Corticosteroid binding globulin (CBG) concentrations in maternal plasma have been measured throughout pregnancy in a series of 100 singleton pregnancies in 89 normotensive women. Plasma CBG concentrations were monitored also in 10 women with essential or renovascular hypertension. Plasma albumin, cortisol and oestriol were measured concurrently. Plasma CBG increased two and a half to three times during pregnancy. In those women who developed hypertension in pregnancy (mean arterial pressure greater than 107 mmHg), the plasma CBG concentrations were significantly lower than in those who remained normotensive. In women who developed hypertension, the CBG either failed to increase at the same rate as in normal pregnancies or the level fell before the appearance of hypertension. The earlier the onset of hypertension, the greater the decline in CBG. In all subjects, the CBG concentration at 34-36 weeks gestation was directly related to the birthweight of the infant. Plasma cortisol levels were depressed in hypertension relative to that in the normotensive women. Whilst plasma albumin levels decreased at least 30% in most women during pregnancy, the fall tended to be less in hypertensive women, but there was marked overlap between patient groups. Plasma oestriol concentrations were depressed only in the very severely affected cases. It is suggested the CBG concentration is a further reflection of the metabolic abnormalities associated with hypertension in pregnancy, and that it can be used as a marker to identify and monitor those patients at risk.
Hypertensive disorders are important causes of premature delivery, IUGR and intra uterine fetal death. It accounts for 15% to 20% of maternal deaths in developing as well as developed nations. An association of serum uric acid with hypertensive disorders of pregnancy. The main objective of the present study was measuring and evaluating serum uric acid values in normal pregnant and preeclamptic and eclamptic cases to see the trend in the rise of serum uric acid in toxemic cases. Therefore we planned this study. The present study was conducted on Control (15 Normal non pregnant healthy women) and 140 cases they were further sub divided as, 60 Normal pregnant women in different trimesters, 60-Preeclampticcases, 20-Eclampticcases. Then Preeclampsia was divided into3groups (Mild preeclampsia-BP at least 140/90 mmHg. Moderate preeclampsia-BP more than 140/90 but <160/110mmHg. Severe preeclampsia-BP>160/110 mmHg but without convulsions). Estimation of serum uric acid was done at Department of Biochemistry, Rajendra Institute of Medical Sciences, Ranchi, Jharkhand during June 2008 to Sept.2009. The cases were selected from outdoor, indoor and emergency of department of Obstetrics and Gynecology, RIMS, Ranchi. The serum value of uric acid was studied in 60 preeclamptic cases and 20 cases of eclampsia.. The mean ± S.D. values of serum uric acid in normal non pregnant cases was 3.68±0.66, in normal pregnant cases in 1 st trimester was 3.60±0.78, normal pregnant cases in 2 nd trimester was 3.40±0.33, normal pregnant cases in 3 rd trimester was 4.64±0.70. in preeclamptic patients, the mean was 6.70±0.78 and in eclamptic patients it was 7.52±0.95. on doing analysis of this it shows significant changing patterns in serum uric acid level between normal non-pregnant cases and normal pregnant cases in the 3 rd trimester. Also there is a good significance between normal cases in 3 rd trimester and preeclamptic cases as a whole. The above study undertaken shows a definite rise in serum uric acid level in diseased subjects as early as first and early second trimester, although difference rise in serum uric acid in mild cases when compared to normal cases was not statistically significant. But, it can be concluded that serum uric acid measurement is one of the best markers of the diagnosis as well as severity of preeclampsia and will be a useful index for the management of the same.
1. Circadian patterns of blood pressure and pressor hormones were studied in late pregnancy in ten normotensive women and twenty-one hypertensives. 2. Plasma renin activity, angiotensin II and free adrenaline and noradrenaline leves were highest at 0900 h in normotensives and uncomplicated hypertensives. Catecholamine sulphate levels were lowest at 0900 h. 3. In eight pre-eclamptic hypertensives, plasma renin activity, and angiotensin II were suppressed. 4. Adrenaline sulphate levels were raised in hypertensives. 5. Four pre-eclamptics with noctural hypertension had the highest blood pressures; their diurnal rhythm for noradrenaline sulphate was reversed but they showed no consistent pattern of pressor hormones. However failure of angiotensin II, adrenaline or noradrenaline to fall at night in subjects with increased vascular reactivity could contribute to their nocturnal hypertension.
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