Hm. Harms et al., PULSE AMPLITUDE AND FREQUENCY-MODULATION OF PARATHYROID-HORMONE IN EARLY POSTMENOPAUSAL WOMEN BEFORE AND ON HORMONE REPLACEMENT THERAPY, The Journal of clinical endocrinology and metabolism, 78(1), 1994, pp. 48-52
Although the pathophysiology of postmenopausal osteoporosis has been i
nvestigated extensively, it is still not established in what respect P
TH is related to the events. Recently, consistent data on the pulsatil
e secretion of PTH in man have been published. In this study intact PT
H was measured in six early postmenopausal women before and after 6 mo
nths of hormone replacement therapy (HRT; 0.6 mg conjugated estrogens
and 5 mg medrogestone). In addition to parameters of calcium metabolis
m and bone mass and to control HRT, intact PTH was measured in blood d
rawn over 6 h every 2 min. With HRT there was a 30% reduction in PTH s
ecretion. Both the amount secreted per pulse (baseline, 26.8 +/- 6.9 n
g/L; HRT, 21.4 +/- 7.6 ng/L; P < 0.05) as well as the basal secretion
(baseline, 232.6 +/- 117.6 ng/L h; HRT, 145.5 +/- 80.0 ng/L h; P < 0.0
1) were reduced, whereas the pulse count per h remained constant (base
line, 5.1 +/- 2.2; HRT, 5.1 +/- 1.3). Power spectrum analysis showed a
shift in spectral maxims consistent with these findings. Ionized and
total calcium were slightly, but nonsignificantly, reduced with treatm
ent. In summary we conclude that in early postmenopausal women, HRT re
duces the secretion of PTH by reducing both the basal secretion and th
e amount secreted per pulse. It is conceivable that some of the known
effects of HRT on bone metabolism might be mediated by the modulation
of PTH secretion.