Treatment with ethinyl estradiol or norethindrone reduces the bone-turnover rate and plasma calcium levels in normal postmenopausal women, without affecting the secretion of calcium-regulating hormones. To assess the effect of these sex steroids in patients with primary hyperparathyroidism, we treated postmenopausal women who had hyperparathyroidism with either ethinyl estradiol (n = 6) or norethindrone (n = 11). After three weeks of treatment, the bone-turnover rate declined and plasma calcium fell from a mean (+/- 1 SE) of 2.77 +/- 0.07 mmol per liter (11.1 +/- 0.3 mg per deciliter) to 2.58 +/- 0.05 mmol per liter (10.3 +/- 0.2 mg per deciliter; P less than 0.01) in the group treated with ethinyl estradiol, and from 2.93 +/- 0.08 mmol per liter (11.7 +/- 0.3 mg per deciliter) to 2.84 +/- 0.08 mmol per liter (11.4 +/- 0.3 per deciliter; P less than 0.05) in the patients who received norethindrone. No significant changes in the plasma levels of parathyroid hormone, calcitonin, or calcitriol were observed after the estrogen-induced increases in vitamin D-binding protein had been taken into account. Since the decline in plasma calcium levels did not stimulate secretion of parathyroid hormone, we conclude that treatment with either sex steroid resets the threshold for secretion of parathyroid hormone. Thus, although the reductions in plasma calcium levels were moderate, sex-hormone therapy may be useful in the treatment of mild hyperparathyroidism in postmenopausal women.
This article has been cited by other articles:
Carrillo-Lopez, N., Roman-Garcia, P., Rodriguez-Rebollar, A., Fernandez-Martin, J. L., Naves-Diaz, M., Cannata-Andia, J. B.
(2009). Indirect Regulation of PTH by Estrogens May Require FGF23. J. Am. Soc. Nephrol.
20: 2009-2017
[Abstract][Full Text]
Khan, A., Grey, A., Shoback, D.
(2009). Medical Management of Asymptomatic Primary Hyperparathyroidism: Proceedings of the Third International Workshop. J. Clin. Endocrinol. Metab.
94: 373-381
[Abstract][Full Text]
Iglesias, P, Diez, J J
(2009). Current treatments in the management of patients with primary hyperparathyroidism. Postgrad. Med. J.
85: 15-23
[Abstract][Full Text]
Kawata, T., Imanishi, Y., Kobayashi, K., Kenko, T., Wada, M., Ishimura, E., Miki, T., Nagano, N., Inaba, M., Arnold, A., Nishizawa, Y.
(2005). Relationship between parathyroid calcium-sensing receptor expression and potency of the calcimimetic, cinacalcet, in suppressing parathyroid hormone secretion in an in vivo murine model of primary hyperparathyroidism. Eur J Endocrinol
153: 587-594
[Abstract][Full Text]
Strewler, G. J.
(2005). A 64-Year-Old Woman With Primary Hyperparathyroidism. JAMA
293: 1772-1779
[Full Text]
Lambert, L. A., Shapiro, S. E., Lee, J. E., Perrier, N. D., Truong, M., Wallace, M. J., Hoff, A. O., Gagel, R. F., Evans, D. B.
(2005). Surgical Treatment of Hyperparathyroidism in Patients With Multiple Endocrine Neoplasia Type 1. Arch Surg
140: 374-382
[Abstract][Full Text]
Shoback, D. M., Bilezikian, J. P., Turner, S. A., McCary, L. C., Guo, M. D., Peacock, M.
(2003). The Calcimimetic Cinacalcet Normalizes Serum Calcium in Subjects with Primary Hyperparathyroidism. J. Clin. Endocrinol. Metab.
88: 5644-5649
[Abstract][Full Text]
Maruani, G., Hertig, A., Paillard, M., Houillier, P.
(2003). Normocalcemic Primary Hyperparathyroidism: Evidence for a Generalized Target-Tissue Resistance to Parathyroid Hormone. J. Clin. Endocrinol. Metab.
88: 4641-4648
[Abstract][Full Text]
Rubin, M. R., Lee, K. H., McMahon, D. J., Silverberg, S. J.
(2003). Raloxifene Lowers Serum Calcium and Markers of Bone Turnover in Postmenopausal Women with Primary Hyperparathyroidism. J. Clin. Endocrinol. Metab.
88: 1174-1178
[Abstract][Full Text]
Parker, C. R., Blackwell, P. J., Fairbairn, K. J., Hosking, D. J.
(2002). Alendronate in the Treatment of Primary Hyperparathyroid-Related Osteoporosis: A 2-Year Study. J. Clin. Endocrinol. Metab.
87: 4482-4489
[Abstract][Full Text]
Hak, A. E., Pols, H. A. P., van Hemert, A. M., Hofman, A., Witteman, J. C. M.
(2000). Progression of Aortic Calcification Is Associated With Metacarpal Bone Loss During Menopause : A Population-Based Longitudinal Study. Arterioscler. Thromb. Vasc. Bio.
20: 1926-1931
[Abstract][Full Text]
Khan, A., Bilezikian, J.
(2000). Primary hyperparathyroidism: pathophysiology and impact on bone. CMAJ
163: 184-187
[Abstract][Full Text]
Bone, H. G.
(1999). Who Needs Parathyroid Surgery? The Case for Parathyroidectomy in Nonclassical Primary Hyperparathyroidismb. J. Clin. Endocrinol. Metab.
84: 2278-2282
[Full Text]
Finkelstein, J. S., Schoenfeld, D. A.
(1999). Effects of Gonadal Suppression on the Regulation of Parathyroid Hormone and 1,25-Dihydroxyvitamin D Secretion in Women. J. Clin. Endocrinol. Metab.
84: 2151-2156
[Abstract][Full Text]
Silverberg, S. J., Bone, H. G., Marriott, T. B., Locker, F. G., Thys-Jacobs, S., Dziem, G., Kaatz, S., Sanguinetti, E. L., Bilezikian, J. P.
(1997). Short-Term Inhibition of Parathyroid Hormone Secretion by a Calcium-Receptor Agonist in Patients with Primary Hyperparathyroidism. NEJM
337: 1506-1511
[Abstract][Full Text]
Bhagat, K., Collier, J., Vallance, P.
(1996). Local Venous Responses to Endotoxin in Humans. Circulation
94: 490-497
[Abstract][Full Text]
Stancer, H. C., Forbath, N.
(1989). Hyperparathyroidism, Hypothyroidism, and Impaired Renal Function After 10 to 20 Years of Lithium Treatment. Arch Intern Med
149: 1042-1045
[Abstract]
Lafferty, F. W., Hubay, C. A.
(1989). Primary Hyperparathyroidism: A Review of the Long-term Surgical and Nonsurgical Morbidities as a Basis for a Rational Approach to Treatment. Arch Intern Med
149: 789-796
[Abstract]
Previous
