Does estrogen replacement therapy influence parathyroid hormone responsiveness to exogenous hypercalcemia in postmenopausal women?
Jazyk angličtina Země Itálie Médium print
Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem
PubMed
8320422
DOI
10.1007/bf03348845
Knihovny.cz E-zdroje
- MeSH
- chlorid vápenatý * MeSH
- estradiol terapeutické užití MeSH
- estrogenní substituční terapie * MeSH
- hyperkalcemie chemicky indukované patofyziologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- menopauza krev MeSH
- parathormon biosyntéza metabolismus MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
- Názvy látek
- chlorid vápenatý * MeSH
- estradiol MeSH
- parathormon MeSH
In postmenopausal women PTH suppression by exogenous calcium is reduced. To test whether this finding might be caused by estrogen deficiency 9 postmenopausal women were given transdermal estradiol (E2) treatment for 3 months at a dose of 100 micrograms/day. PTH reactivity to iv administration of CaCl2 was determined before and at the end of the E2-treatment period. Compliance to treatment was checked by determination of serum levels of E2 and FSH. The E2 level rose from 0.1 +/- 0.02 (mean +/- SE) to 0.46 +/- 0.10 mmol/l p < 0.01), whereas the corresponding FSH level declined from 77.5 +/- 7.4 to 33.9 +/- 5.7 U/l p < 0.01). This suggests good compliance. At the end of E2-treatment period calcium administration induced a higher PTH suppression as compared with control value (the PTH decremental area 2123 +/- 270 vs 1253 +/- 253 ng/l x min, p < 0.05), although a lower calcemic response was attained (the Ca incremental area 32.6 +/- 6.1 vs 47.4 +/- 4.5 mmol/ml x min, p < 0.05). These results imply that parathyroid glands are dependent on an adequate estrogen provision to respond normally to serum calcium changes.
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Horm Metab Res. 1985 Dec;17(12):696-7 PubMed
Science. 1988 Jul 1;241(4861):81-4 PubMed
J Clin Endocrinol Metab. 1990 Apr;70(4):1119-23 PubMed
Lancet. 1981 Mar 28;1(8222):693-5 PubMed
J Clin Invest. 1989 Feb;83(2):537-42 PubMed
Endocrinology. 1992 May;130(5):2617-24 PubMed
Lancet. 1982 Feb 27;1(8270):475-8 PubMed
J Clin Endocrinol Metab. 1985 Oct;61(4):595-600 PubMed
Proc Natl Acad Sci U S A. 1991 Jun 15;88(12):5134-8 PubMed
Horm Metab Res. 1985 Jul;17(7):370-3 PubMed
Exp Clin Endocrinol. 1988 Mar;92(3):257-61 PubMed
J Clin Endocrinol Metab. 1989 Apr;68(4):831-6 PubMed
Clin Sci (Lond). 1985 Sep;69(3):265-71 PubMed
J Clin Endocrinol Metab. 1989 Jan;68(1):223-6 PubMed
J Clin Endocrinol Metab. 1980 Dec;51(6):1359-64 PubMed
J Clin Invest. 1989 Mar;83(3):1073-7 PubMed
Calcif Tissue Int. 1983 Jul;35(4-5):502-7 PubMed
J Clin Endocrinol Metab. 1991 Feb;72(2):350-5 PubMed
Front Horm Res. 1975;3:150-76 PubMed
J Clin Endocrinol Metab. 1989 Mar;68(3):684-7 PubMed
J Clin Endocrinol Metab. 1990 Nov;71(5):1284-7 PubMed
