Abstract
Renal osteodystrophy with secondary hyperparathyroidism is a troublesome complication in hemodialysis patients. It has recently been reported that intermittent oral administration of 1, 25-dihydrocholecalciferol (1, 25-(OH)2D3) suppressed serum parathyroid hormone (PTH) levels in nine hemodialysis patients. We examined this pharmacological parathyroidectomy (pulse therapy) in uremic patients in 15 hemodialysis units. Two to 6mg of 1, 25-(OH)2D3 was administered orally twice weekly to 26 hemodialysis patients whose serum carboxy-terminal PTH (C-PTH) levels were greater than 7.0ng/ml.
Five of the 26 patients withdrew from treatment because of hypercalcemia (>11.0mg/dl). Serum midregion PTH fragment (HS-PTH) was measured using the PTH kit “Yamasa” before and 4, 8 and 12 weeks after 1, 25-(OH)2D3 administration. A marked decrease in HS-PTH level was noted in 21 patients 12 weeks after the pulse therapy, but in 5 patients HS-PTH levels were elevated or unchanged at 4 weeks after therapy compared with the level before treatment (slow responder). The HS-PTH levels of 16 other patients were decresed by 28% at 4 weeks compared with the initial values (fast responder). In one patient, the HS-PTH level was decreased after the administration of 1, 25-(OH)2D3 (2mg), This decrease occurred although her plasma Ca was not elevated (8.5mg/dl).
Our results indicated that the suppression of serum parathyroid hormone level by 1, 25-(OH)2D3 was not uniform among hemodialysis patients, as indicated by the fast and slow responders. It was also suggested that 1, 25-(OH)2D3 directly suppressed parathyroid function.
