Delling G, Lühmann H, Bulla M, Fuchs C, Henning H V, Jansen J L, Kohnle W, Schulz W
Contrib Nephrol. 1980;18:105-21. doi: 10.1159/000403278.
Fibroosteoclasia as well as osteoidosis are reduced by 1,25(OH)2D3 treatment if secondary hyperparathyroidism preexists. Fibrosteoclasia completely disappeared after 6 months therapy in some cases. 1,25(OH)2D3 has no or only a very slight effect on the disturbed mineralization in type II of renal bone disorder (osteoidosis only, no signs of secondary hyperparathyroidism). The appositional rate of the osteoblasts increases under 1,25(OH)2D3 treatment if serum PTH values are raised. 1,25(OH)2D3 seemed to have, in the chosen dosage of this study, a self-limiting effect by reducing the bone-forming cells, i.e. the osteoblasts. This state already represents an overtreatment of the underlying bone disease.
如果预先存在继发性甲状旁腺功能亢进,1,25(OH)₂D₃治疗可使纤维骨炎以及骨样骨病减轻。在某些病例中,经过6个月治疗后纤维骨炎完全消失。1,25(OH)₂D₃对Ⅱ型肾性骨病(仅骨样骨病,无继发性甲状旁腺功能亢进体征)中紊乱的矿化没有影响或仅有非常轻微的影响。如果血清甲状旁腺激素(PTH)值升高,在1,25(OH)₂D₃治疗下成骨细胞的贴壁率会增加。在本研究选择的剂量下,1,25(OH)₂D₃似乎通过减少骨形成细胞即成骨细胞而具有自限性作用。这种状态已经代表了对潜在骨病的过度治疗。