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      The ‘Oral 1,25-Dihydroxyvitamin D 3 Pulse Therapy’ in Hemodialysis Patients with Severe Secondary Hyperparathyroidism

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          Many hemodialysis patients are still suffering from secondary hyperparathyroidism although 1,25-dihydroxyvitamin D<sub>3</sub> (1,25(OH)<sub>2</sub>D<sub>3</sub>) has been used to treat renal osteodystrophy for the last two decades. The main reason for its failure to correct the secondary hyperparathyroidism is that in patients, hypercalcemia occurs before adequate parathyroid hormone (PTH) suppression is obtained when a large daily dose of 1,25(OH)<sub>2</sub>D<sub>3</sub> is started. In this study, the oral dose of 1,25(OH)<sub>2</sub>D<sub>3</sub> (4.0 μg) was administered only twice a week at the end of hemodialysis (‘oral 1,25(OH)<sub>2</sub>D<sub>3 </sub>pulse therapy’), in 19 patients with severe secondary hyperparathyroidism. Serum immunoreactive PTH started to decrease after 6 weeks of therapy, and the original level of 41.2 ± 7.24 was reduced to 24.4 ± 6.12 ng/ml by the end of the 6-month therapy (p < 0.001). Serum alkaline phosphatase also was reduced by 64.4%. Three out of 19 patients suffered from hypercalcemia during the 4th month of therapy. Calcium supplement given to 6 other patients with severe secondary hyperparathyroidism did not lower serum PTH levels significantly after 6 weeks of therapy, although serum calcium levels increased and were sustained above 10 mg/dl for the last 5 weeks. These findings strongly suggest that the suppressive effect of the oral 1,25(OH)<sub>2</sub>D<sub>3</sub> pulse therapy was attained by a direct action of 1,25(OH)<sub>2</sub>D<sub>3</sub> on the parathyroid gland rather than by its ability to elevate serum calcium levels. In conclusion, the oral 1,25(OH)<sub>2</sub>D<sub>3</sub> pulse therapy effectively lowered PTH levels in hemodialysis patients who cannot tolerate large daily doses of 1,25(OH)<sub>2</sub>D<sub>3</sub>.

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          Author and article information

          S. Karger AG
          11 December 2008
          : 57
          : 1
          : 23-28
          aDepartment of Medicine, Kitasato University School of Medicine, bSagamidai Hospital and cKitasato Biochemical Laboratories of SMI Bristoles, Sagamihara; dSecond Department of Internal Medicine, Tokyo Medical and Dental University, Tokyo, Japan
          186210 Nephron 1991;57:23–28
          © 1991 S. Karger AG, Basel

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          Pages: 6
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