Incidence Of Pregnancy-induced Hypertension Research Articles

Incidence of Pregnancy-Induced Hypertension Among Gestational Diabetics

Although hypertensive disorders of pregnancy are more likely to occur in pregestational diabetics, the question of whether they occur more frequently in gestational diabetics or certain subsets of gestational diabetics remains unclear. This study compared 197 gestational diabetics with 197 control patients matched on the basis of age, race, parity, and prepregnancy weight. No significant difference was found between the two groups in the incidence of either pregnancy-induced hypertension or preeclampsia. There was, however, a small but significant elevation in mean arterial blood pressure in the third trimester in gestational diabetics compared with control patients (90.1 versus 87.5 mm Hg; p = 0.006). Mean arterial pressures were also higher in diabetic patients on insulin compared with those on diet, and higher in diabetic patients diagnosed early (less than 24 weeks) compared with those diagnosed late (more than 24 weeks) in pregnancy; however, there were larger numbers of chronic hypertensives in these two groups. We conclude that gestational diabetics do not develop pregnancy-induced hypertension more frequently. Small increases in blood pressure late in pregnancy in these patients achieve statistical significance, but their clinical relevance is unclear.

Prevention of Pregnancy‐Induced Hypertension by Calcium Dietary Supplement: A Preliminary Report

The purpose of this study is to clarify whether the taking of a calcium dietary supplement is able to prevent the development of pregnancy-induced hypertension (PIH) in Japanese people. Forty-five nulliparous women (Ca-group) with various high-risk factors for PIH started to take a calcium supplement (1 g/day in the form of calcium salts) from the 12th gestational week (GW). Obstetrical outcome of Ca-group was compared to that of the nullipara (n = 453) who did not take a calcium supplement during pregnancy (Non-Ca Group) and that of the nullipara (n = 413) who did not develop PIH among Non-Ca group (normotensive group). The incidence of PIH in the Ca-group was 2.2%, compared to 8.8% of Non-Ca group. The decrease in blood pressure after taking calcium during the first half of the pregnancy was much greater in Ca-group than in the normotensive group. The urinary excretion of sodium and calcium and serum free calcium at the 28th GW were much lower in a woman with PIH, despite of the taking of a calcium supplement, than in the normotensive calcium group. Also, the parathyroid hormone level at the 28th GW was higher in the calcium-taking woman with PIH than in the normotensive calcium group. Our preliminary study suggests that among the possible effects of taking a calcium supplement are a decrease in blood pressure and the prevention of PIH in Japanese people, and that calcium metabolism might be related to the development of PIH. However, more study is needed before it will be possible to reach a final conclusion.

Relationship between lupus anticoagulant (LAC) and pregnancy-induced hypertension.

Lupus anticoagulant (LAC), a serum antiphospholipid autoantibody, is believed to be one of the causes of infertility or fetal loss. The purpose of the present study was to evaluate the role of LAC in the pathogenesis of hypertension during pregnancy. In this study, 20 pregnant women with hypertension were classified into two groups: 14 patients who did not have hypertension before the pregnancy but developed it during the pregnancy (pregnancy-induced hypertension; Group A) and 6 patients who had hypertensive or renal disease before the pregnancy, and developed further hypertension during the pregnancy (pregnancy-aggravated hypertension; Group B). A LAC coagulation assay was performed, and the presence of LAC in each group was compared. All 14 patients in group A were LAC-negative. In contrast, 3 of the 6 patients in group B were LAC-positive, and had clinical autoimmune diseases. The incidence of pregnancy-induced hypertension was also examined in 15 pregnancies from 9 LAC-positive women who had a history of repeated fetal loss but no systemic autoimmune disease (Group C). None of these 15 pregnancies had hypertensive complications, even when they reached term. In the placentas of LAC-positive women, no characteristic changes other than fibrinoid degeneration and microscopic infarction were observed upon histological examination. These results suggest that LAC does not relate with the onset of hypertension during pregnancy.

Association of pregnancy-induced hypertension with duration of sexual cohabitation before conception

Summary Pregnancy-induced hypertension affects at least 10% of all pregnancies. An association with first pregnancy or a change in paternity for subsequent pregnancies has been suggested. We studied the duration of sexual cohabitation with the father prior to conception and the incidence of pregnancy-induced hypertension. During a five-month period, 1011 consecutive women who delivered in an obstetric unit were interviewed about paternity and duration of sexual cohabitation before conception. Obstetric charts were abstracted to identify three groups: those with pregnancy-induced hypertension, chronic hypertension, and normal blood pressure. The incidence of pregnancy-induced hypertension was 11·9% among primigravidae, 4·7% among same-paternity multigravidae, and 24·0% among new-paternity multigravidae. For both primigravidae and multigravidae, length of sexual cohabitation before conception was inversely related to the incidence of pregnancy-induced hypertension (p<0·0001). Similar results were observed after control for race, education, maternal age, marital status, and number of pregnancies. Pregnancy-induced hypertension may be a problem of primipaternity rather than primigravidity. Furthermore, an extended duration of sexual cohabitation before conception may protect against pregnancy-induced hypertension.

Prevention of Pregnancy‐Induced Hypertension in Twins by Early Administration of Low‐Dose Aspirin: A Preliminary Report

Effectiveness of early administered low-dose aspirin in prevention of pregnancy-induced hypertension (PIH) and fetal growth retardation in twin pregnancies was investigated in a randomized placebo controlled, double-blind trial in 47 twin pregnancies. Twenty-four women received 100 mg of aspirin daily from mean gestational age of 17.7 wk, and 23 women ingested placebo from a mean gestational age of 18 wk until delivery. The placebo and aspirin group were similar in age, weight gain, zygosity, gravidity, parity, and obstetrical antecedents. Treatment lasted for a mean period of 16.8 wk and 18.3 wk in the placebo and aspirin groups, respectively. The mean gestational age at birth was 35.0 wk and 36.4 wk in the placebo and aspirin groups, respectively. PIH was noted in six women (26%) in the placebo group, but in only one woman (4%) in the aspirin treated patients (P < .05). The mean combined fetal weights of both twins, and the mean weight of the second twin at delivery were significantly higher in the aspirin treated mothers than in the placebo treated gravidas (mean difference of 781 g, P < .02 and mean difference of 488 g, P < .005, respectively). Intrauterine growth retardation (< 10th percentile) concerned 11 (24%) and six (13%) fetuses in the placebo and aspirin groups, respectively. No adverse effects of treatment to either the mothers or the infants were noted. Low-dose aspirin reduces the incidence of PIH and has a beneficial effect on fetal growth in twin pregnancies. Additional clinical trials are needed in order to define and select subgroups of twins where aspirin treatment is recommended.

Sodium transport inhibitors in pregnancy-induced hypertension

In blacks and whites of similar socioeconomic background, the incidence of pregnancy-induced hypertension (PIH) is probably the same. In underdeveloped countries, however. PIH is often a life-threatening complication of pregnancy. Recent theories as to the etiology of PIH include the suggestion that vascular tone may be increased as a result of inhibition of active sodium transport in vascular smooth muscle. This may be the result of an inhibitor of sodium transport present in the serum. The literature concerning the demonstration of endogenous sodium transport inhibitors and endogenous digoxinlike immunoreactivity (EDLI) in PIH is reviewed and discussed.

The Association of Pregnancy-Induced Hypertension and Uterine Malformations

To evaluate the incidence of pregnancy-induced hypertension (PIH) in women with congenital uterine malformations, we examined the pregnancy complications of 67 women with uterine anomalies demonstrated by hysterosalpingography (HSG). The study group was compared with a control group of 130 women with normal-shaped uterus proven by HSG-matched for age, parity and presenting complaint. A significantly increased (p less than 0.04) rate of PIH was found for women with uterine malformation as well as a 2-fold higher frequency of preeclampsia. The etiology for this association is unknown, however; it is suggested that uterine malformation is a predisposing condition to PIH.

Biochemical changes associated with blood pressure reduction induced by calcium supplementation during pregnancy

In a study population that comprised 34 normal black pregnant women, biochemical changes are compared between a group of women who received 1.5 gm of calcium supplementation a day and a group of women who received placebos. The blood pressure-lowering effect of calcium supplementation appears to involve a mechanism that relates parathyroid hormone and plasma renin activity. Other alterations in calcium and magnesium metabolism, as reflected by increased urinary calcium excretion and serum magnesium levels, may also contribute to this effect. Subgroups of study participants with initial (less than 26 weeks' gestation) low levels of serum calcium and plasma renin activity are the ones with the largest reductions in blood pressure. Whether these alterations can produce a reduction in the incidence of pregnancy-induced hypertension is the next question to be answered in this area.

Response of skin thickness and metacarpal index to estradiol therapy in postmenopausal women

Fifty-two healthy pregnant women were enrolled in a double-blind, randomized, controlled clinical trial. After the 26th week of gestation, the women were given either 1.5 g of elemental calcium per day or a placebo. Subjects in the calcium group, after adjustment for race and initial blood pressure (BP), had a term mean systolic and diastolic BP value of 4-5 mmHg lower than those in the placebo group (P less than .05). The incidence of pregnancy-induced hypertension was 11.1% in the placebo group and 4.0% in the calcium group, a nonsignificant difference. Combining these values with previous data, we found a dose-effect relationship between calcium intake and BP reduction during the third trimester of pregnancy. Further research should be directed at understanding the mechanism of this effect and trying to demonstrate a reduction in pregnancy-induced hypertension with calcium supplementation in a larger population.

The relationship between calcium intake and pregnancy-induced hypertension: Up-to-date evidence

In 1980 we pointed to a relationship between calcium intake and pregnancy-induced hypertension. The original epidemiologic observations showed an inverse association between calcium intake and incidence of eclampsia after adjusting by several confounding factors. A series of recent randomized clinical trials have demonstrated a reduction in blood pressure with calcium supplementation in animals, in healthy and mildly hypertensive subjects, and in pregnant women. It is hypothesized that parathyroid hormone plays a role since it is affected by calcium intake and can partially regulate the concentration of free cytosolic ionized calcium, thus triggering smooth muscle contraction. Randomized clinical trials showing a reduction in the incidence of pregnancy-induced hypertension with calcium supplementation have not as yet been published. However, preliminary observations appear to support this hypothsis.

Effect of low-dose aspirin on angiotensin II pressor response in human pregnancy

Recent clinical studies have reported a significant reduction in the incidence of pregnancy-induced hypertension after the ingestion of low-dose aspirin. The effect of 80 mg of acetylsalicylic acid on vascular sensitivity to exogenous angiotensin II (Hypertensin, Ciba-Geigy Limited, Basel, Switzerland) was examined in 13 normotensive pregnant patients. The effective pressor dose before treatment (17.4 ± 2.2 ng/kg/min) (mean ± SE) was significantly less (p < 0.001) than that after treatment (35.1 ± 4.2 ng/kg/min). Low-dose aspirin therapy resulted in an enhancement of the pregnancy-acquired refractoriness to angiotensin II. It can be speculated that prostglandin synthetase inhibitors at a low dose may alter the thromboxane A2/prostacyclin ratio in favor of the latter.

The relationship between abortion in the first pregnancy and development of pregnancy-induced hypertension in the subsequent pregnancy

The relation between pregnancy-induced hypertension and reproductive history was assessed in 29,484 women receiving obstetric care at Parkland Memorial Hospital. The incidence of pregnancy-induced hypertension was 25.4% in primigravid women, somewhat lower (22.3%) in women whose only previous pregnancy terminated in abortion, and much lower (10%) in women who carried two or more successive pregnancies to viability.

Effect of calcium supplementation on the vascular sensitivity to angiotensin II in pregnant women

Pregnant woment destined to develop pregnancy-induced hypertension lose refractoriness to the pressor effects of infused angiotensin II. The effect of calcium supplementation on the vascular sensitivity to angiotensin II was investigated in pregnant women. We administered orally 600 mg of calcium l-aspartate daily to 22 pregnant women from 20 weeks of gestation to delivery. The values for the effective pressor dose of angiotensin II in the calcium-supplemented women were compared with those in 72 nonsupplemented pregnant women. The vascular sensitivity was significantly decreased after calcium supplementation. The values for the effective pressor dose of angiotensin II in the calcium-supplemented patients were 18.1 ± 1.2 ng/kg/min at 20 weeks of gestation, 32.2 ± 2.6 ng/kg/min at the twenty-sixth week, 41.1 ± 3.4 ng/kg/min at the thirtieth week, and 25.9 ± 2.9 ng/kg/min at the thirty-sixth week (mean ± SEM), while those in the nonsupplemented patients were 17.3 ± 1.2, 17.7 ± 1.6, 17.6 ± 1.2, and 15.0 ± 1.6 ng/kg/min, respectively. Assessment of the changes in the effective pressor dose of angiotensin II in the individual patients indicated that the percentile changes from 20 weeks of gestation in the calcium-supplemented patients were also significantly greater than those in 22 nonsupplemented patients. These findings suggest that calcium supplementation tends to reduce the vascular sensitivity in pregnancy. The present dosage of calcium did not affect the blood chemical parameters and did not reduce the blood pressure. The incidence of pregnancy-induced hypertension in the calcium-supplemented patients was 4.5%, which was smaller than that (21.2%) in the nonsupplemented patients. Although there is no clear explanation of the mechanisms involved in such an effect of calcium, the present results do provide evidence to support the idea that oral calcium intake can prevent the onset of pregnancy-induced hypertension.

Zinc supplementation during pregnancy: effects on selected blood constituents and on progress and outcome of pregnancy in low-income women of Mexican descent

The effects of zinc supplementation on levels of various blood constituents and the outcome of pregnancy in 213 Hispanic women attending a prenatal clinic in Los Angeles was assessed in this double-blind study. The women were randomized into either a control (C) or a zinc-supplemented (Z) group and received similar vitamin and mineral supplements except that 20 mg zinc was added to the Z group's capsules. At the final interview, women (C + Z) with low serum Zn levels (≤ 53 μg/dl) had higher (p < 0.01) mean ribonuclease activity and lower (p < 0.01) mean δ-aminolevulinic acid dehydratase activity than women with acceptable serum zinc levels. The incidence of pregnancy-induced hypertension was higher (p < 0.003) in the C than in the Z group, but pregnancy-induced hypertension was not associated with low serum zinc levels at either the initial or final interview. The expected increase in serum copper levels was greater (p < 0.001) in women with pregnancy-induced hypertension (C + Z) than in normotensives. Except for pregnancy-induced hypertension, there was a higher incidence of abnormal outcomes of pregnancy in the noncompliers than in the compilers (C + Z).

The incidence of pregnancy-induced hypertension is increased among Colorado residents at high altitude

Both pregnancy-induced hypertension and high-altitude residence are associated with fetal growth retardation, thereby leading us to hypothesize that pregnancy-induced hypertension would be more common at high than at low altitude. Retrospectively collected data in Colorado revealed that pregnancy-induced hypertension was more common at 3,100 m (12%) than at 2,410 m (4%) or 1,600 m (3%) (P < 0.001). Proteinuria and edema in the upper extremities were also more frequent at 3,100 m than at 1,600 m (proteinuria = 28% versus 9%, P < 0.001; edema of upper extremities = 22% versus 13%, P < 0.01). Blood pressure during pregnancy increased with altitude among all women and those without pregnancy-induced hypertension (analysis of variance, P < 0.05). In a prospective study at 3,100 m, women with pregnancy-induced hypertension had no change in blood pressure during pregnancy prior to the onset of hypertension (analysis of variance, P = NS), whereas blood pressure decreased in the normal women (analysis of variance, P < 0.05). Arterial oxygen saturation during the third trimester was inversely related to the degree of hypertension in women with pregnancy-induced hypertension at 3,100 m (r = 0.8, P < 0.05), thus suggesting that maternal hypoxia may play a previously unsuspected role in the etiology of pregnancy-induced hypertension.

Enhanced prediction of pregnancy-induced hypertension by combining supine pressor test with mean arterial pressure of middle trimester

Both the impact of the mean arterial pressure of the second trimester (MAP-2) on the development of pregnancy-induced hypertension (PIH) and the accuracy of the supine pressor test (SPT) for the prediction of PIH have been demonstrated. Despite good over-all predictability of the SPT, a large percentage of false positive SPT's have been reported, ranging from 6 to 60 per cent with an average of 34 per cent. In an effort to reduce the incidence of false positive SPT's and provide a more accurate method for identifying those primigravidas at risk for PIH, weekly or biweekly SPT's were performed. There were 251 SPT's performed on 97 primigravidas between 28 and 32 weeks' gestation. Along with the performance of serial SPT's, each subject's MAP-2 was calculated. Those primigravidas with an MAP-2 greater than 85 mm. Hg or two or more positive SPT's had a greater incidence of PIH (45 and 46 per cent, respectively). Of greater significance, those women who exhibited both an MAP-2 greater than 85 mm. Hg and two or more positive SPT's had an 88 per cent chance of developing PIH. These results were highly significant (chi square = 9.7, p < 0.005).