目的 探讨磷酸肌酸钠联合复合辅酶对肿瘤患儿多柔比星化疗所致心肌损伤的保护作用.方法 2012年2月至2014年2月在首都医科大学附属北京世纪坛医院化疗的肿瘤患儿153例.其中男112例,女41例;年龄10个月~5岁,中位年龄2.3岁.均给予含多柔比星的方案化疗,其中多柔比星剂量为每疗程20~30mg/(m2 ·d),3d,共3~6疗程.随机分为3组,A组:静脉滴注磷酸肌酸钠(1.0 g/d)联合复合辅酶(1支/d),共7d;B组:仅静脉滴注磷酸肌酸钠,1.0 g/d,共7d;C组:仅静脉输注复合辅酶,1支/d,共7d.每组均于化疗前2d开始保护心肌治疗,化疗前ld和化疗结束后第2天复查血清丙二醛(MDA)、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、心肌肌钙蛋白(cTnT),N端脑钠肽前体(NT-proBNP)、高敏C反应蛋白(hsCRP)、心电图、超声心动图等.比较化疗前后及各组间以上指标的变化.结果 多柔比星心肌损伤的发生率随剂量增加而升高,差异有统计学意义(x2=18.462,P<0.05);磷酸肌酸钠联合复合辅酶预防性治疗患儿心肌损伤的发生率较单用磷酸肌酸钠或复合辅酶者显著下降,差异有统计学意义(x2=4.883、5.971,P均<0.05).与化疗前比较,A组患儿血清cTnT(t=2.561,P<0.05)、NT-proBNP(t=6.654,P<0.01)、hsCRP(t=3.149,P<0.01)水平显著降低;B组患儿血清MDA(t=2.170,P<0.05)、CK-MB(t=2.596,P<0.05)和hsCRP(t=2.604,P<0.05)水平升高;C组患儿血清MDA(t =2.151,P<0.05)和CK-MB(t =4.109,P<0.05)水平显著升高,差异均有统计学意义.化疗后各组间测定结果显示:与A组比较,B组血清MDA(t=4.461,P<0.01)、CK-MB(t=3.273,P<0.01)、eTnT(t=3.476,P <0.01)、NT-proBNP(t =7.081,P <0.01)、hsCRP(t=5.941,P<0.01)水平明显增高,差异均有统计学意义.C组血清MDA(t=4.064,P<0.01)、CK-MB(t=5.452,P<0.01)、cTnT(t=2.768,P<0.05)、NT-proBNP(t=4.806,P<0.01)和hsCRP(t=3.436,P<0.05)水平明显增高,差异均有统计学意义.结论 磷酸肌酸钠和复合辅酶均可减轻多柔比星对心肌细胞的损伤,二者联合应用能更有效地预防蒽环类药物所致心肌损伤,有助于改善肿瘤患儿的预后及提高患儿远期生存质量.
目的 探討燐痠肌痠鈉聯閤複閤輔酶對腫瘤患兒多柔比星化療所緻心肌損傷的保護作用.方法 2012年2月至2014年2月在首都醫科大學附屬北京世紀罈醫院化療的腫瘤患兒153例.其中男112例,女41例;年齡10箇月~5歲,中位年齡2.3歲.均給予含多柔比星的方案化療,其中多柔比星劑量為每療程20~30mg/(m2 ·d),3d,共3~6療程.隨機分為3組,A組:靜脈滴註燐痠肌痠鈉(1.0 g/d)聯閤複閤輔酶(1支/d),共7d;B組:僅靜脈滴註燐痠肌痠鈉,1.0 g/d,共7d;C組:僅靜脈輸註複閤輔酶,1支/d,共7d.每組均于化療前2d開始保護心肌治療,化療前ld和化療結束後第2天複查血清丙二醛(MDA)、肌痠激酶(CK)、肌痠激酶同工酶(CK-MB)、心肌肌鈣蛋白(cTnT),N耑腦鈉肽前體(NT-proBNP)、高敏C反應蛋白(hsCRP)、心電圖、超聲心動圖等.比較化療前後及各組間以上指標的變化.結果 多柔比星心肌損傷的髮生率隨劑量增加而升高,差異有統計學意義(x2=18.462,P<0.05);燐痠肌痠鈉聯閤複閤輔酶預防性治療患兒心肌損傷的髮生率較單用燐痠肌痠鈉或複閤輔酶者顯著下降,差異有統計學意義(x2=4.883、5.971,P均<0.05).與化療前比較,A組患兒血清cTnT(t=2.561,P<0.05)、NT-proBNP(t=6.654,P<0.01)、hsCRP(t=3.149,P<0.01)水平顯著降低;B組患兒血清MDA(t=2.170,P<0.05)、CK-MB(t=2.596,P<0.05)和hsCRP(t=2.604,P<0.05)水平升高;C組患兒血清MDA(t =2.151,P<0.05)和CK-MB(t =4.109,P<0.05)水平顯著升高,差異均有統計學意義.化療後各組間測定結果顯示:與A組比較,B組血清MDA(t=4.461,P<0.01)、CK-MB(t=3.273,P<0.01)、eTnT(t=3.476,P <0.01)、NT-proBNP(t =7.081,P <0.01)、hsCRP(t=5.941,P<0.01)水平明顯增高,差異均有統計學意義.C組血清MDA(t=4.064,P<0.01)、CK-MB(t=5.452,P<0.01)、cTnT(t=2.768,P<0.05)、NT-proBNP(t=4.806,P<0.01)和hsCRP(t=3.436,P<0.05)水平明顯增高,差異均有統計學意義.結論 燐痠肌痠鈉和複閤輔酶均可減輕多柔比星對心肌細胞的損傷,二者聯閤應用能更有效地預防蒽環類藥物所緻心肌損傷,有助于改善腫瘤患兒的預後及提高患兒遠期生存質量.
목적 탐토린산기산납연합복합보매대종류환인다유비성화료소치심기손상적보호작용.방법 2012년2월지2014년2월재수도의과대학부속북경세기단의원화료적종류환인153례.기중남112례,녀41례;년령10개월~5세,중위년령2.3세.균급여함다유비성적방안화료,기중다유비성제량위매료정20~30mg/(m2 ·d),3d,공3~6료정.수궤분위3조,A조:정맥적주린산기산납(1.0 g/d)연합복합보매(1지/d),공7d;B조:부정맥적주린산기산납,1.0 g/d,공7d;C조:부정맥수주복합보매,1지/d,공7d.매조균우화료전2d개시보호심기치료,화료전ld화화료결속후제2천복사혈청병이철(MDA)、기산격매(CK)、기산격매동공매(CK-MB)、심기기개단백(cTnT),N단뇌납태전체(NT-proBNP)、고민C반응단백(hsCRP)、심전도、초성심동도등.비교화료전후급각조간이상지표적변화.결과 다유비성심기손상적발생솔수제량증가이승고,차이유통계학의의(x2=18.462,P<0.05);린산기산납연합복합보매예방성치료환인심기손상적발생솔교단용린산기산납혹복합보매자현저하강,차이유통계학의의(x2=4.883、5.971,P균<0.05).여화료전비교,A조환인혈청cTnT(t=2.561,P<0.05)、NT-proBNP(t=6.654,P<0.01)、hsCRP(t=3.149,P<0.01)수평현저강저;B조환인혈청MDA(t=2.170,P<0.05)、CK-MB(t=2.596,P<0.05)화hsCRP(t=2.604,P<0.05)수평승고;C조환인혈청MDA(t =2.151,P<0.05)화CK-MB(t =4.109,P<0.05)수평현저승고,차이균유통계학의의.화료후각조간측정결과현시:여A조비교,B조혈청MDA(t=4.461,P<0.01)、CK-MB(t=3.273,P<0.01)、eTnT(t=3.476,P <0.01)、NT-proBNP(t =7.081,P <0.01)、hsCRP(t=5.941,P<0.01)수평명현증고,차이균유통계학의의.C조혈청MDA(t=4.064,P<0.01)、CK-MB(t=5.452,P<0.01)、cTnT(t=2.768,P<0.05)、NT-proBNP(t=4.806,P<0.01)화hsCRP(t=3.436,P<0.05)수평명현증고,차이균유통계학의의.결론 린산기산납화복합보매균가감경다유비성대심기세포적손상,이자연합응용능경유효지예방은배류약물소치심기손상,유조우개선종류환인적예후급제고환인원기생존질량.
Objective To explore the protective effect of creatine phosphate sodium and compound coenzyme on tumor children with Adriamycin(ADM)-induced myocardial injury.Methods From Feb.2012 to Feb.2014,there were 153 tumor children administered in Shijitan Hospital,the Capital Medical University,among which there were 112 male and 41 female,aged from 10 months to 5 years,and the median age was 2.3 years.All the cases were randomly divided into 3 groups,with the dose of ADM at 20-30 mg/(m2 · d) for 3 days,and for 3 to 6 courses of treatment.All cases were rolled in the ADM chemotherapy:group A,intravenous infusion of creatine phosphate sodium(1.0 g/d) and compound coenzyme(1 injection/d),at a total of 7 days;group B with only intravenous infusion of creatine phosphate sodium(1.0 g/d) for a total of 7 days;group C with only intravenous infusion compound coenzyme(1 injection/d) for a total of 7 days.Two days before ADM chemotherapy,creatine phosphate sodium and / or compound coenzyme were administrated to protect the musculus cardiacus.One day before chemotherapy and two days after chemotherapy,the peripheral blood was taken to determine levels of malondialdehyde (MDA),creatine kinase (CK),creatine kinase MB (CK-MB),cardiac troponin(cTnT),N terminal pro-brain natriuretic peptide(NT-proBNP),high-sensitivity C-reactive protein(hsCRP),electrocardiogram,echocardiogram and so on.Then the changes of all those indicators before and after the chemotherapy between the groups were compared.Results The morbidity of myocardial damage induced by ADM was increased significantly with its dose accumulation (x2 =18.462,P < 0.05).Creatine phosphate sodium combined with compound coenzyme could decrease the morbidity of myocardial damage induced by ADM (x2 =4.883,5.971,all P < 0.05).Compared with those before chemotherapy,the cTnT (t =2.561,P < 0.05),NT-proBNP (t =6.654,P < 0.01) and hsCRP(t =3.149,P < 0.01) levels of group A decreased markedly.Serum levels of MDA (t =2.170,P <0.05),CK-MB(t =2.596,P <0.05) and hsCRP(t =2.604,P <0.05) of group B increased obviously.Serum levels of MDA (t =2.151,P < 0.05) and CK-MB (t =4.109,P < 0.05) of group C also increased obviously.After chemotherapy,the detection of serum indexes of all groups showed as below.Contracted with those of group A,the serum MDA(t =4.461,P < 0.01),CK-MB (t =3.273,P < 0.01),cTnT (t =3.476,P < 0.01),NT-proBNP (t =7.081,P < 0.01) and hsCRP(t =5.941,P < 0.01) levels of group B increased distinctly.Meanwhile,the MDA (t =4.064,P <0.01),CK-MB(t =5.452,P <0.01),cTnT(t =2.768,P <0.05),NT-proBNP(t =4.806,P <0.01)and hsCRP(t =3.436,P < 0.05) levels of group C also increased significantly.Conclusions Both creatine phosphate and compound coenzyme could reduce the myocardial damage induced by ADM.Combination of them has important clinical value for better prevention of cardiac toxicity of ADM,enhancement of the prognosis of childhood tumor,and improvement of the long-term quality life of those children.