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作 者:应若素[1] 李粤平[1] 戴朝霞[1] 刘惠媛[1] 林路平[1] 肖蕾[1] 石裕明[1] 杨湛[1] 许敏[1]
出 处:《中华生物医学工程杂志》2014年第6期464-466,共3页Chinese Journal of Biomedical Engineering
摘 要:目的探讨核苷(酸)类似物致慢性乙型肝炎患者乳酸性酸中毒(LA)的临床表现及其发生机制。方法回顾性分析本科室2012至2013年应用核苷(酸)类似物抗乙型肝炎病毒(HBV)治疗过程中发生LA的2例患者的临床资料,包括患者的临床表现、实验室检查资料。采用双标准曲线相对定量PCR法测定2例患者外周血单个核细胞线粒体DNA拷贝数。结果2例患者应用核苷(酸)类似物抗病毒治疗后血乳酸均升高,例1患者血乳酸为4.0mmol/L、例2患者血乳酸最高达31.8mmol/L。例1患者停用替比夫定2个月后血乳酸恢复正常,例2患者及时行连续。肾J往替代治疗后病情改善。2例患者急性期外周血单个核细胞线粒体DNA拷贝数测定显示DNA拷贝数较正常对照均减少,例2患者恢复期线粒体DNA拷贝数较急性期增加。结论核苷(酸)类似物抗病毒治疗引起LA与线粒体损伤有关,临床治疗过程中应高度警惕LA的发生。Objective To investigate the clinical features and pathogenic mechanisms of lactie acidosis (LA) caused by nueleoside analogues in patients with chronic hepatitis B. Methods The clinical data of 2 patients who experienced LA during anti-hepatitis B virus medication with nucleoside analogues between 2012 and 2013 in our department were retrospectively analyzed, including the clinical features and laboratory findings. The DNA copies in the mitoehondria of peripheral blood mononuelear cells (PBMCs) in the 2 patients were examined by relative quantification PCR with double reference calibration curve method. Results After medication with nucleoside analogues as part of the anti-viral treatment, the blood lactic acid increased in both patients, reaching 4.0 mmol/L and 31.8 mmol/L, respectively. The blood lactic acid level returned to normal in Case 1 at 2 months after discontinuation of telbivudine. Case 2 showed clinical improvement after timely performance of the continuous renal replacement therapy. PCR showed fewer DNA copies in the PBMCs mitoehondria in both patients during the acute stage compared with the normal controls, and the mitochondrial DNA copies in Case 2 were increased during the convalescent stage compared with acute stage. Conclusions LA caused by anti-viral treatment with nueleoside analogues is associated with mitoehondrial damage. Physicians should be highly alerted to occurrence of LA during the clinical treatment.
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