原発性副甲状腺機能亢進症ならびに特発性高カルシウム尿症にみられる高カルシウム尿症の成因,ことにカルシウム調節ホルモンの働きについて

Abstract

Calcium regulation hormones, parathyroid hormone (PTH), 1, 25-dihydroxyvitamin D (1, 25(OH)2D3) and calcitonin (CT) were measured and calcium and phosphate metabolism investigated in primary hyperparathyroidism (PHP, n=15), normocalcemic idiopathic hypercalciuria (IHC, n= 12) and related metabolic disorders of calcium, and pathogenesis of hypercalciuria was discussed. Calcium-47 dynamic study using whole body counter consisting of intestinal absorption and body retention rates of calcium was also applied in those patients. 1. Elevations of serum 1, 25(OH)2D3 and urinary calcium excretion were seen as a common feature between PHP and IHC and increased intestinal calcium absorption and decreased serum phosphorus as a similar directional change. 2. Biochemical differences were seen between adenoma and hyperplasia in PHP. In hyperplasia, while serum 1, 25(OH)2D3 increased significantly, serum phosphate and urinary excretion of calcium increased and PTH decreased, but these were not significant changes. In adenoma, alkaline phosphatase significantly increased. 3. In PHP, excessive production of PTH stimulates production of 1, 25(OH)2D3 in the kidney, which enhances intestinal absorption of calcium. Hypophosphatemia had no effects on serum 1, 25(OH)2D3 and urinary excretion of calcium. 4. In IHC, although the subgroup, either absorptive or reabsorptive, should be classified, elevation of serum 1, 25(OH)2D3 was a characteristic feature, which enhanced intestinal absorption of calcium, resulting in increased urinary excretion of calcium. However, increased levels of 1, 25 (OH)2D3 did not parallel the amount of intestinal absorption. Since there was a good correlation between serum 1, 25(OH)2D3 and phosphorus or urinary excretion of calcium and serum phosphorus, hypohophosphatemia is a factor which stimulates the production of 1, 25(OH)2D3 in the kidney. PTH levels were within normal limits. 5. Serum CT levels were normal in those patients in spite of alterations of PTH and 1, 25(OH)2D3. 6. Except that elevations of serum calcium and PTH were seen in PHP, the level of 1, 25 (OH)2D3 in the hyperplasia group of PHP was similar to that in IHC. Levels of serum phosphorus and the amount of urinary calcium excretion in hyperplasia group showed a similar directional changes to those in IHC. It is suggested that an intermediate form possibly exists between reabsorption type in IHC and hyperplasia in PHP.