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Intravenous calcitriol therapy in an early stage prevents parathyroid gland growth.

Taniguchi M, Tokumoto M, Tsuruya K, Hirakata H, Iida M - Nephrol. Dial. Transplant. (2008)

Bottom Line: Both groups showed similar reductions of the serum PTH level and similar increases in serum calcium.Long-term daily oral calcitriol therapy failed to prevent the increase of both maximum PT volume and total volume, as assessed by ultrasonography; however, intravenous calcitriol therapy successfully suppressed this progression.In the daily, oral group, both the bone-specific alkaline phosphatase (BAP) and the N-telopeptide cross-linked of type I collagen (NTX) significantly decreased, which was probably due to the PTH suppression.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Higashi-Ku, Fukuoka 812-8582, Japan. masatomo@kcu.med.kyushu-u.ac.jp

ABSTRACT

Background: Both the phenotypic alterations of parathyroid (PT) cells, e.g. down-regulation of the calcium-sensing receptor, and the increase of the PT cell number in nodular hyperplasia are the main causes of refractory secondary hyperparathyroidism. It is of great importance to prevent PT growth in an early stage.

Methods: To examine a more effective method of calcitriol therapy for the prevention of PT hyperplasia, we randomized haemodialysis patients with mild hyperparathyroidism to receive either daily orally administered calcitriol (n = 33) or intravenous calcitriol (n = 27) over a 12-month study period. Calcitriol was modulated so as to keep the serum intact PTH level between 100 and 150 pg/ml.

Results: Both groups showed similar reductions of the serum PTH level and similar increases in serum calcium. In both groups, there were no significant changes in the serum phosphate level. Long-term daily oral calcitriol therapy failed to prevent the increase of both maximum PT volume and total volume, as assessed by ultrasonography; however, intravenous calcitriol therapy successfully suppressed this progression. In the daily, oral group, both the bone-specific alkaline phosphatase (BAP) and the N-telopeptide cross-linked of type I collagen (NTX) significantly decreased, which was probably due to the PTH suppression. However, these bone metabolism markers remained stable in the intravenous group. The total dosage of calcitriol during the study was comparable in both groups.

Conclusions: These data indicate that intravenous calcitriol therapy in an early stage of secondary hyperparathyroidism is necessary to prevent PT growth and to keep a good condition of bone metabolism.

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Changes of maximum and total parathyroid gland volume during the treatment with daily oral and intravenous calcitriol. DO, the daily oral group; IV, the intravenous group. Median values and interquartile ranges were given.
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Figure 3: Changes of maximum and total parathyroid gland volume during the treatment with daily oral and intravenous calcitriol. DO, the daily oral group; IV, the intravenous group. Median values and interquartile ranges were given.

Mentions: There were no significant differences in the maximum PT gland volume at the start of administration nor total volume between the two groups (Table 1). We additionally evaluated the PT volume 12 months after the start of administration (Figure 2). In the DO group, the maximum PT gland volume significantly increased (49 ± 73 mm3 → 101 ± 141 mm3, P = 0.007). In the IV group, there were no changes in the volume (96 ± 215 mm3 → 89 ± 170 mm3). In the DO group, the total volume also increased (65 ± 108 mm3 → 134 ± 196 mm3, P = 0.006). In the IV group, there was no significant increase (150 ± 292 mm3 → 135 ± 250 mm3). There was a significant difference in the change of the PT volume between the two groups (Figure 3). The changes of both maximum and total gland volume were significantly larger in the DO group than those in the IV group (P = 0.047 and 0.015, respectively).


Intravenous calcitriol therapy in an early stage prevents parathyroid gland growth.

Taniguchi M, Tokumoto M, Tsuruya K, Hirakata H, Iida M - Nephrol. Dial. Transplant. (2008)

Changes of maximum and total parathyroid gland volume during the treatment with daily oral and intravenous calcitriol. DO, the daily oral group; IV, the intravenous group. Median values and interquartile ranges were given.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2568009&req=5

Figure 3: Changes of maximum and total parathyroid gland volume during the treatment with daily oral and intravenous calcitriol. DO, the daily oral group; IV, the intravenous group. Median values and interquartile ranges were given.
Mentions: There were no significant differences in the maximum PT gland volume at the start of administration nor total volume between the two groups (Table 1). We additionally evaluated the PT volume 12 months after the start of administration (Figure 2). In the DO group, the maximum PT gland volume significantly increased (49 ± 73 mm3 → 101 ± 141 mm3, P = 0.007). In the IV group, there were no changes in the volume (96 ± 215 mm3 → 89 ± 170 mm3). In the DO group, the total volume also increased (65 ± 108 mm3 → 134 ± 196 mm3, P = 0.006). In the IV group, there was no significant increase (150 ± 292 mm3 → 135 ± 250 mm3). There was a significant difference in the change of the PT volume between the two groups (Figure 3). The changes of both maximum and total gland volume were significantly larger in the DO group than those in the IV group (P = 0.047 and 0.015, respectively).

Bottom Line: Both groups showed similar reductions of the serum PTH level and similar increases in serum calcium.Long-term daily oral calcitriol therapy failed to prevent the increase of both maximum PT volume and total volume, as assessed by ultrasonography; however, intravenous calcitriol therapy successfully suppressed this progression.In the daily, oral group, both the bone-specific alkaline phosphatase (BAP) and the N-telopeptide cross-linked of type I collagen (NTX) significantly decreased, which was probably due to the PTH suppression.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University, Higashi-Ku, Fukuoka 812-8582, Japan. masatomo@kcu.med.kyushu-u.ac.jp

ABSTRACT

Background: Both the phenotypic alterations of parathyroid (PT) cells, e.g. down-regulation of the calcium-sensing receptor, and the increase of the PT cell number in nodular hyperplasia are the main causes of refractory secondary hyperparathyroidism. It is of great importance to prevent PT growth in an early stage.

Methods: To examine a more effective method of calcitriol therapy for the prevention of PT hyperplasia, we randomized haemodialysis patients with mild hyperparathyroidism to receive either daily orally administered calcitriol (n = 33) or intravenous calcitriol (n = 27) over a 12-month study period. Calcitriol was modulated so as to keep the serum intact PTH level between 100 and 150 pg/ml.

Results: Both groups showed similar reductions of the serum PTH level and similar increases in serum calcium. In both groups, there were no significant changes in the serum phosphate level. Long-term daily oral calcitriol therapy failed to prevent the increase of both maximum PT volume and total volume, as assessed by ultrasonography; however, intravenous calcitriol therapy successfully suppressed this progression. In the daily, oral group, both the bone-specific alkaline phosphatase (BAP) and the N-telopeptide cross-linked of type I collagen (NTX) significantly decreased, which was probably due to the PTH suppression. However, these bone metabolism markers remained stable in the intravenous group. The total dosage of calcitriol during the study was comparable in both groups.

Conclusions: These data indicate that intravenous calcitriol therapy in an early stage of secondary hyperparathyroidism is necessary to prevent PT growth and to keep a good condition of bone metabolism.

Show MeSH
Related in: MedlinePlus