中南大学学报(医学版)
中南大學學報(醫學版)
중남대학학보(의학판)
JOURNAL OF CENTRAL SOUTH UNIVERSITY (MEDICAL SCIENCES)
2013年
7期
681-685
,共5页
罗玉梅%姜文玲%许丹焰%姜德谦
囉玉梅%薑文玲%許丹燄%薑德謙
라옥매%강문령%허단염%강덕겸
代谢综合征%心血管重构%过氧化物酶体增殖物激活受体-γ
代謝綜閤徵%心血管重構%過氧化物酶體增殖物激活受體-γ
대사종합정%심혈관중구%과양화물매체증식물격활수체-γ
metabolic syndrome%cardiovascular remodeling%peroxisome proliferator-activated receptor-γ
目的:通过观察吡格列酮干预对代谢综合征患者颈动脉内中膜厚度、斑块阳性率的影响,为改善代谢综合征患者动脉重构寻找新的方法。方法:将代谢综合征患者分为对照组(n=60)和吡格列酮组(n=61),所有患者均给予降压、降胆固醇、降糖等基础治疗,吡格列酮组加用吡格列酮(15 mg/d),对照组加用安慰剂(维生素C)干预24周。采用彩色多普勒超声测量2组患者干预后颈动脉内中膜厚度及斑块阳性率,用日本日立7600-020自动生化分析仪测定空腹血清三酰甘油、总胆固醇、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、游离脂肪酸、空腹血糖、餐后2小时血糖及肝肾功能等生化指标;分析比较干预后吡格列酮组和对照组患者颈动脉内中膜厚度、斑块阳性率及各血生化指标的差异。结果:干预后,与对照组比较,吡格列酮组患者颈动脉斑块阳性率较对照组明显降低(P<0.05),颈动脉内中膜厚度无明显差异(P>0.05),血清三酰甘油、游离脂肪酸水平降低(P<0.05),其他生化指标无明显差异(P>0.05)。结论:吡格列酮干预可改善代谢综合征组患者颈动脉重构,较基础治疗更显著地抑制其斑块形成。
目的:通過觀察吡格列酮榦預對代謝綜閤徵患者頸動脈內中膜厚度、斑塊暘性率的影響,為改善代謝綜閤徵患者動脈重構尋找新的方法。方法:將代謝綜閤徵患者分為對照組(n=60)和吡格列酮組(n=61),所有患者均給予降壓、降膽固醇、降糖等基礎治療,吡格列酮組加用吡格列酮(15 mg/d),對照組加用安慰劑(維生素C)榦預24週。採用綵色多普勒超聲測量2組患者榦預後頸動脈內中膜厚度及斑塊暘性率,用日本日立7600-020自動生化分析儀測定空腹血清三酰甘油、總膽固醇、高密度脂蛋白膽固醇、低密度脂蛋白膽固醇、遊離脂肪痠、空腹血糖、餐後2小時血糖及肝腎功能等生化指標;分析比較榦預後吡格列酮組和對照組患者頸動脈內中膜厚度、斑塊暘性率及各血生化指標的差異。結果:榦預後,與對照組比較,吡格列酮組患者頸動脈斑塊暘性率較對照組明顯降低(P<0.05),頸動脈內中膜厚度無明顯差異(P>0.05),血清三酰甘油、遊離脂肪痠水平降低(P<0.05),其他生化指標無明顯差異(P>0.05)。結論:吡格列酮榦預可改善代謝綜閤徵組患者頸動脈重構,較基礎治療更顯著地抑製其斑塊形成。
목적:통과관찰필격렬동간예대대사종합정환자경동맥내중막후도、반괴양성솔적영향,위개선대사종합정환자동맥중구심조신적방법。방법:장대사종합정환자분위대조조(n=60)화필격렬동조(n=61),소유환자균급여강압、강담고순、강당등기출치료,필격렬동조가용필격렬동(15 mg/d),대조조가용안위제(유생소C)간예24주。채용채색다보륵초성측량2조환자간예후경동맥내중막후도급반괴양성솔,용일본일립7600-020자동생화분석의측정공복혈청삼선감유、총담고순、고밀도지단백담고순、저밀도지단백담고순、유리지방산、공복혈당、찬후2소시혈당급간신공능등생화지표;분석비교간예후필격렬동조화대조조환자경동맥내중막후도、반괴양성솔급각혈생화지표적차이。결과:간예후,여대조조비교,필격렬동조환자경동맥반괴양성솔교대조조명현강저(P<0.05),경동맥내중막후도무명현차이(P>0.05),혈청삼선감유、유리지방산수평강저(P<0.05),기타생화지표무명현차이(P>0.05)。결론:필격렬동간예가개선대사종합정조환자경동맥중구,교기출치료경현저지억제기반괴형성。
Objective:To observe the effect of pioglitazone on carotid artery intima-media thickness (IMT) and plaque-positive rate in patients with metabolic syndrome, and to ifnd a new way to improve arterial remodeling in patients with metabolic syndrome. Methods:Patients with metabolic syndrome were randomly divided into a control group (n=60) and a pioglitazone group (n=61). All subjects received basic therapeutic measures, i.e, appropriate medication to control blood pressure, blood sugar and cholesterol. Pioglitazone (15 mg/d) was given to patients in the pioglitazone group, and placebo (vitamin C) in the control group for 24 weeks. Color doppler ultrasound was used to measure carotid artery IMT and plaque-positive rate of patients in the 2 groups atfer the intervention. Japan’s Hitachi 7600-020 automatic biochemical analyzer was used to measure fasting serumal triglycerides, total cholesterol, high density lipoprotein cholesterol, low-density lipoprotein cholesterol, free fatty acids, fasting blood glucose, 2-hour postprandial glucose and liver and kidney function, etc. The differences between groups after the intervention were analyzed and compared in IMT, plaque-positive rate and all blood biochemical indicators. Results:Atfer the intervention, compared with the control group, carotid artery plaque-positive rate and the levels of triglyceride and free fatty acid decreased in the pioglitazone group (P<0.05), but there was no difference in IMT of carotid artery and other blood biochemical indicators between the 2 groups (P>0.05). Conclusion:Pioglitazone intervention can significantly improve pathologic artery remodeling, and it can more effectively inhibit the arterial plaque-formation than basic therapeutic measures in patients with metabolic syndrome.