Giachino G, Giacchino F, Basolo B, Giraudo G, Boero R, Bancale E, Nigra M, Garetto A, Jeantet A, Piccoli G
Arch Sci Med (Torino). 1983 Jul-Sep;140(3):259-66.
Thirty-seven osteodystrophic and chronically haemodialyzed patients have been treated for 1-22 months by means of 1,25(OH)2D3. Under treatment a marked improvement of symptomatology and radiographic findings has been observed in the majority of cases; from the haematochemical viewpoint a rise of calcemia and phosphoremia, a fall in alkaline phosphatase and a variable course of PTH have been observed. Several episodes of asymptomatic hypercalcemia ceased with posology reduction; only 3 cases needed stopping the treatment for this reason, one of them definitively; 12/37 cases needed hypophosphoric diets and increase in oral aluminium hydroxide doses to control hyperphosphoremia. The Authors conclude that, to achieve a correct management of a 1,25(OH)2D3 therapy for renal osteodystrophy, is mandatory a strict and accurate biochemical control: in this way is possible to obtain an effective modulation of the posology avoiding the appearance of side-effects as hypercalcemia and ectopic calcifications.
37例骨营养不良且长期接受血液透析的患者接受了1,25(OH)₂D₃治疗，疗程为1至22个月。治疗期间，多数病例的症状及影像学表现有显著改善；从血液生化角度看，血钙和血磷升高，碱性磷酸酶降低，甲状旁腺激素（PTH）变化不一。几例无症状高钙血症发作通过减少剂量得以缓解；仅3例因此需要停止治疗，其中1例为永久性停药；37例中有12例需要低磷饮食并增加口服氢氧化铝剂量以控制高磷血症。作者得出结论，为正确管理肾性骨营养不良的1,25(OH)₂D₃治疗，严格准确的生化监测必不可少：通过这种方式，可有效调整剂量，避免出现高钙血症和异位钙化等副作用。
