药物不良反应杂志
藥物不良反應雜誌
약물불량반응잡지
ADVERSE DRUG REACTIONS JOURNAL
2014年
2期
91-94
,共4页
龙靓%李璐璐%阎敏%尹桃
龍靚%李璐璐%閻敏%尹桃
룡정%리로로%염민%윤도
他克莫司%肾损害%老年人
他剋莫司%腎損害%老年人
타극막사%신손해%노년인
Tacrolimus%Kidney injury%Aged
目的 探讨他克莫司致老年患者肾损害的发生情况和相关因素. 方法 以2010年11月1日至2013年10月31日在中南大学湘雅医院住院期间使用他克莫司、年龄＞60岁并有完整病历资料的所有患者为研究对象,收集其病历资料进行回顾性分析.主要分析指标为用药后血清肌酐水平变化、他克莫司全血谷浓度和联合用药情况.以他克莫司全血谷浓度＞ 15.0 μg/L为阳性,对肾损害组和无肾损害组患者应用他克莫司后全血谷浓度阳性率进行比较. 结果 共收集到127例患者,肾损害组11例(肾损害发生率为8.7％),无肾损害组116例.肾损害组男性6例,年龄60 ～ 85(71±6)岁;女性5例,年龄61 ～80(69±11)岁;无肾损害组男性64例,年龄60～89(74±9)岁;女性52例,年龄60～85(70±6)岁,2组性别分布和年龄差异无统计学意义(P＞0.05).应用他克莫司前,肾损害组患者血清肌酐浓度为57 ～ 363(179±90) μmol/L,无肾损害组为42 ～350(150±65) μmol/L,组间差异无统计学意义(P＞0.05).肾损害组患者应用他克莫司5～20(11±6)d后血清肌酐升高为176 ～ 639(358±183)μmol/L,与用药前比较差异有统计学意义(P＜0.05).肾损害组11例患者他克莫司全血谷浓度为5.9～15.1 μg/L,其中9例＞15.0 μg/L,阳性率为81.8％;无肾损害组116例患者为4.7～16.9 μg/L,其中42例＞15.0 μg/L,阳性率为36.2％.2组他克莫司全血谷浓度阳性率差异有统计学意义(P=0.00).11例肾损害患者均联用细胞色素P450 3A酶诱导剂或抑制剂及糖皮质激素,3例同时联用肾毒性药物.11例患者中9例出现肾损害后立即改用其他免疫抑制剂,2例调整给药剂量,均未发生不可逆肾损害. 结论 他克莫司可导致老年患者发生肾损害,该药全血谷浓度及与联用药物的相互作用可能与肾损害的发生相关.
目的 探討他剋莫司緻老年患者腎損害的髮生情況和相關因素. 方法 以2010年11月1日至2013年10月31日在中南大學湘雅醫院住院期間使用他剋莫司、年齡＞60歲併有完整病歷資料的所有患者為研究對象,收集其病歷資料進行迴顧性分析.主要分析指標為用藥後血清肌酐水平變化、他剋莫司全血穀濃度和聯閤用藥情況.以他剋莫司全血穀濃度＞ 15.0 μg/L為暘性,對腎損害組和無腎損害組患者應用他剋莫司後全血穀濃度暘性率進行比較. 結果 共收集到127例患者,腎損害組11例(腎損害髮生率為8.7％),無腎損害組116例.腎損害組男性6例,年齡60 ～ 85(71±6)歲;女性5例,年齡61 ～80(69±11)歲;無腎損害組男性64例,年齡60～89(74±9)歲;女性52例,年齡60～85(70±6)歲,2組性彆分佈和年齡差異無統計學意義(P＞0.05).應用他剋莫司前,腎損害組患者血清肌酐濃度為57 ～ 363(179±90) μmol/L,無腎損害組為42 ～350(150±65) μmol/L,組間差異無統計學意義(P＞0.05).腎損害組患者應用他剋莫司5～20(11±6)d後血清肌酐升高為176 ～ 639(358±183)μmol/L,與用藥前比較差異有統計學意義(P＜0.05).腎損害組11例患者他剋莫司全血穀濃度為5.9～15.1 μg/L,其中9例＞15.0 μg/L,暘性率為81.8％;無腎損害組116例患者為4.7～16.9 μg/L,其中42例＞15.0 μg/L,暘性率為36.2％.2組他剋莫司全血穀濃度暘性率差異有統計學意義(P=0.00).11例腎損害患者均聯用細胞色素P450 3A酶誘導劑或抑製劑及糖皮質激素,3例同時聯用腎毒性藥物.11例患者中9例齣現腎損害後立即改用其他免疫抑製劑,2例調整給藥劑量,均未髮生不可逆腎損害. 結論 他剋莫司可導緻老年患者髮生腎損害,該藥全血穀濃度及與聯用藥物的相互作用可能與腎損害的髮生相關.
목적 탐토타극막사치노년환자신손해적발생정황화상관인소. 방법 이2010년11월1일지2013년10월31일재중남대학상아의원주원기간사용타극막사、년령＞60세병유완정병력자료적소유환자위연구대상,수집기병력자료진행회고성분석.주요분석지표위용약후혈청기항수평변화、타극막사전혈곡농도화연합용약정황.이타극막사전혈곡농도＞ 15.0 μg/L위양성,대신손해조화무신손해조환자응용타극막사후전혈곡농도양성솔진행비교. 결과 공수집도127례환자,신손해조11례(신손해발생솔위8.7％),무신손해조116례.신손해조남성6례,년령60 ～ 85(71±6)세;녀성5례,년령61 ～80(69±11)세;무신손해조남성64례,년령60～89(74±9)세;녀성52례,년령60～85(70±6)세,2조성별분포화년령차이무통계학의의(P＞0.05).응용타극막사전,신손해조환자혈청기항농도위57 ～ 363(179±90) μmol/L,무신손해조위42 ～350(150±65) μmol/L,조간차이무통계학의의(P＞0.05).신손해조환자응용타극막사5～20(11±6)d후혈청기항승고위176 ～ 639(358±183)μmol/L,여용약전비교차이유통계학의의(P＜0.05).신손해조11례환자타극막사전혈곡농도위5.9～15.1 μg/L,기중9례＞15.0 μg/L,양성솔위81.8％;무신손해조116례환자위4.7～16.9 μg/L,기중42례＞15.0 μg/L,양성솔위36.2％.2조타극막사전혈곡농도양성솔차이유통계학의의(P=0.00).11례신손해환자균련용세포색소P450 3A매유도제혹억제제급당피질격소,3례동시련용신독성약물.11례환자중9례출현신손해후립즉개용기타면역억제제,2례조정급약제량,균미발생불가역신손해. 결론 타극막사가도치노년환자발생신손해,해약전혈곡농도급여련용약물적상호작용가능여신손해적발생상관.
Objective To explore the occurrence and related factors of kidney injury induced by tacrolimus in elderly patients.Methods The clinical data of patients who were hospitalized in Xiangya Hospital during December 2011 to October 2013 and had complete medical records,aged ≥ 60 years,and received tacrolimus treatments were collected and analyzed retrospectively.The main analytic indicators included the change of serum creatinine before and after tacrolimus treatment,the blood trough concentration of tacrolimus,and the drug combinations.The tacrolimus trough concentration ＞ 15.0 μg/L was considered as a positive result and the positive rates after tacrolimus treatment in patients in the renal damage and the no renal damage groups were compared.Results A total of 127 patients were enrolled in this study.There were 11 (8.7％)patients in the renal damage group and 116 patients in the no renal damage group.It comprised 6 men with age of 61 to 80 (69 ± 11) years,and 5 women with age of 60 to 85 (69 ± 11) years in the renal damage group; while it comprised 64 men with age of 60 to 89 (74 ± 9) years,and 52 women with age of 60 to 85 (70 ± 6) years in the no renal damage group.There were no statistical significance in gender and age distribution in patients between the 2 groups (P ＞ 0.05).The serum creatinine levels before tacrolimus treatment were 57-363 (179 ± 90) μmol/L in patients in the renal damage group and 42-350 (150 ± 65) μmol/L in patients in the no renal damage group.The difference was no statistical significance between the 2 groups (P ＞0.05).The serum creatinine levels increased to 176-639 (358 ± 183) μmol/L after 5 to 20 (11 ± 6) days receiving tacrolimus treatments in patients in the renal damage group.The difference before and after treatment was statistically significant (P ＜ 0.05).The blood trough concentration of tacrolimus was 5.9-15.1 μg/L in 11 patients in the renal damage group and ＞ 15.0 μg/L (81.8％) in 9 of them; the tacrolimus trough concentration was 4.7-16.9 μg/L in 116 patients in the no renal damage group and ＞ 15.0 μg/L (36.2％) in 42 of them.The difference between the 2 groups was statistically significant (P =0.00).Eleven patients with renal damage were treated with cytochrome P450 3A inducers/ inhibitors combined with glucocorticoid; 3 of them combined with nephrotoxic drug at the same time.When the kidney injury appeared in the 11 patients,tacrolimus was stopped immediately and changed to other immunosuppressants in 9 patients and the drug dosages were adjusted in 2 patients.No irreversible kidney injury occurred in any of the patients.Conclusion Tacrolimus may induce renal damage in elderly patients,which may be related to the blood trough concentration of tacrolimus as well as potential interactions among combined drugs.
