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Severe rebound effect and multiple fractures after denosumab discontinuation in patient with chronic kidney disease stage 5

机译:慢性肾病阶段患者Denosumab停止后的严重反弹效果和多重骨折

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We report a 46-year old woman with diabetes mellitus type 1, receiving hemodialysis therapy for 7 years. In history it was indicated that she many years took aluminum hydroxide containing antacids to reveal stomach pains. On the 4 th year of that practice she suffered fractures of both heel bones. Low BMD was revealed. The patient consulted by endocrinologist and therapy with denosumab 60 mg given subcutaneously every 6 months was started. Four injections of denosumab were performed, the last one in December 2016. Lumbar spine BMD increased after first year of treatment by 7%. However bone mineral of the distal forearm decreased by 16%. The patient stopped the therapy with denosumab. In August 2017 she suffered bilateral femoral neck fracture after falling down from dialysis chair. In 6 months multiple rib and scapular fractures were revealed. Laboratory analysis showed low level of phosphates (0.42 mmol/l), 25(OH) Vit D (22 ng/ml), high level of alkaline Fig. 1. Study design. Abstracts 77 phosphatase and bone metabolites (β-isomers of CTX - 1.620 ng/ml; PINP - 1425 ng/ml. Intact PTH was 12.1 pmol/l (lab reference ranges: 0.7-5.6 pmol/l). This condition was diagnosed as hypophosphatemic osteomalacia and rebound effect of denosumab discontinuation. High doses of alfacalcidol and phosphate-rich diet were prescribed. Seven months later plasma phosphates level raised to 0.79 mmol/l, intact PTH lowered to 5.2 pmol/l, level of calcium raised slightly, but alkaline phosphatase did not change significantly. However bone resorption continued and patient suffered spontaneous fracture of the right arm. To stop this progressive, parathyroid hormone independent, bone loss we had to administer zoledronic acid. Denosumab is not contraindicated for patients with chronic kidney disease, however it should not be used in hemodialysis patients without serious reasons. If one starts therapy with denosumab, one must envisage what to do after its discontinuation.
机译:我们举办了一名46岁的女性,患有糖尿病型1型,接受血液透析治疗7年。在历史中,它表明许多年份服用含有抗酸盐的氢氧化铝,露出胃痛。在那个练习的第4年,她遭受了两个脚跟的骨折。低BMD被揭示。通过内分泌学家和治疗患者用DeNOSumab咨询60mg每6个月进行一次咨询,每6个月进行一次鉴定。进行了四次掺入的Denosumab,2016年12月的最后一个。腰椎BMD在第一年治疗后增加了7%。然而,远端前臂的骨矿物占16%。患者用Denosumab停止治疗。 2017年8月,她从透析椅下降后,她遭受了双侧股骨颈骨折。在6个月内,揭示了多个肋骨和肩胛骨骨折。实验室分析显示出低水平的磷酸盐(0.42mmol / L),25(OH)Vit D(22ng / ml),高水平的碱性图1.研究设计。摘要77磷酸酶和骨代谢物(CTX的β-异构体 - 1.620ng / ml; PINP-1425 Ng / ml。完整的PTH为12.1 pmol / L(实验室参考范围:0.7-5.6 pmol / L)。这种情况被诊断为低磷酸骨癌和脱肌肉停止的反弹效果。规定了高剂量的阿尔法甲酰胺和富含磷酸盐的饮食。七个月后血浆磷酸盐水平升至0.79mmol / L,完整的Pth降至5.2 pmol / L,钙水平升高,但碱性磷酸酶没有显着变化。然而,骨吸收持续,患者患有右臂的自发性骨折。为了阻止这种进步,甲状旁腺激素独立,我们不得不施用唑妥酸的骨质损失。对于慢性肾脏疾病的患者,DeNOSumab对慢性肾脏疾病的患者没有禁忌,然而,在没有严重的原因,它不应该在血液透析患者中​​使用。如果一个人开始用DeNOSumab进行治疗,必须设想停止后该怎么办。

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