic hypertension. A maternal blood pressure measurement of 140/90 mm Hg or greater on two occasions before 20 weeks of gestation indicates chronic hypertension. Pharmacologic treatment is needed to prevent maternal end-organ damage from severely elevated blood pressure (150 to 180/100 to 110 mm Hg); treatment of mild to moderate chronic hypertension does not improve neonatal outcomes or prevent superimposed preeclampsia. Gestational hypertension is a provisional diagnosis for women with new-onset, nonproteinuric hypertension after 20 weeks of gestation; many of these women are eventually diagnosed with preeclampsia or chronic hypertension. Preeclampsia is the development of new-onset hypertension with proteinuria after 20 weeks of gestation. Adverse pregnancy outcomes related to severe preeclampsia are caused primarily by the need for preterm delivery. HELLP (i.e., hemolysis, elevated liver enzymes, and low platelet count) syndrome is a form of severe preeclampsia with high rates of neonatal and maternal morbidity. Magnesium sulfate is the drug of choice to prevent and treat eclampsia. The use of magnesium sulfate for seizure prophylaxis in women with mild preeclampsia is controversial because of the low incidence of seizures in this population.
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PMID:Hypertensive disorders of pregnancy. 1864 16

Pregnancy-induced hypertension (PIH) is a life-threatening disorder for both mother and fetus; cardiac dysfunction is the major complication and can result in further deterioration. Recently, it has been recognized that aberrant activation of angiotensin type 1 receptor (AT1) signaling contributes to the pathogenesis of PIH, but the details of the relationship between cardiac injury and enhanced AT1 signaling in PIH are still unclear. We previously generated a transgenic mouse model of pregnancy-associated hypertension (PAH) via overproduction of angiotensin II, an endogenous ligand of AT1, in the maternal circulation during late pregnancy. In the present study, we administered olmesartan, an AT1 blocker, to suppress redundant AT1 signaling in PAH mice and evaluated the efficacy of this treatment in cardiac remodeling. Olmesartan treatment significantly lowered the blood pressure of PAH mice, and hypertrophy as well as increased plasma levels of cardiac injury markers were also markedly reduced. Histological analyses revealed that morphological abnormalities and fibrosis in the hearts of PAH mice recovered to the levels of normal pregnant wild-type mice after the administration of olmesartan. Moreover, in fibrotic regions of PAH hearts, olmesartan treatment significantly decreased the extent of cardiac injury and apoptosis. These results indicate that the activation of AT1 signaling pathways during maternal hypertension plays a critical role in cardiac remodeling in PAH mice, and suggest that treatment with an AT1 blocker could effectively ameliorate cardiac dysfunction during pregnancy with hypertension in vivo.
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PMID:Angiotensin type 1 receptor blockade prevents cardiac remodeling in mice with pregnancy-associated hypertension. 1913 6

Gestational hypertension is a recognized risk factor for the development of complications during pregnancy. The present study retrospectively assessed the respective values of blood pressure components derived from conventional and 24-h recordings (ABPM) as predictors of premature delivery in women with gestational hypertension based on office readings from 26th week of gestation onwards. Blood pressures were measured conventionally and over 24 h. Standard medical and obstetric history, and standard laboratory work-up were taken into account. The mean (+/- standard deviation, SD) age of 123 women was 29 +/- 6 years. Current pregnancy was, on average, the second. The conventional systolic (SBP)/diastolic (DBP) blood pressure averaged 140 +/- 19/92 +/- 14 mmHg, and pulse pressure (PP) and mean arterial pressure (MBP) averaged 48 +/- 10 and 108 +/- 15 mmHg. The corresponding values derived from ABPM were 135 +/- 16/90 +/- 11, 47 +/- 9 and 105 +/- 12 mmHg. The 24-h blood pressures had better prognostic value than the conventional blood pressures. The 24-h SBP predicted risk of premature delivery and was inversely related to the duration of pregnancy and birth weight. After the exclusion of 41 women with white-coat hypertension, the highest predictive value was associated with PP. PP wider by 1SD was associated with 66% higher risk of premature delivery, and was associated with shortening of pregnancy by 2 weeks and 400 g lower birth weight, even after adjustment for SBP. In conclusion, ABPM is superior to conventional blood pressure measurements in predicting adverse outcome of pregnancy. Twenty-four-hour PP, of all classic indices, seems to be most closely related to increase of that risk.
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PMID:Twenty-four-hour and conventional blood pressure components and risk of preterm delivery or neonatal complications in gestational hypertension. 1935 10

The most important task of classification of hypertension in pregnancy is to establish whether hypertension predates pregnancy (so-called pre-existing hypertension) or whether this is pregnancy-induced hypertension (so-called gestational hypertension). Pre-existing hypertension is diagnosed either before pregnancy or within 20 weeks of gestation. Gestational hypertension is characterized by poor perfusion of several organs, and the elevated blood pressure (BP) represents usually only one of the characteristic features. Non-pharmacological treatment of hypertension should be considered in pregnant females with systolic BP 140-150 mm Hg or diastolic BP 90-99 mm Hg. Salt restriction or weight reduction is not recommended. Systolic BP > or = 170 or diastolic BP > or = 110 mm Hg in a pregnant woman should be regarded as an emergency requiring hospitalization. Drug treatment with intravenous labetalol, or oral methyldopa or nifedipine should be considered. The thresholds at which to initiate antihypertensive therapy is systolic BP of 140 mm Hg or diastolic BP of 90 mm Hg in women with gestational hypertension without proteinuria or in those with pre-existing hypertension before 28 weeks' gestation. Drug treatment is to be initiated at the same threshold levels in females with gestational hypertension and proteinuria or those presenting with symptoms at any time during the pregnancy, those with pre-existing hypertension in the presence of associated conditions or organ damage and, also, those with pre-existing hypertension and superimposed gestational hypertension. In other cases, it is recommended to institute antihypertensive medication at systolic BP of 150 mm Hg or diastolic BP of 95 mm Hg. For non-severe hypertension, methyldopa, labetalol, calcium-channel blockers should be considered the drugs of choice. ACE inhibitors and angiotensin II antagonists (AT1-blockers) are contraindicated in pregnancy.
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PMID:[Hypertension in pregnancy]. 1963 40

Gestational hypertension, preeclampsia, and diabetes are all associated with increased risks of poor maternal and perinatal outcomes. Pregnant women with gestational diabetes have been shown in population studies to have increased risk of pregnancy-associated hypertension compared with nondiabetic women. Moreover, pregnant patients with hypertension are at increased risk for developing gestational diabetes mellitus. It has been hypothesized that this association could be due, at least in part, to insulin resistance. Although insulin resistance is a physiologic phenomenon in normal pregnancy, in predisposed individuals this could lead to hyperinsulinemia with the development of gestational hypertension, gestational diabetes mellitus, or both.
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PMID:Insulin resistance: the possible link between gestational diabetes mellitus and hypertensive disorders of pregnancy. 1964 Mar 43

Gestational hypertension and gestational diabetes mellitus are the most frequent obstetric disorders during pregnancy. The rates of both disorders are expected to increase as a result of delayed pregnancy at a later maternal age, the epidemic of obesity and the increased frequency of using assisted reproductive technology in women with infertility. Pregnancies complicated one or both of these disorders are also associated with adverse consequences for the mother and infant (both acute and long-term). The objectives of this review are to describe the association between gestational hypertension and gestational diabetes, and to discuss approaches to management and summarize long-term consequences of gestational hypertension.
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PMID:Hypertension in gestational diabetes mellitus: pathophysiology and long-term consequences. 2012 95

Pregnancy induced hypertension (PIH) is a major complication of pregnancy and is associated with high maternal and perinatal morbidity and mortality. The aim of this study was to investigate the possible causal association of PIH with maternal serum PAPP-A and urinary protein-creatinine ratio (UPCr) as well as to evaluate the usefulness of these two variables as predictive markers of PIH. A total 200 women of 8-16 weeks of pregnancy were enrolled in this study. All the patients were followed up till delivery for the development of pregnancy induced hypertension. Thirty patients were lost in the follow up, 3(1.76%) developed preeclampsia (PE) and 14(8.23%) gestational hypertension (GH). By a nested case-control design the 17 pregnancy induced hypertension cases were compared with 48 Controls with normal pregnancy outcome. Maternal serum PAPP-A was significantly lower in the pregnancy induced hypertension group compared to Control [mIU/ml, median (range) 1.8(0.70-4.1) vs. 5.45(2.7-10), p<0.001]. UPCr was significantly higher in the pregnancy induced hypertension group compared to Control (mg/mmol, mean+/-SD, 6.86+/-1.56 vs. 4.75+/-0.96, p<0.001). When tested as a predictive marker of pregnancy induced hypertension the sensitivity, specificity, positive predictive value (PPV) and negative predictive value (NPV) of maternal serum PAPP-A in the lowest 25th percentile were 82%, 95%, 87% and 93%. At 75th percentile the sensitivity, specificity, PPV and NPV of UPCr were 52%, 85%, 56% and 83% respectively.
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PMID:Early pregnancy maternal serum PAPP-A and urinary protein-creatinine ratio as predictive markers of pregnancy induced hypertension. 2039 25

Preterm birth is the major cause of perinatal mortality and morbidity. During the last decade, it has become an important issue in public health policies of developing countries. Gestational diabetes mellitus and Pregnancy induced hypertension are two important high-risk factors for preterm birth. The proposed study aimed to make a macroscopic analysis on the functional tissues (Parenchymal tissues) in preterm placenta in respect of Gestational diabetes mellitus (GDM) and pregnancy induced hypertension (PIH). The study was observational and cross sectional. The patients under this study were selected from the Obstetric ward of BSMMU and BIRDEM hospital, from June 2005 to October 2005. Sixty-six samples were collected from women during 28 weeks to 36 weeks of gestation. Among them, twenty-two samples were from gestational diabetic mothers, twenty-two were from pregnancy induced hypertensive mothers and twenty-two were from mothers who were non-diabetic and non-hypertensive in current pregnancy. Placentas were fixed and preserved in 10% formal saline solution. The volume proportions of parenchymal and non-parenchymal components were measured by using a point counting technique on formalin fixed placentas. In this study, the GDM group had significantly more absolute volume and mean proportional volume of the parenchyma but less mean proportional volume of the non-parenchyma when compared with Control and PIH group. However, the PIH group had significantly less absolute volume of the parenchyma than the control group and the mean value of the absolute volume of non parenchyma was also less than control value but did not reach a significant level. The results obtained from diseased and control groups demonstrated a significant change in some events, and some trends were also observed among these groups. However, it could be suggest that, in these two pregnancy-induced disorders, there is placental insufficiency where the placenta tries to exert its reserve capacity by changing its functional structures and consequently overcomes the possible damage to the fetus.
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PMID:Quantitative macroscopic study on preterm placenta in gestational diabetes mellitus and pregnancy induced hypertension. 2152 1


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