TY - JOUR
T1 - Postmenopausal osteoporosis as a manifestation of renal hypercalciuria with secondary hyperparathyroidism
AU - Sakhaee, K.
AU - Nicar, M. J.
AU - Glass, K.
AU - Pak, C. Y C
N1 - Copyright:
Copyright 2016 Elsevier B.V., All rights reserved.
PY - 1985/8
Y1 - 1985/8
N2 - An apparently unique presentation of osteoporosis was encountered in eight postmenopausal women (mean age, 56.8 yr). They had renal hypercalciuria, since they had fasting hypercalciuria [0.17 ± 0.04 (±SD) mg/100 ml glomerular filtrate (GF)] ]in the setting of normocalcemia and parathyroid stimulation (high serum immunoreactive PTH and/or urinary cAMP). Serum 1, 25-dihydroxyvitamin D was not significantly different (28 ± 7 vs. 34 ± 2 pg/ml) from that in a nonelderly control group, but fractional intestinal calcium (Ca) absorption was significantly lower (0.382 ±0.123 vs. 0.49 ±0.06; P <0.025). Thus, the patients did not have compensatory intestinal hyperabsorption of Ca despite PTH excess. Treatment with hydrochlorothiazide (50 mg/day) produced a decline in fasting urinary Ca (to 0.07 ± 0.02 mg/100 ml GF; P < 0.01), serum PTH (from 39 ± 19 to 21 ± 1 μl eq/ml; P< 0.05), and urinary cAMP excretion (from 5.30 ± 0.57 to 3.57 ± 0.59 nmol/100 ml GF; P < 0.0025). The results suggested that hyperparathyroidism was secondary. Histomorphometric analysis of bone showed reduced trabecular bone volume without mineralization defect, compatible with osteoporosis. Four of eight patients had high or high normal fractional resorption surfaces, fractional formation surfaces, and fractional osteoid volumes. That these abnormalities may reflect PTH-dependent osteoclastic resorption and bone turnover was supported by the reduction of these indices after correction of secondary hyperparathyroidism with hydrochlorothiazide therapy. The remaining four patients, however, had normal histomorphometric results. In summary, postmenopausal osteoporosis may occur sometimes with renal hypercalciuria and secondary hyperparathyroidism. The lack of compensatory intestinal hyperabsorption of Ca predisposes to negative Ca balance, and the hyperparathyroid state may be manifested by stimulated osteoclastic and osteoblastic activities.
AB - An apparently unique presentation of osteoporosis was encountered in eight postmenopausal women (mean age, 56.8 yr). They had renal hypercalciuria, since they had fasting hypercalciuria [0.17 ± 0.04 (±SD) mg/100 ml glomerular filtrate (GF)] ]in the setting of normocalcemia and parathyroid stimulation (high serum immunoreactive PTH and/or urinary cAMP). Serum 1, 25-dihydroxyvitamin D was not significantly different (28 ± 7 vs. 34 ± 2 pg/ml) from that in a nonelderly control group, but fractional intestinal calcium (Ca) absorption was significantly lower (0.382 ±0.123 vs. 0.49 ±0.06; P <0.025). Thus, the patients did not have compensatory intestinal hyperabsorption of Ca despite PTH excess. Treatment with hydrochlorothiazide (50 mg/day) produced a decline in fasting urinary Ca (to 0.07 ± 0.02 mg/100 ml GF; P < 0.01), serum PTH (from 39 ± 19 to 21 ± 1 μl eq/ml; P< 0.05), and urinary cAMP excretion (from 5.30 ± 0.57 to 3.57 ± 0.59 nmol/100 ml GF; P < 0.0025). The results suggested that hyperparathyroidism was secondary. Histomorphometric analysis of bone showed reduced trabecular bone volume without mineralization defect, compatible with osteoporosis. Four of eight patients had high or high normal fractional resorption surfaces, fractional formation surfaces, and fractional osteoid volumes. That these abnormalities may reflect PTH-dependent osteoclastic resorption and bone turnover was supported by the reduction of these indices after correction of secondary hyperparathyroidism with hydrochlorothiazide therapy. The remaining four patients, however, had normal histomorphometric results. In summary, postmenopausal osteoporosis may occur sometimes with renal hypercalciuria and secondary hyperparathyroidism. The lack of compensatory intestinal hyperabsorption of Ca predisposes to negative Ca balance, and the hyperparathyroid state may be manifested by stimulated osteoclastic and osteoblastic activities.
UR - http://www.scopus.com/inward/record.url?scp=0021827119&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0021827119&partnerID=8YFLogxK
U2 - 10.1210/jcem-61-2-368
DO - 10.1210/jcem-61-2-368
M3 - Article
C2 - 4008611
AN - SCOPUS:0021827119
VL - 61
SP - 368
EP - 373
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
SN - 0021-972X
IS - 2
ER -