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目的:对阿德福韦酯(ADV)致低血磷性骨软化症病例进行临床分析,提高对此病的认识。方法:回顾性分析11例ADV致低血磷性骨软化症病例的病史资料及生化检查(转氨酶、白蛋白、肌酐、尿酸、血糖、血pH、BE)、骨代谢标志物检查(25OHD_3、PTH、tP1NP、β-CTX、OC)、尿液检查(尿pH、24 h尿钙、24 h尿磷、24 h尿蛋白、尿肌酐)、X线双能骨密度值、骨扫描结果。并分别于停用ADV 1个月和2016年7月对11例患者症状、血磷及AKP水平、尿常规进行复查随访。结果:11例患者服用ADV时间(5.7±1.2)年,骨痛时间(2.2±0.6)年,血磷水平(0.45±0.099)mmol·L~(-1),24h尿磷水平(17.9±4.8)mmol,AKP(248±107)U·L~(-1),肾磷酸根阈值(0.31±0.10)mmol·L~(-1)。停用ADV1个月后随访:患者骨痛缓解,在补磷情况下血磷上升。2016年7月随访:平均停用ADV(18.3±10.7)月;相较于入院时及停药1个月时血磷显著升高、AKP显著降低(P均<0.05);2例血磷恢复正常,血磷恢复率为20%(2/10)。回归分析显示:影响入院时血磷的因素是肾磷酸根阈值和tP1NP(P<0.05);影响最后随访时血磷的因素是入院时的骨密度值(P<0.05)。结论:低血磷性骨软化症是用ADV潜在不良反应,所致肾损害并不完全可逆,在临床工作中应引起重视。
OBJECTIVE: To analyze the clinical data of adefovir dipivoxil-induced hypophosphatemia osteomalacia (CFRP) and to raise awareness of the disease. Methods: The clinical data, biochemical tests (aminotransferase, albumin, creatinine, uric acid, blood glucose, blood pH, BE) and bone metabolic markers (25OHD_3, PTH , TP1NP, β-CTX, OC), urinalysis (urinary pH, 24 h urinary calcium, 24 h urinary phosphate, 24 h urinary protein, urinary creatinine), X-ray dual energy BMD and bone scan results. The follow-up of 11 patients with symptoms, serum phosphorus and AKP levels and urinary routine examination was performed in 1 month after discontinuation of ADV and July 2016 respectively. Results: Eleven patients took ADV (5.7 ± 1.2) years, bone pain time (2.2 ± 0.6) years, serum phosphate level (0.45 ± 0.099) mmol·L -1, 24h urine phosphate level (17.9 ± 4.8) ), AKP (248 ± 107) U · L -1, and the threshold of renal phosphate (0.31 ± 0.10) mmol·L -1. Discontinuation of ADV1 months after follow-up: Patients with bone pain relief, phosphorus uptake in the case of phosphorus. The July follow-up in July 2016: mean discontinuation of ADV was (18.3 ± 10.7) months; AKP was significantly lower than that on admission and 1 month after withdrawal (all P <0.05); 2 cases of recovery of serum phosphorus Normal, phosphorus recovery rate was 20% (2/10). Regression analysis showed that the factors influencing phosphorus on admission were the threshold of renal phosphate and tP1NP (P <0.05). The factors influencing the final blood phosphorus at the final follow-up were the bone mineral density at admission (P <0.05). CONCLUSION: Hypophosphatemia osteomalacia is a potential adverse reaction with ADV. Renal damage is not completely reversible, and should be paid more attention in clinical practice.