细胞因子和糖尿病心肌病

Diabetic cardiomyopathy (DCM), as an independent diabetic cardiac complication, has been paid more attention to. In clinical study, DCM was characterized by left ventricular diastolic dysfunction at the early stage. The pathogenesis of DCM is characterized by myocyte hypertrophy and cardiac fibrosis,ex-tracellular matrix accumulation and deposition. The development of DCM is multifactorial, the mechanism is still unclear. Several mechanisms are involved in the pathogenesis of DCM including myocardial fibrosis,in-terstitial inflammation and endothelial dysfunction. Cytokines can involve in multiple pathophysiological processes. In this review, the relationships between transforming growth factor-β1, connective tissue growth factor, tumor necrosis factor-α, insulin-like growth factor-1 ,adiponectin ,thrombospondin-1 and DCM are sum-marized. It may be the basis of therapeutic approaches for ameliorating DCM.     

地塞米松切不可长期使用

最近我们收治的一位男性患者患支气管哮喘多年,中西药治疗效果不好。医师介绍他服用地塞米松,服后平喘效果很好,于是6年来他经常服用地塞米松,以致发生了严重的医源性类固醇性糖尿病。数年来的高血糖毒性损害了他的胰岛B细胞功能,导致多种口服降糖药治疗均无效,经胰岛素治疗后血糖才得以控制。该患者由于长期服用地塞米松,使下丘脑-垂体-肾上腺轴（HPA轴）功能受到严重抑制,表现为肾上腺皮质功能低下,需给予氢化可的松替代治疗。     

从血糖说起

血糖是指血液中的葡萄糖，在诊断时主张用静脉血浆测定，空腹是指至少8小时内无任何热量摄入时的血糖。空腹血糖正常范围为3．9～5．6mmol／L，临床上常嘱患者晚餐后不再进食，直至第二天早晨空腹采取静脉血测定，即为空腹血糖。     

慢性淋巴细胞性甲状腺炎15例误诊分析

慢性淋巴细胞性甲状腺炎(桥本甲状腺炎)极易误诊,本文分析15例误诊病例,供提高诊断参考。一、临床资料:见表1。     

风湿病·遗传·感染

说起风湿病,人们就会联想起风湿热和风湿性心脏病。这是一种由于溶血性链球菌感染引起的延迟过敏反应所致的疾病。然而,风湿病所涉及的范围很广泛,其中较常见的有系统性红斑狼疮、类风湿关节炎、系统性硬化症、多发性肌炎、皮肌炎、干燥综合征等疾病。这     

老年糖尿病患者自由基与微血管并发症关系的探讨

目的　探讨老年糖尿病患者自由基和抗氧化能力的变化及其与微血管并发症的关系。　方法　测定 6 5例老年糖尿病患者和 6 5例健康老年对照者血浆或红细胞中脂质过氧化物 (LPO)、超氧化物岐化酶 (SOD)、过氧化氢酶 (CAT)、谷胱甘肽过氧化物酶 (GSH PX)、维生素C(VC)、维生素E(VE)、β 胡萝卜素 (β CAR)、谷胱甘肽 (GSH) ,同时测定患者的空腹血糖、餐后 2h血糖、糖化血红蛋白(HbA1c)、空腹和餐后 2hC肽、血脂、尿微量白蛋白排泄率、肌电图。　结果　老年糖尿病患者LPO(42 97± 6 99)nmol/g高于健康老年组 (31 5 9± 7 4 4 )nmol/g ,SOD(1712 4 4± 15 7 0 4 )U/L、CAT(2 17 0 1± 2 9 36 ) μg/g、GSH PX(2 1 0 1± 3 38)× 10 -10 U/RBC、VC(40 98± 10 5 1) μmol/L、VE(16 4 4± 2 4 5 ) μmol/L、β CAR(1 19± 0 2 3) μmol/L、GSH(0 98± 0 16 )nmol/L低于健康老年组〔分别为 (192 8 38± 14 3 4 4 )U/L、(2 6 4 4 0± 6 3 5 5 ) μg/g、(2 5 16± 6 4 1)× 10 -10 U/RBC、(5 2 2 3± 10 5 1) μmol/L、(2 3 0 4± 5 38) μmol/L、(1 6 3± 0 4 0 ) μmol/L、(1 2 5± 0 2 0 )nmol/L〕 ,合并糖尿病微血管并发症者变化更加明显 ,LPO和年龄呈正相关 (r=0 310 ,P <0 0 5 ) ,SOD、C     

吡格列酮临床应用进展

噻唑烷二酮类药物(Thiazoli dilsdioms,TDs)是一类新型的胰岛素增敏剂,主要包括:噻格列酮(Ciglitazone)、曲格列酮(Troglitazone)、罗格列酮(Rosigtiaxone)、吡格列酮(Pi-ogltazone)、嗯格列酮(Enlitazone)等.1997年曲格列酮被欧美及日本最早应用于临床,结果发现曲格列酮可引起严重的肝脏毒性,甚至肝坏死,现已禁止使用.1999年,吡格列酮作为该类药中的第二个新药被美国食品和药品管理局批准上市.该药降糖作用比曲格列酮强10倍,且无明显毒副作用.目前国内已生产(顿灵),并已全面进入临床应用.     

细胞因子和糖尿病心肌病

Diabetic cardiomyopathy (DCM), as an independent diabetic cardiac complication, has been paid more attention to. In clinical study, DCM was characterized by left ventricular diastolic dysfunction at the early stage. The pathogenesis of DCM is characterized by myocyte hypertrophy and cardiac fibrosis,ex-tracellular matrix accumulation and deposition. The development of DCM is multifactorial, the mechanism is still unclear. Several mechanisms are involved in the pathogenesis of DCM including myocardial fibrosis,in-terstitial inflammation and endothelial dysfunction. Cytokines can involve in multiple pathophysiological processes. In this review, the relationships between transforming growth factor-β1, connective tissue growth factor, tumor necrosis factor-α, insulin-like growth factor-1 ,adiponectin ,thrombospondin-1 and DCM are sum-marized. It may be the basis of therapeutic approaches for ameliorating DCM.     

Graves病患者血清中凋亡抑制因子sFas、Bcl-2的初步研究

用ELISA法检测 3 0例Graves病患者治疗前后及 3 2例正常对照组血清中凋亡抑制因子sFas、Bcl 2 ,发现Graves病患者治疗前sFas〔(0 .76± 0 .2 4)ng/L〕、Bcl 2〔1.0 2± 0 .2 3 )ng/L〕含量升高 ;治疗后 (0 .5 2±0 .0 8)ng/L ;(0 .87± 0 .15 )ng/L〕下降 ,与正常对照组〔(0 .5 3± 0 .0 9)ng/L ;(0 .81± 0 .15 )ng/L〕差异无显著性 ,提示sFas、Bcl 2可能参与Graves病的发病。     

细胞因子和糖尿病心肌病

Diabetic cardiomyopathy (DCM), as an independent diabetic cardiac complication, has been paid more attention to. In clinical study, DCM was characterized by left ventricular diastolic dysfunction at the early stage. The pathogenesis of DCM is characterized by myocyte hypertrophy and cardiac fibrosis,ex-tracellular matrix accumulation and deposition. The development of DCM is multifactorial, the mechanism is still unclear. Several mechanisms are involved in the pathogenesis of DCM including myocardial fibrosis,in-terstitial inflammation and endothelial dysfunction. Cytokines can involve in multiple pathophysiological processes. In this review, the relationships between transforming growth factor-β1, connective tissue growth factor, tumor necrosis factor-α, insulin-like growth factor-1 ,adiponectin ,thrombospondin-1 and DCM are sum-marized. It may be the basis of therapeutic approaches for ameliorating DCM.