Bone mineral density in patients with chronic hypoparathyroidism.

Photon absorptiometry was used to measure skeletal mass in the proximal femur, lumbar spine, and distal radius in 19 females with hypoparathyroidism after operation for either thyroid carcinoma or hyperparathyroidism. Healthy subjects as well as normocalcemic patients who had undergone the same surgical procedure without developing hypoparathyroidism were used as controls. Skeletal mass was measured after a mean postoperative time of 13 and 10 yr in patients operated on for thyroid carcinoma and hyperparathyroidism, respectively. Bone mass was 10-32% greater in hypoparathyroid patients than in controls. In patients with retained parathyroid function after total thyroidectomy and surgical treatment of hyperparathyroidism, bone mass did not differ from that in age-matched healthy controls. Long term T4 medication in doses that suppressed endogenous TSH production was not associated with a decreased bone mass. Reduced PTH production, vitamin D treatment, and calcium supplementation may all have contributed to the increased bone mass found in the patients with postsurgical hypoparathyroidism.

Skeletal remineralization after surgery for primary and secondary hyperparathyroidism.

Bone mineral was measured by photon absorptiometry before and after parathyroid surgery in patients with primary or secondary hyperparathyroidism (HPT). The mean bone mineral density of lumbar vertebrae was 0.82 +/- 0.04 (SEM) gm/cm2 in primary HPT (n = 7) and 0.86 +/- 0.05 gm/cm2 in secondary HPT (n = 11). These values are significantly lower than for age-matched normal subjects. After successful parathyroid surgery, the bone mass of the distal radius and lumbar vertebrae increased by approximately 10% within 3 months after operation and then remained stable during the first postoperative year. In conclusion, parathyroid surgery is followed by a significant increase of bone mass in primary and secondary HPT. The substantial increase in bone mass in parts of the skeleton consisting predominantly of trabecular bone, as well as in sites with predominantly cortical bone, indicates that remineralization after operation involves a generalized increase in bone mass.

Rickets induced by calcium or phosphate depletion.

We studied the effects of calciopenia and phosphopenia on longitudinal growth, skeletal mineralization, and development of rickets in young Sprague-Dawley rats. At an age of 21 days, two experimental groups were given diets containing 0.02% calcium or 0.02% phosphorus; otherwise the diets were nutritionally adequate. After 7, 14, and 21 days, five animals from each group were randomly chosen. The animals were anaesthetized and blood samples were drawn for analysis of calcium, phosphorus, and immunoreactive parathyroid hormone, whereupon the animals were killed. Length, weight, and specific weight of the left femur were measured. After 28 days on the respective diet the remaining animals were killed and one proximal tibia from each animal was processed for light microscopy and subjected to stereological analysis. Both experimental groups developed progressive growth retardation, more so the phosphate-depleted group. The calciopenic animals developed severe hypocalcaemia and secondary hyperparathyroidism, whereas the phosphate-depleted animals, in spite of marked secondary hypercalcaemia, had unaltered levels of immunoreactive parathyroid hormone. By 28 days both experimental groups displayed rachitic changes, more pronounced in the phosphate-depleted animals. This paper provides quantitative data demonstrating that calciopenia per se may cause rickets in young rats, but that the rachitic changes in this condition are less severe, and the growth pattern different from those in phosphate depletion.

Effect of calcium supplementation on bone mass in patients operated on for hyperparathyroidism.

Photon absorptiometry was used to measure bone mass in the lumbar vertebrae, proximal femur, mid-radius and distal radius in eight pairs of closely matched female patients with primary hyperparathyroidism before, and 1, 3 and 6 months after operation. One of each pair was randomised to receive 3 g of oral calcium supplementation/day for three months postoperatively, and the other to serve as a control. After successful operations on the parathyroids, the bone mass in the lumbar vertebrae, proximal femur, and distal radius increased by roughly 7% during the first six months in both the treated and the control patients. This study shows that oral calcium supplementation after operation for hyperparathyroidism does not result in any additional increase in bone mass beyond the effect that is caused by the operation.

Bone mineral density in patients with familial hypocalciuric hypercalcaemia (FHH).

OBJECTIVE: To find out whether chronic hypercalcaemia and excessive secretion of parathyroid hormone (PTH) is associated with skeletal demineralisation in familial hypocalciuric hypercalcaemia (FHH). DESIGN: Open study. SETTING: Huddinge University Hospital, Sweden. SUBJECTS: Nine affected and three unaffected members of two kindreds with FHH, and 12 age- and sex-matched controls. INTERVENTIONS: Measurement of bone mineral density (g/cm2) in the proximal femur and lumbar spine by dual photon absorptiometry, and of bone mineral content in the distal radius and midradius (g/cm) by single photon absorptiometry. Measurement of serum concentrations of PTH, total and ionised calcium, phosphate, and magnesium, and alkaline phosphatase activity, and 24 hour urinary calcium excretion were also made. RESULTS: Bone mineral density was significantly higher in Wards's triangle of the femur (p < 0.05) in the members of families with FHH than in control subjects. In the other parts of the femur and in the lumbar vertebrae it was slightly but not significantly higher, as was the bone mineral content of the distal radius and midradius. Family members with FHH all had increased total and ionised serum calcium concentrations, except for the index case in one of the families who developed hypoparathyroidism postoperatively. Twenty-four urinary calcium excretion was less than 5 mmol (the upper limit of the reference range for FHH) in all the affected patients. CONCLUSION: Chronic hypercalcaemia in affected members of families with FHH is not the result of an increase rate of bone mineralisation, because they have normal bone mass. They seem to be relatively insensitive to the deleterious effects of PTH on bone mineral state, because raised concentrations of PTH were not associated with reduced bone mass.