Jd. Lalau et al., CALCIUM-METABOLISM, PLASMA PARATHYROID-HORMONE, AND CALCITRIOL IN TRANSIENT HYPERTENSION OF PREGNANCY, American journal of hypertension, 6(6), 1993, pp. 522-527
In order to know if abnormalities of calcium metabolism may be involve
d in the pathophysiology of pregnancy-induced hypertension (PIH), as i
t has been incriminated in essential hypertension, we measured plasma
and urinary calcium and phosphate as well as plasma PTH and free calci
triol index (ratio of total calcitriol on the D binding protein) in no
rmotensive pregnant women (n = 25), in women with PIH after the same d
uration of amenorrhea (> 28 wk, n = 21: preeclampsia and 20 transient
hypertensions), and in age-matched nonpregnant women (n = 15). The sev
erity of PIH was mild since blood uric acid was not increased and plas
ma volume, measured with the Evans blue technique, was found only mode
rately decreased (-10.5 +/- 3.1% of normal value). The results show th
at normotensive pregnant women showed the expected increase of the vit
amin D parameters in comparison to nonpregnant controls. Hypertensive
pregnant women were not different from the normotensive ones regarding
plasma corrected calcium and phosphate and urinary excretion of calci
um and phosphate, but had higher plasma PTH (13 +/- 1 v 8.8 +/- 1.6 pg
/mL) and lower total and free calcitriol index (86 +/- 7 v 110 +/- 6 p
g/mL and 1.72 +/- 0.10 v 2.25 +/- 0.13 X 10(-5)). Correlative studies
showed PIH having a negative correlation between blood pressure and pl
asma corrected calcium (r = -0.43, P < .05), which is in agreement wit
h epidemiological studies of essential hypertension. In conclusion, di
sturbances of calcium regulating hormones do exist in transient forms
of pregnancy-induced hypertension. In contrast to their increase in es
sential hypertension, plasma calcitriol levels are not so high in tran
sient hypertension of pregnancy as compared to normotensive pregnancy,
as it has been already shown in preeclampsia. All the above data take
n together suggest that in both forms of pregnancy-induced hypertensio
n, there is a primary defect of calcitriol synthesis in contrast to es
sential hypertension.