Development of osteomalacia in a post-liver transplant patient receiving adefovir dipivoxil
Development of osteomalacia in a post-liver transplant patient receiving adefovir dipivoxil
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DOI：
10.4254/wjh.v2.i12.442
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发表时间：
2010-12-27
影响因子：
2.4
通讯作者：
Sugiyama, Toshiro
中科院分区：
文献类型：
--
作者：
Minemura, Masami;Tokimitsu, Yoshiharu;Sugiyama, Toshiro
我们报告了一例接受活体供肝相关肝移植治疗的患者，该患者在接受含阿德福韦酯（ADV）的抗病毒治疗拉米夫定耐药的B型肝炎病毒感染期间发生骨软化。患者在接受ADV治疗20个月后出现全身性骨痛和严重低磷血症。影像学研究表明存在骨软化。ADV 10 mg/d给药后血浆ADV峰值为38 ng/mL。同时发现ADV影响钙调神经磷酸酶抑制剂他克莫司的代谢，并引起他克莫司血浆浓度升高。停用ADV和补充矿物质可逆转残疾。ADV可引起血浆他克莫司水平升高，这可能与肾功能不全有关。高水平的ADV和他克莫司可引起肾毒性和骨软化。这个病例强调了在接受ADV和他克莫司治疗的肝移植受者中考虑骨软化症诊断的重要性。(C)2010年百世登。All rights reserved.
We report the case of a patient treated with living donor-related liver transplantation who suffered from osteomalacia during adefovir dipivoxil (ADV)-containing antiviral therapy for lamivudine-resistant hepatitis B virus infection. The patient had generalized bone pain, with severe hypophosphatemia after 20 mo of ADV therapy. Radiographic studies demonstrated the presence of osteomalacia. The peak plasma ADV level was 38 ng/mL after administration of ADV at 10mg/day. It was also found that ADV affected the metabolism of tacrolimus, a calcineurin-inhibitor, and caused an increase in the plasma levels of tacrolimus. The disability was reversed with the withdrawal of ADV and with mineral supplementation. ADV can cause an elevation of plasma tacrolimus levels, which may be associated with renal dysfunction. High levels of ADV and tacrolimus can cause nephrotoxicity and osteomalacia. This case highlights the importance of considering a diagnosis of osteomalacia in liver transplantation recipients treated with both ADV and tacrolimus. (C) 2010 Baishideng. All rights reserved.