Abstract
Oral 1α, 25 (OH) 2D3 pulse therapy and conventional therapy were performed in 9 hemodialysis patients with secondary hyperparathyroidism. The times during which the patients underwent pulse and conventional therapies were divided into four periods. The first period was 86.3 days (20-160 days) for pulse therapy. The second period was 84.1 days (37-210 days) for conventional therapy, the third period was 79.6 days (44-120 days) for pulse therapy, and the fourth period was 53.8 days (30-80 days) for conventional therapy. Under pulse therapy, 4.0μg of 1α, 25 (OH) 2D3 was administered orally at the end of each dialysis session (twice a week). Under conventional therapy, 0.25 to 1.0 μg of 1α (OH) D3 or 1α, 25 (OH) 2D3 was administered every day, During each therapy, CaCO3 and Al (OH)3 were administered to serve as phosphate binders.
A month after pulse therapy started, the serum C-PTH level had decreased and the pain in bones and joints had disappeared. A month after pulse therapy stopped and conventional therapy started, the serum C-PTH level had increased and the pain in bones and joints had recurred. The serum ALP level decreased during the first pulse therapy period and did not change significantly during the following conventional, pulse and conventional therapy periods.
The changes in the serum C-PTH level and in bone and joint pain suggests that PTH may be a pain activator. When the pain in bones and joints disappeared, the mean serum C-PTH level was 14.5ng/ml (n=13), a significantly high level.
