Metabolic balance studies in patients with Paget's disease receiving salmon calcitonin over long periods.

Metabolic balance and calcium kinetic studies were performed in four patients with Paget's disease before treatment with salmon calcitonin and during the early and late stages of the treatment, which lasted 9 to 19 months, A significant decrease in bone turnover and 24-hour urine hydroxyproline and serum alkaline phosphatase values was observed in all patients. In contrast, the calcium, phosphorus and magnesium balances did not change significantly. In agreement with this, the partial body calcium, measured by in vivo neutron activation analysis, did not change. Intestinal calcium absorption increased initially, but returned to baseline levels 9 to 19 months after the study began. During the initial period there was a small, significant, but transient decrease in tubular reabsorption of phosphorus; this was accompanied by a significant decrease in serum phosphorus values--probably a direct effect of calcitonin rather than evidence of secondary hyperparathyroidism. Administration of salmon calcitonin to patients with Paget's disease decreases bone turnover without affecting calcium and phosphorus balances.     

Morphology, progression, and regression of arterial and periarterial calcifications in patients with end-stage renal disease

The appearance of arterial calcifications over time was studied radiographically in 143 patients with end-stage renal disease. Of these, 85 patients had only slight calcifications; 58 had the well-known, linear, pipe stem-like arterial calcifications. In 44 of the 58, small nodular calcifications were noted, often external to the linear calcifications. Nine patients had larger periarterial calcifications, which have not been previously described to our knowledge. Arterial calcifications progressed in 82 of 143 patients (57%) and regressed in 19 (13%). During progression, thickening of the linear calcifications was often observed, and in ten patients this caused definite luminal narrowing. From 1976 to 1984, five of 71 patients (7%) required amputations; all five had marked arterial calcifications. Better controlled clinical studies are indicated to detect factors that may prevent the progression and promote the regression of arterial calcifications.     

Correlations between peripheral and central skeletal mineral content in chronic renal failure patients and in osteoporotics

Partial-body calcium measurements by in vivo neutron activation analysis (IVNAA) were correlated with radiographic measurements of bone mineral mass and density, external diameter, and combined cortical thickness of the proximal radius in three groups of subjects: normals, osteoporotics, and chronic renal failure patients. The radial bone mineral mass (in g/cm) correlated best with IVNAA measurements in normal subjects (r=0.94), reasonably well in osteoporotics (r=0.83), and less well in chronic renal failure patients (r=0.65). Simple combined cortical thickness measurements correlated moderately well both in normal subjects (r=0.82) and in osteoporotic subjects (r=0.74).     

Detection and pathogenesis of visceral calcification in dialysis patients and patients with malignant disease

Scintiscanning to detect the uptake of bone-seeking radioactive isotopes by soft tissue is a promising technique for the in vivo study of visceral calcification. Visceral uptake of such radioisotopes was studied in 40 patients: 22 undergoing long-term dialysis, 9 with malignant disease and hypercalcemia and 9 with primary hyperparathyroidism and hypercalcemia.

Fifteen patients, 11 undergoing dialysis and 4 with malignant disease, had radioisotope uptake in the lungs, and 5, 3 undergoing dialysis and 2 with malignant disease, had uptake in the stomach. None of the patients with primary hyperparathyroidism had visceral uptake, nor did the patients with uptake have radiologic evidence of pulmonary or gastric calcification. The dialysis patients with visceral uptake had a mean calcium × phosphate product of 84.3 ± 23.7 (standard deviation), which was significantly greater (P < 0.001) than that of patients without such uptake (59.2 ± 14.0). Similarly, in patients with malignant disease and visceral uptake the Ca × P product was 72.2 ± 6.4 — significantly greater (P < 0.005) than that of patients without such uptake (49.3 ± 6.7).

These findings indicate that scintiscanning for the visceral uptake of a bone-seeking radioisotope is a simple and effective technique for the in vivo study of visceral calcification. An elevation in the Ca × P product seems to be the single most important factor in the production of visceral calcification.