目的 比较氟伐他汀及缬沙坦对2型糖尿病早期肾病相关炎症因子的影响及对糖尿病肾病的保护作用.方法 2型糖尿病早期肾病共90例,其中常规降糖治疗组作为对照组(DN1组),在常规降糖治疗基础上加用缬沙坦作为缬沙坦组(DN2组),在常规降糖治疗基础上加用氟伐他汀作为氟伐他汀组(DN3组).分别测定各组患者治疗前后的血糖、血脂、血肌酐(SCr)、C反应蛋白(CRP)、24 h尿蛋白定量、尿白蛋白排泄率(UAER)及数种炎症因子.结果 (1)干预前3组的血清CRP、转化生长因子-β1(TGF-β1)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、白细胞介素-18(IL-18)浓度差异无统计学意义.DN2组治疗后与治疗前相比,IL-6[(15.99±2.87)ng/L与(17.64±2.91)ng/L,t=-3.091,P<0.01]、TNF-α[(48.72±14.62)ng/L与(52.56±17.02)ng/L,t=-2.131,P<0.05]、TGF-β1[(33.54±10.69)μg/L与(40.11±12.08)μg/L,t=-2.921,P<0.01]、IL-18[(139.65±66.37)ng/L与(158.74±74.20)μg/L,t=-2.053,P<0.05]、CRP[(5.12±3.54)mg/L与(6.08±3.39)mg/L,t=-2.072,P<0.05]均明显降低;DN3组治疗后与治疗前相比,IL-6[(15.39±2.77)ng/L与(16.49±2.81)ng/L,t=-2.071,P<0.05]、TNF-α[(45.89 ±16.22)ng/L与(53.04 ±17.02)ng/L,t=-3.651,P<0.01]、TGF-β1[(31.19±10.48)μg/L与(37.11±11.76)μg/L,t=-2.963,P<0.01]、IL-18[(141.54±66.65)ng/L与(158.01±73.23)ng/L,t=-2.182,P<0.05]、CRP[(4.94±3.61)mg/L与(5.86±3.46)mg/L,t=-2.110,P<0.05]亦均明显降低.DN2、DN3组治疗后的炎症因子含量差异无统计学意义(P>0.05).(2)在DN2、DN3组治疗前后血压均无差异情况下,DN2组治疗后与治疗前比较,UAER[(63.1±31.7)μg/min与(82.9±40.0)μg/min,t=-2.145,P<0.05]、24 h尿蛋白定量[(0.14±0.11)g/24 h与(0.18±0.15)g/24 h,t=-2.438,P<0.05]、尿微量白蛋白/肌酐(ALb/Cr)[(114.7±68.1)mg/g与(162.0 ±83.8)mg/g,t=-2.399,P<0.05]均明显降低,DN3组治疗后与治疗前比较,UAER[(65.5±32.6)μg/min与(83.5±42.1)μg/min,t=-2.131,P<0.05]、24 h尿蛋白定量[(0.15±0.12)g/24 h与(0.18±0.13)g/24h,t=-2.611,P<0.05]、尿ALb/Cr[(119.1±78.2)mg/g与(160.0±82.3)mg/g,t=-2.213,P<0.05]亦均明显降低,但2组治疗后结果 比较差异均无统计学意义(P均>0.05).结论 2型糖尿病肾病患者用缬沙坦、氟伐他汀均能降低尿蛋白,降低相关血清炎症因子含量,提示对肾功能具有保护作用.
目的 比較氟伐他汀及纈沙坦對2型糖尿病早期腎病相關炎癥因子的影響及對糖尿病腎病的保護作用.方法 2型糖尿病早期腎病共90例,其中常規降糖治療組作為對照組(DN1組),在常規降糖治療基礎上加用纈沙坦作為纈沙坦組(DN2組),在常規降糖治療基礎上加用氟伐他汀作為氟伐他汀組(DN3組).分彆測定各組患者治療前後的血糖、血脂、血肌酐(SCr)、C反應蛋白(CRP)、24 h尿蛋白定量、尿白蛋白排洩率(UAER)及數種炎癥因子.結果 (1)榦預前3組的血清CRP、轉化生長因子-β1(TGF-β1)、白細胞介素-6(IL-6)、腫瘤壞死因子-α(TNF-α)、白細胞介素-18(IL-18)濃度差異無統計學意義.DN2組治療後與治療前相比,IL-6[(15.99±2.87)ng/L與(17.64±2.91)ng/L,t=-3.091,P<0.01]、TNF-α[(48.72±14.62)ng/L與(52.56±17.02)ng/L,t=-2.131,P<0.05]、TGF-β1[(33.54±10.69)μg/L與(40.11±12.08)μg/L,t=-2.921,P<0.01]、IL-18[(139.65±66.37)ng/L與(158.74±74.20)μg/L,t=-2.053,P<0.05]、CRP[(5.12±3.54)mg/L與(6.08±3.39)mg/L,t=-2.072,P<0.05]均明顯降低;DN3組治療後與治療前相比,IL-6[(15.39±2.77)ng/L與(16.49±2.81)ng/L,t=-2.071,P<0.05]、TNF-α[(45.89 ±16.22)ng/L與(53.04 ±17.02)ng/L,t=-3.651,P<0.01]、TGF-β1[(31.19±10.48)μg/L與(37.11±11.76)μg/L,t=-2.963,P<0.01]、IL-18[(141.54±66.65)ng/L與(158.01±73.23)ng/L,t=-2.182,P<0.05]、CRP[(4.94±3.61)mg/L與(5.86±3.46)mg/L,t=-2.110,P<0.05]亦均明顯降低.DN2、DN3組治療後的炎癥因子含量差異無統計學意義(P>0.05).(2)在DN2、DN3組治療前後血壓均無差異情況下,DN2組治療後與治療前比較,UAER[(63.1±31.7)μg/min與(82.9±40.0)μg/min,t=-2.145,P<0.05]、24 h尿蛋白定量[(0.14±0.11)g/24 h與(0.18±0.15)g/24 h,t=-2.438,P<0.05]、尿微量白蛋白/肌酐(ALb/Cr)[(114.7±68.1)mg/g與(162.0 ±83.8)mg/g,t=-2.399,P<0.05]均明顯降低,DN3組治療後與治療前比較,UAER[(65.5±32.6)μg/min與(83.5±42.1)μg/min,t=-2.131,P<0.05]、24 h尿蛋白定量[(0.15±0.12)g/24 h與(0.18±0.13)g/24h,t=-2.611,P<0.05]、尿ALb/Cr[(119.1±78.2)mg/g與(160.0±82.3)mg/g,t=-2.213,P<0.05]亦均明顯降低,但2組治療後結果 比較差異均無統計學意義(P均>0.05).結論 2型糖尿病腎病患者用纈沙坦、氟伐他汀均能降低尿蛋白,降低相關血清炎癥因子含量,提示對腎功能具有保護作用.
목적 비교불벌타정급힐사탄대2형당뇨병조기신병상관염증인자적영향급대당뇨병신병적보호작용.방법 2형당뇨병조기신병공90례,기중상규강당치료조작위대조조(DN1조),재상규강당치료기출상가용힐사탄작위힐사탄조(DN2조),재상규강당치료기출상가용불벌타정작위불벌타정조(DN3조).분별측정각조환자치료전후적혈당、혈지、혈기항(SCr)、C반응단백(CRP)、24 h뇨단백정량、뇨백단백배설솔(UAER)급수충염증인자.결과 (1)간예전3조적혈청CRP、전화생장인자-β1(TGF-β1)、백세포개소-6(IL-6)、종류배사인자-α(TNF-α)、백세포개소-18(IL-18)농도차이무통계학의의.DN2조치료후여치료전상비,IL-6[(15.99±2.87)ng/L여(17.64±2.91)ng/L,t=-3.091,P<0.01]、TNF-α[(48.72±14.62)ng/L여(52.56±17.02)ng/L,t=-2.131,P<0.05]、TGF-β1[(33.54±10.69)μg/L여(40.11±12.08)μg/L,t=-2.921,P<0.01]、IL-18[(139.65±66.37)ng/L여(158.74±74.20)μg/L,t=-2.053,P<0.05]、CRP[(5.12±3.54)mg/L여(6.08±3.39)mg/L,t=-2.072,P<0.05]균명현강저;DN3조치료후여치료전상비,IL-6[(15.39±2.77)ng/L여(16.49±2.81)ng/L,t=-2.071,P<0.05]、TNF-α[(45.89 ±16.22)ng/L여(53.04 ±17.02)ng/L,t=-3.651,P<0.01]、TGF-β1[(31.19±10.48)μg/L여(37.11±11.76)μg/L,t=-2.963,P<0.01]、IL-18[(141.54±66.65)ng/L여(158.01±73.23)ng/L,t=-2.182,P<0.05]、CRP[(4.94±3.61)mg/L여(5.86±3.46)mg/L,t=-2.110,P<0.05]역균명현강저.DN2、DN3조치료후적염증인자함량차이무통계학의의(P>0.05).(2)재DN2、DN3조치료전후혈압균무차이정황하,DN2조치료후여치료전비교,UAER[(63.1±31.7)μg/min여(82.9±40.0)μg/min,t=-2.145,P<0.05]、24 h뇨단백정량[(0.14±0.11)g/24 h여(0.18±0.15)g/24 h,t=-2.438,P<0.05]、뇨미량백단백/기항(ALb/Cr)[(114.7±68.1)mg/g여(162.0 ±83.8)mg/g,t=-2.399,P<0.05]균명현강저,DN3조치료후여치료전비교,UAER[(65.5±32.6)μg/min여(83.5±42.1)μg/min,t=-2.131,P<0.05]、24 h뇨단백정량[(0.15±0.12)g/24 h여(0.18±0.13)g/24h,t=-2.611,P<0.05]、뇨ALb/Cr[(119.1±78.2)mg/g여(160.0±82.3)mg/g,t=-2.213,P<0.05]역균명현강저,단2조치료후결과 비교차이균무통계학의의(P균>0.05).결론 2형당뇨병신병환자용힐사탄、불벌타정균능강저뇨단백,강저상관혈청염증인자함량,제시대신공능구유보호작용.
Objective To compare the effects of fluvastatin and valsartan on the inflammatory cytokines in the early stage of type 2 diabetic nephropathy and their protective effects on to diabetic nephropathy. Methods Ninety patients with early stage of type 2 diabetic nephropathy were divided into three groups, 30 patients receiving routine hypoglycemic agents (DN1) as control,30 patients receiving routine hypoglycemic agents plus valsartan (DN2) and the other 30 receiving routine hypoglycemic agents plus fluvastatin (DN3). Blood glucose, blood lipid,serum creatinine and C reactive protein(CRP),24-hour urine protein,urinary albumin excretion rate (UAER) and several inflammatory cytokine were measured before and after treatment. Results ( 1 ) No significant difference of the levels of serum CRP,TGF-β1,IL-6,TNF-α, IL-18 at the baseline were observedamong these three groups.In the DN2 group,after treatment,IL.6 was([15.99±2.87]ng/L and[17.64±2. 131 ,P <0. 05) ,TGF-β1 was ( [33.54 ±10. 69] μg/L and [40. 11 ± 12. 08] μg/L,t = -2. 921 ,P <0. 01 ),IL-18 was ( [139.65±66. 37] ng/L and [158.74±74. 20]ng/L,t = -2.053,P <0. 05),CRP was ( [5. 12±3. 54] mg/L and [6. 08 ±3. 39] mg/L, t = - 2. 072, P < 0. 05 ) after and before treatment, respectively. All abovemented indices significantly decreased after treatment. In the DN3 group, IL-6 was ( [15. 39 ±2. 77] ng/L ng/L,t = -3. 651 ,P <0. 01 ) ,TGF-β1 was ( [31.19 ±10. 48] μg/L and [37. 11± 11.76] μg/L,t = -2. 963,P<0.01),IL-18 was ([141.54 ±66.65] ng/L and [158.01±73.23] ng/L,t = -2. 182,P <0.05),CRP respectively. All abovemented indices significantly decreased after treatment No significant difference was observed on inflamaory factors after treatment between the DN2 and DN3 group ( P > 0. 05). (2) In the subgroup that there was no difference in blood pressure between before and after treatment in both the DN2 and DN3 group,in the DN3 group,UAER was ([63. 1 ±31.7] μg/min and[82.9±40.0] μg/min,t = -2. 145,P <0. 05) ,24 h total urokinase protein was ( [0. 14 ±0. 11] g/24 h and [0. 18±O. 15] g/24 h, t = - 2. 438, P <0. 05 ), microalbuminuria/urine creatinine was ( [ALb/Cr] [114. 7±68. 1] mg/g and [162.0±83.8] mg/g,t = - 2. 399, P < 0. 05 ) after and before treatment. All abovemention indices significantly decreased after treatment. In the DN3 group, UAER was ( [65.5 ±32. 6]μg/min and [83.5 ±42. 1]μg/min,t = - 2. 131, P <0. 05 ),24 h total urine protein was ( [0. 14 ±0. 11] g/24 h and [0. 18±0. 15] g/24 h, t = - 2. 438, P < 0. 05 ),0. 05 ) after and before treatment. All abovemention indices significantly decreased after treatment. No significant difference was observed after treatment between the DN2 and ON3 group ( P > 0. 05 ). Conclusion Both valsartan and fluvastatin are able to protect the renal function of patients with type 2 diabetic nephropathy by decreasing the levels of urine proteins and correlated serum inflammatory cytokines.
