TY - JOUR
T1 - Assessment of combined 24,25(oh)2d3 and 1α(oh)d3 therapy for bone disease in dialysis patients
AU - Popovtzer, M. M.
AU - Levi, J.
AU - Bar-Khayim, Y.
AU - Shasha, S. M.
AU - Boner, G.
AU - Bernheim, J.
AU - Chaimovitz, C.
AU - Rubinger, D.
AU - Gafter, U.
AU - Gazit, D.
AU - Edelstein, S.
AU - Slatopolsky, E.
AU - Weiner, B. Z.
AU - Kafka, D. R.
AU - Kadosh, S.
AU - Ladkani, D.
AU - Mazor, Z.
AU - Shalita, B.
AU - Bab, I.
PY - 1992
Y1 - 1992
N2 - An increasing body of experimental data suggests a role for 24,25(OH)2D3 in bone metabolism. The present study was carried out to assess a possible therapeutic role of this vitamin D metabolite in renal osteodystrophy. Twenty-two chronic dialysis patients, most of whom were previously maintained on 1α(OH)D3 therapy, received additional treatment with 10 μg/day 24,25(OH)2D3 and were compared to 19 patients receiving 1α(OH)D3 alone. Analysis of transiliac bone biopsies obtained at study entry and following 10-16 months of treatment revealed that the combined therapy produced a decrease in bone turnover. Specifically, the addition of 24,25(OH)2D3 inhibited an increase in trabecular bone volume ( BV TV) and suppressed osteoclastic parameters. Thus BV TV increased from 26.2 ± 8.6 to 32.1 ± 7.5% (p < 0.01) in the 1α(OH)D3 group, but it remained unchanged in the combined therapy group. In contrast, the eroded surface ( ES BS), the osteoclast surface ( Oc.S BS), and the osteoclast numbers were significantly suppressed in patients receiving both 24,25(OH)2D3 and 1α(OH)D3, as compared with those receiving 1α(OH)D3 alone (p < 0.01, p < 0.01, and p < 0.001, respectively). These improvements were independent of changes in 1α(OH)D3 dosage. The extent of bone aluminium deposits was unrelated to the administration of 24,25-(OH)2D3 or to its effect. 24,25(OH)2D3 therapy was not associated with any adverse effects.
AB - An increasing body of experimental data suggests a role for 24,25(OH)2D3 in bone metabolism. The present study was carried out to assess a possible therapeutic role of this vitamin D metabolite in renal osteodystrophy. Twenty-two chronic dialysis patients, most of whom were previously maintained on 1α(OH)D3 therapy, received additional treatment with 10 μg/day 24,25(OH)2D3 and were compared to 19 patients receiving 1α(OH)D3 alone. Analysis of transiliac bone biopsies obtained at study entry and following 10-16 months of treatment revealed that the combined therapy produced a decrease in bone turnover. Specifically, the addition of 24,25(OH)2D3 inhibited an increase in trabecular bone volume ( BV TV) and suppressed osteoclastic parameters. Thus BV TV increased from 26.2 ± 8.6 to 32.1 ± 7.5% (p < 0.01) in the 1α(OH)D3 group, but it remained unchanged in the combined therapy group. In contrast, the eroded surface ( ES BS), the osteoclast surface ( Oc.S BS), and the osteoclast numbers were significantly suppressed in patients receiving both 24,25(OH)2D3 and 1α(OH)D3, as compared with those receiving 1α(OH)D3 alone (p < 0.01, p < 0.01, and p < 0.001, respectively). These improvements were independent of changes in 1α(OH)D3 dosage. The extent of bone aluminium deposits was unrelated to the administration of 24,25-(OH)2D3 or to its effect. 24,25(OH)2D3 therapy was not associated with any adverse effects.
KW - 1α(OH)D
KW - 24,25-(OH)D
KW - Aluminium
KW - Bone biopsy
KW - Dialysis
KW - Renal osteodystrophy
UR - http://www.scopus.com/inward/record.url?scp=0026701813&partnerID=8YFLogxK
U2 - 10.1016/8756-3282(92)90453-4
DO - 10.1016/8756-3282(92)90453-4
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AN - SCOPUS:0026701813
SN - 8756-3282
VL - 13
SP - 369
EP - 377
JO - Bone
JF - Bone
IS - 5
ER -