Improvement in Bone Density with Calcitriol Substitution for Cholecalciferol in Refractory Osteoporosis induced by Prednisone

U. Kabadi, Salina Esmail
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引用次数: 1

Abstract

Introduction/ Purpose: Decline in BMD following prednisone therapy is attributed to osteoporosis. However, osteomalacia due to low 125 OH Vitamin D and resulting hyperparathyroidism may also be contributors. Therefore, administration of 125 OH vitamin D3, Calcitriol on BMD was examined in subjects receiving chronic prednisone therapy and low BMD (T< 2.5) refractory to therapy with bisphosphanate, calcium and vitamin D3, Cholecalciferol. Methods: 21 subjects, ages 45–56 years receiving prednisone ≥3 years with declining BMD despite therapy with Cholecalciferol, CaCO3 and bisphosphanate were divided into 2 groups. Both groups continued Calcium and bisphosphanate. 10 subjects (group 1) received increased dose of Cholecalciferol, 2000 units daily while in 11 subjects (group 2), it was substituted by Calcitriol. Comprehensive metabolic panels (CMP) including serum calcium and alkaline phosphatase as well as 25 OH Vit D and 125 OH Vit D levels were determined every 6 months. BMD was determined at yearly interval. Results: CMP including calcium and phosphorus remained normal in both groups while alkaline phosphatase declined in group 2 alone. Serum 25 OH Vit D levels were subnormal (<20 pg/ml) in both groups and normalized (53 ±6 pg/ml) only in group 2. BMD continued to decline in group1 while improving (p<0.01) in group 2; BMD being significantly greater than group 1 (p<0.01). Conclusion: In subjects receiving chronic prednisone therapy, low BMD is induced by multiple mechanisms: osteomalacia caused by decreased 125 OH Vit D and osteoporosis caused by matrix collagen breakdown, hypogonadism and secondary hyperparathyroidism. Role of osteomalacia is confirmed by rising BMD on substituting active 125 OH vitamin D3, Calcitriol for inactive vitamin D3, Cholecalciferol.
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骨化三醇替代胆钙化醇改善泼尼松诱导的难治性骨质疏松症的骨密度
介绍/目的:强的松治疗后骨密度下降归因于骨质疏松。然而,低125 OH维生素D导致的骨软化症和由此导致的甲状旁腺功能亢进也可能是原因之一。因此,在接受慢性强的松治疗和对双磷酸盐、钙和维生素D3、胆骨化醇治疗难治的低骨密度(T< 2.5)患者中,研究了125 OH维生素D3、骨化三醇对骨密度的影响。方法:21例患者,年龄45-56岁,接受强的松治疗≥3年,经胆骨化醇、碳酸钙和二磷酸盐治疗后骨密度下降,随机分为两组。两组均继续使用钙和双磷酸盐。10例(1组)增加胆骨化醇剂量,每日2000单位;11例(2组)用骨化三醇替代。每6个月测定一次综合代谢组(CMP),包括血清钙和碱性磷酸酶以及25 OH Vit D和125 OH Vit D水平。骨密度每隔一年测定一次。结果:两组CMP包括钙、磷均保持正常,而单组碱性磷酸酶下降。两组血清25oh - Vit D水平均低于正常水平(<20 pg/ml),仅在2组血清25oh - Vit D水平正常(53±6 pg/ml)。1组骨密度持续下降,2组骨密度升高(p<0.01);BMD显著大于1组(p<0.01)。结论:在慢性强的松治疗的受试者中,低骨密度是由多种机制引起的:由125 OH - Vit D降低引起的骨软化,由基质胶原分解、性腺功能减退和继发性甲状旁腺功能亢进引起的骨质疏松。骨软化症的作用是通过用活性125 OH维生素D3、骨化三醇取代非活性维生素D3、胆骨化醇来提高骨密度来证实的。
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