Prevalence of normal coronary angiography in the acute phase of suspected ST-elevation myocardial
中医“治未病”理念在脂肪肝防治中的体现
总第22卷256期2020年12月大众科技Popular Science&TechnologyVol.22No.12December2020中医“治未病"理念在脂肪肝防治中的体现刘谢盛庆寿(广西中医药大学，广西南宁530001)【摘要】中医"治未病”是预防医学的重要组成部分，其理念涵盖了未病先防、既病防变、瘻后防复三个层面。
脂肪性肝病是我国最常见慢性肝病，文章将中医"治未病”理念贯穿脂肪肝的防治始末，对脂肪肝早防御、早发现、早治疗，从而降低治疗成本，提高治疗效率，为临床实践提供新思路。
【关键词】治未病；脂肪肝；防治【中图分类号】R575【文献标识码】A【文章编号】1008-1151(2020)12-0092-03 Embodiment of the Concept of"Preventive Treatment of Disease"of TraditionalChinese Medicine in the Prevention and Treatment of Fatty Liver Abstract:"Preventive treatment of disease**in traditional Chinese medicine is an important part of preventive medicine.Its concept covers three aspects:prevention before disease,prevention of b oth diseases,prevention and recovery after treatment.IF a tty liver disease is the most common chronic liver disease in China.In this paper,the concept of"preventive treatment of disease*'in traditional Chinese medicine runs through the prevention and treatment of fatty liver,so as to prevent,detect and treat fatty liver early,and so as to reduce the treatment cost and improve the treatment efficiency,and provide new ideas for clinical practice.Key words:preventive treatment of disease;fatty liver;prevention引言脂肪性肝病(Fatty Liver Disease,FLD)是由多种病因引起的肝细胞内脂肪堆积过多闪、肝细胞变性、炎性渗出、甚至肝细胞坏死的肝脏病理性表现。
医学论文写作英语：Glamour of Grammar
It can work as grammatical connectors.
e.g.: If dysphagia is present, the radiologist
should… In the presence of dysphagia but a normal
barium swallow endoscopy is indicated.
cf.：
Immunohistochemical analysis of paraffin embedded specimens of eight colon tumours and normal colon mucosa in rats treated with AOM was performed.
English for Writing Medical Research Papers
Glamour of Grammar
I. Nominalization
Definition
Nominalization refers to the use of nouns in place of adjectives, verbs or even clauses.
aggressive immunosuppressive marrow ablative treatment of the recipient.
Fronting is preferred. In EMP and other EST articles, more information is put into the subject. This way of building up the subject is called fronting, which can catch the reader’s attention. e.g.:
铁死亡在心血管疾病中的调节途径及作用
syndromes in patients with angiographically normal or nearnormal(non-obstructive)coronary arteries[J].T rends in CardiovascularMedicine,2018,28(8):541-551.[16]SCALONE G,NICCOLI G,CREA F.Editor's Choice-pathophysiology,diagnosis and management of MINOCA:anupdate[J].European Heart Journal Acute Cardiovascular Care,2019,8(1):54-62.[17]RIEBER J,HUBER A,ERHARD I,et al.Cardiac magneticresonance perfusion imaging for the functional assessment ofcoronary artery disease:a comparison with coronary angiographyand fractional flow reserve[J].European Heart Journal,2006,27(12):1465-1471.[18]PEDRIZZETTI G,CLAUS P,KILNER P J,et al.Principles ofcardiovascular magnetic resonance feature tracking andechocardiographic speckle tracking for informed clinical use[J].Journal of Cardiovascular Magnetic Resonance,2016,18(1):1-12.[19]刘敏.心脏磁共振成像技术临床应用及进展[J].中华老年心脑血管病杂志,2021,23(5):449-451.[20]ZOU Q A,ZHENG T A,ZHOU S L,et al.Quantitative evaluation ofmyocardial strain after myocardial infarction with cardiovascularmagnetic resonance tissue-tracking imaging[J].InternationalHeart Journal,2020,61(3):429-436.[21]李坤成,张振.心脏MR特征追踪技术进展及其临床应用[J].中国医学影像技术,2022,38(1):1-5.[22]CARBERRY J,CARRICK D,HAIG C,et al.Persistence of infarctzone T2hyperintensity at6months after acute ST-segment-elevation myocardial infarction:Incidence,pathophysiology,andprognostic implications[J].Circ Cardiovasc Imaging,2017,10(12):e006586-e006586.[23]SONG L S,MA X H,ZHAO X X,et al.Validation of black blood lategadolinium enhancement(LGE)for evaluation of myocardialinfarction in patients with or without pathological Q-wave onelectrocardiogram(ECG)[J].Cardiovascular Diagnosis andTherapy,2020,10(2):124-134.[24]REINSTADLER S J,STIERMAIER T,LIEBETRAU J,et al.Prognostic significance of remote myocardium alterationsassessed by quantitative noncontrast T1mapping in ST-segmentelevation myocardial infarction[J].JACC:CardiovascularImaging,2018,11(3):411-419.[25]KIM R J,ALBERT T S,WIBLE J H,et al.Performance of delayed-enhancement magnetic resonance imaging with gadoversetamidecontrast for the detection and assessment of myocardialinfarction:an international,multicenter,double-blinded,randomizedtrial[J].Circulation,2008,117(5):629-637.[26]万俊义,赵世华.心脏磁共振钆对比剂延迟强化的临床意义及判断预后的价值[J].中国医学影像技术,2012,28(8):1600-1603. [27]VICENTE-IBARRA N,FELIU E,BERTOMEU-MARTÍNEZ V,et al.Role ofcardiovascular magnetic resonance in the prognosis of patientswith myocardial infarction with non-obstructive coronary arteries[J].Cardiovasc Magn Reson,2021,23(1):83.(收稿日期:2022-08-29)(本文编辑邹丽)铁死亡在心血管疾病中的调节途径及作用王世远,李虹摘要阐述铁死亡的调节途径及其在心血管疾病(CVD)中的作用㊂CVD是我国乃至世界人口死亡和影响生活质量的主要原因,目前,经典的细胞死亡不能完全解释CVD的发生㊁发展,铁死亡的发现进一步补充了CVD发生的可能原因,同时,自噬在铁死亡中发挥着重要作用㊂关键词铁死亡;心血管疾病;自噬;综述d o i:10.12102/j.i s s n.1672-1349.2023.15.016心血管疾病(cardiovascular disease,CVD)是指一组包括心脏病㊁血管病㊁心力衰竭㊁心律失常㊁心脏瓣膜病㊁心肌病㊁心内膜炎等的循环系统疾病㊂CVD的预防㊁治疗㊁预后成为世界范围内生命健康的重要问题㊂细胞死亡在CVD的发生中至关重要㊂一般情况下,心肌细胞和血管细胞死于调节性细胞死亡(RCD),而非意外细胞死亡(ACD),铁死亡(ferroptosis)作为RCD中的新成员,补充了CVD的发生,且自噬在其中发挥重要作用㊂了解铁死亡的调节途径及其在CVD 中的作用,为CVD病人获取更大收益㊂1铁及铁死亡铁是一种微量元素,成人体内含有3~5g的总铁,其中2/3以血红蛋白和肌红蛋白的形式存在,近1/3储存在蛋白中即铁蛋白,而细胞外铁仅占全身铁的0.1%作者单位山西医科大学第二医院(太原030001)通讯作者李虹,E-mail:**********************引用信息王世远,李虹.铁死亡在心血管疾病中的调节途径及作用[J].中西医结合心脑血管病杂志,2023,21(15):2799-2802.左右㊂在机体内,补充铁流失的途径主要有两种,一是在脾脏和其他器官巨噬细胞的作用下,吞噬衰老或损伤的红细胞,释放其中的铁到循环中用于合成血红素[1];二是通过饮食摄入铁[2]㊂铁是参与多种生物过程的必需矿物质元素,如血红素合成㊁DNA合成㊁蛋白质合成㊁催化反应㊁细胞呼吸㊁整体代谢等[3-5]㊂机体铁稳态主要依靠铁调素(hepcidin,阻止细胞铁外流作用)-膜铁转运蛋白(FPN)轴来调节[1]㊂CVD的发生与铁的过载或缺乏密切相关㊂目前,细胞死亡可分为ACD和RCD两种形式[6]㊂RCD主要包括:细胞凋亡(apoptosis)㊁自噬(autophagy)㊁坏死性凋亡(necroptosis)㊁细胞焦亡㊁依赖性细胞死亡(parthanatos)㊁内源性细胞死亡(entosis)㊁溶酶体依赖性细胞死亡(lysosome-dependent cell death,LDCD)㊁氧中毒(oxeiptosis)等形式[7]㊂2012年,Dixon等[8]提出一种新型细胞死亡形式,其特点为非凋亡性㊁铁依赖性的,即铁死亡㊂铁死亡作为RCD新的一员,其线粒体具有致密紧凑㊁嵴缺失㊁膜浓缩及外膜破裂的特点[9]㊂其发生过程中,过载铁在细胞内积聚产生活性氧(ROS),氧化多不饱和脂肪酸,造成细胞膜结构的破坏,最终导致细胞死亡[8]㊂研究表明,铁死亡参与CVD㊁神经退行性疾病㊁肿瘤㊁脑卒中㊁中毒性损伤等多种疾病的发生㊂2铁死亡与自噬自噬是生物体内细胞重要的代谢过程,将衰老或损伤的蛋白质㊁细胞器分解成氨基酸和脂肪酸,可进入循环再次被利用和供应能量,以便维持内环境稳态[10]㊂细胞自噬主要分为以下几个过程:初始自体吞噬泡的形成㊁中间自体吞噬泡的形成㊁降解自体吞噬泡的形成[11]㊂按照溶酶体转运方式和生理功能,自噬主要分为巨自噬㊁微自噬㊁分子伴侣介导的自噬[12]㊂已有研究表明,选择性自噬如铁蛋白吞噬㊁脂肪吞噬㊁时钟吞噬㊁分子伴侣介导的自噬等在铁死亡过程中不可或缺[13];自噬的调节因子如Beclin1㊁核因子E2相关因子2(nuclear factor erythroid derived2-like2, Nrf2)㊁信号转导和转录激活因子3(signal transducer and activator of transcription3,STAT3)㊁p53在铁死亡中发挥着重要的调节作用[14]㊂在生物体内,自噬作用的缺乏或过度均会导致不同程度的RCD[15-16]㊂3铁死亡的调节途径3.1铁代谢细胞内的铁稳态取决于铁的吸收㊁利用㊁储存和排泄之间的动态平衡㊂铁具有活跃的氧化还原能力和不成对的电子特点,成为铁死亡重要的基础因素㊂在正常生物机体内,分泌的胃酸将食物中的Fe3+还原为Fe2+,在十二指肠和空肠上段被吸收㊂在芬顿(Fenton)和类芬顿反应中,Fe2+和过氧化氢(H2O2)反应产生大量羟基自由基和脂质过氧化物,最终导致铁死亡[17]㊂血红素加氧酶1(Hmox1)可将血红素降解生成Fe2+,使游离铁水平增加,进一步导致铁死亡的发生[18-19]㊂在铁蛋白吞噬中,核受体共激活因子4 (NCOA4)将铁蛋白转化为细胞内铁的自噬,并产生游离铁[20-22]㊂研究发现,转录因子BTB结构域和CNC 同源物1(BACH1)是铁代谢的调节剂,在铁死亡中发挥一定作用[23]㊂还有研究发现,由铁蛋白应激诱导的Prominin2可抑制铁蛋白细胞的死亡[24]㊂3.2脂质过氧化多不饱和脂肪酸(PUFAs)是构成细胞膜的重要成分,对维持细胞膜的功能起到重要作用,而PUFAs与自由基相互作用发生的脂质过氧化正是铁死亡的主要原因[25]㊂在长链脂酰辅酶A合成酶4(ACSL4)的催化作用下,PUFAs中的花生四烯酸(AA)和肾上腺酸(AdA)分别合成相应的脂酰辅酶AA-CoA和AdA-CoA,参与膜磷脂的合成,其产物在溶血卵磷脂酰基转移酶3 (LPCAT3)的催化作用下,发生酯化反应生成磷脂酰乙醇胺PE-AA和PE-AdA,再被脂氧合酶(LOXs)或细胞色素P450氧化还原酶(POR)氧化成脂质过氧化产物PE-AA-OOH和PE-AdA-OOH[26]㊂正常情况下,这些有害物质可被谷胱甘肽过氧化物酶4(glutathione peroxidase4,GPX4)还原成没有毒性的脂醇;相反,当机体GPX4处于低水平,其抗氧化作用降低,过氧化物产物会过度积累,引起铁死亡的发生[27-29]㊂3.3Xc-谷胱甘肽(GSH)-GPX4途径GSH具有重要的抗氧化和清除自由基的作用,在谷氨酸-半胱氨酸连接酶(GCL)和谷胱甘肽合酶(GSS)的催化作用下,产生谷氨酸㊁半胱氨酸和甘氨酸㊂GSH有两种形式,还原形式(GSH)和氧化二硫化物形式(GSSG),在自由基等条件刺激下,GPX4发挥其抗氧化或催化脂质氢过氧化物的还原作用,将GSH 转化为GSSG,并将脂质过氧化物(L-OOHs)还原为其相应的脂质醇(L-OHs),限制了脂质过氧化在膜中的扩散,从而减少铁死亡的发生[9,30-32]㊂System Xc-是一种胱氨酸/谷氨酸逆向转运蛋白,可促进胱氨酸和谷氨酸在质膜上的交换,合成GSH[33]㊂相关研究表明,当抑制System Xc-时,可进一步抑制GPX4的抗氧化作用,最终发生铁死亡[34]㊂3.4铁死亡抑制蛋白1(FSP1)-辅酶Q10(CoQ10)-NAD(P)H途径FSP1-CoQ10-NAD(P)H途径是一种与Xc-GSH-GPX4通路协同作用的独立系统,其可独立清除过多的脂质过氧化物,抑制铁死亡的发生[35-36]㊂NADPH是除GSH之外的另一种抗氧化化合物,可通过减少脂质ROS来抑制铁死亡;FSP1是一种氧化还原酶,在NAD(P)H作用下,将泛醌(亦称辅酶Q10,CoQ10)还原为泛醇(CoQH2),CoQH2可通过捕获脂质过氧自由基,抑制脂质过氧化和铁死亡的发生[37]㊂CoQH2是甲羟戊酸途径产生的CoQ10还原形式,抑制甲羟戊酸途径可能会减少CoQ10生成量,进而导致铁死亡[38]㊂3.5三磷酸鸟苷环水解酶1(GCH1)-四氢生物蝶呤(BH4)-二氢叶酸还原酶(DHFR)途径GCH1-BH4-DHFR通路是一种独立于Xc-GSH-GPX4途径的通路,在敲除GPX4诱导铁死亡的模型中,GCH1发挥其保护作用,对其他形式的细胞死亡具有选择性[39]㊂GCH1既是BH4的起始酶,又是限速酶,调节着BH4的含量,DHFR可调节BH4的生成[40]㊂BH4是一种内源性自由基捕获抗氧化剂,通过捕获脂质衍生的过氧自由基阻断脂质过氧化,保护脂质膜免受自身氧化[40]㊂因此,可以得出GCH1-BH4-DHFR通路可通过阻断脂质过氧化抑制铁死亡㊂3.6线粒体线粒体的独有特点 电压依赖性阴离子通道(VDAC)是位于线粒体外膜的蛋白质,当这些蛋白细胞越多,发生铁死亡的敏感性就越高[41]㊂线粒体同样参与着铁死亡的发生,其机制还包括胱氨酸饥饿㊁谷氨酰胺分解,升高膜电位和亚铁含量,促进芬顿反应和脂质过氧化发生,最终造成铁死亡[42-43]㊂4铁死亡与心血管疾病4.1动脉粥样硬化(atherosclerosis,AS)AS是一种以脂质代谢异常为特征的病理过程,主要由脂质沉积㊁内皮细胞损伤㊁氧化应激㊁血管平滑肌细胞(VSMC)增殖㊁巨噬细胞转化㊁炎症和免疫功能障碍等引起[44-45]㊂研究表明,抑制铁死亡可通过减轻脂质过氧化和内皮功能障碍缓解AS,在体内,铁死亡抑制剂Fer-1可减轻高脂饮食的ApoE-/-小鼠诱导的AS 和脂质过氧化;体外细胞实验研究表明,Fer-1可改善氧化型低密度脂蛋白(ox-LDL)诱导的铁死亡和内皮功能障碍[46]㊂4.2心肌梗死(myocardial infarction,MI)MI在全世界具有非常高的致死率㊂研究表明,在MI小鼠模型中,MI部位的铁蛋白重链1(FTH1)水平下降,引起游离铁水平升高和氧化应激发生,促进心肌细胞铁死亡,导致心肌细胞死亡和MI发生[47]㊂有研究表明,与正常组织相比,MI组织中GPX4蛋白的数量减少,引起铁死亡,最终导致MI的发生[48]㊂4.3缺血/再灌注损伤(I/R)I/R通常是指急性心肌梗死血管再通最严重的并发症[49]㊂尤其在再灌注阶段,会产生大量的ROS和自由基,引起心肌细胞损伤坏死和铁死亡[50-51]㊂铁死亡抑制剂Liproxstatin-1(Lip-1),通过降低线粒体上的电压依赖性阴离子通道1(VDAC1)㊁ROS水平和增加GPX4水平保护心肌免受I/R损伤[52-53]㊂由此得出,铁死亡可引起I/R损伤[54]㊂4.4心力衰竭(heart failure,HF)HF是大多数CVD的终末阶段,心脏发生重塑由代偿变为失代偿,出现心肌肥厚和纤维化,最终导致心脏功能的下降[55]㊂已有研究表明,在HF中Toll样受体4(TLR4)和NADPH氧化酶4(NOX4)明显上调,而当敲除TLR4和NOX4时可显著抑制自噬和铁死亡,并对抗心脏重塑和改善心脏功能,为治疗HF提供了基础[56]㊂4.5心肌病阿霉素(DOX)是一种常用的第二代蒽环类抗癌药物,具有很强的心肌毒性,最终导致心肌病㊂有研究表明,在DOX小鼠模型中,Nrf2通过增加血红素加氧酶1(heme oxygenase1,Hmox1)的含量,降解血红素,释放游离铁引起铁过载,导致心肌细胞铁死亡[57];而铁死亡抑制剂Fer-1在该模型中能减轻DOX所致心肌病[57]㊂铁死亡可能在糖尿病心肌病(diabetic cardiomyopathy,DCM)中存在一定作用,但目前机制尚不清楚㊂5小结铁死亡作为一种新的调节性细胞死亡形式出现,参与着CVD的发生㊂本研究一方面从铁代谢㊁脂质过氧化㊁Xc-GSH-GPX4途径㊁FSP1-CoQ10-NAD(P)H 途径㊁GCH1-BH4-DHFR通路㊁线粒体来阐明铁死亡的发生,为阻止铁死亡进而引起心血管疾病提供了研究基础;但其他调节途径机制目前尚未明确,例如能量应激(energy stress)㊁热休克蛋白(HSP)等,可成为进一步的研究点㊂另一方面主要阐明了铁死亡在AS㊁MI㊁I/R损伤㊁HF㊁DOX所致心肌病中的作用,为治疗CVD 提供了新的思路㊂参考文献:[1]PAPANIKOLAOU G,PANTOPOULOS K.Systemic iron homeostasis anderythropoiesis[J].IUBMB Life,2017,69(6):399-413.[2]GREEN R,CHARLTON R,SEFTEL H,et al.Body iron excretion inman:a collaborative study[J].The American Journal of Medicine,1968,45(3):336-353.[3]KOBAYASHI M,SUHARA T,BABA Y,et al.Pathological roles ofiron in cardiovascular disease[J].Current Drug Targets,2018,19(9):1068-1076.[4]ABBASPOUR N,HURRELL R,KELISHADI R.Review on iron andits importance for human health[J].Journal of Research inMedical Sciences,2014,19(2):164-174.[5]ALI M K,KIM R Y,BROWN A C,et al.Critical role for ironaccumulation in the pathogenesis of fibrotic lung disease[J].TheJournal of Pathology,2020,251(1):49-62.[6]TANG D L,KANG R,VANDEN BERGHE T,et al.The molecularmachinery of regulated cell death[J].Cell Research,2019,29(5):347-364.[7]王刚,杨飞飞,罗茂.细胞调节性死亡及其机制的研究[J].西南医科大学学报,2021,44(5):511-519.[8]DIXON S J,LEMBERG K M,LAMPRECHT M R,et al.Ferroptosis:an iron-dependent form of nonapoptotic cell death[J].Cell,2012,149(5):1060-1072.[9]LI J,CAO F,YIN H L,et al.Ferroptosis:past,present and future[J].Cell Death&Disease,2020,11(2):88.[10]CÃTANÃC S,ATANASOV A G,BERINDAN-NEAGOE I.Naturalproducts with anti-aging potential:affected targets and molecularmechanisms[J].Biotechnology Advances,2018,36(6):1649-1656.[11]周罗慧,柏亚明,孙毅,等.血管生成过程中的自噬调控作用及自噬信号通路调控机制研究进展[J].山东医药,2021,61(6):108-111.[12]ZHANG X Y,EVANS T D,JEONG S J,et al.Classical andalternative roles for autophagy in lipid metabolism[J].CurrentOpinion in Lipidology,2018,29(3):203-211.[13]LI N,JIANG W Y,WANG W,et al.Ferroptosis and its emergingroles in cardiovascular diseases[J].Pharmacological Research,2021,166:105466.[14]朱婷,范洋.自噬在细胞铁死亡发生中作用机制的研究进展[J].现代肿瘤医学,2021,29(11):1994-1999.[15]NAKA TOGA W A H.Mechanisms governing autophagosome biogenesis[J].Nature Reviews Molecular Cell Biology,2020,21(8):439-458.[16]AMARAVADI R K,KIMMELMAN A C,DEBNATH J.Targetingautophagy in cancer:recent advances and future directions[J].Cancer Discovery,2019,9(9):1167-1181.[17]HASSANNIA B,VANDENABEELE P,VANDEN BERGHE T.Targeting ferroptosis to iron out cancer[J].Cancer Cell,2019,35(6):830-849.[18]T ANG M Z,CHEN Z,WU D,et al.Ferritinophagy/ferroptosis:iron-relatednewcomers in human diseases[J].Journal of CellularPhysiology,2018,233(12):9179-9190.[19]CHANG L C,CHIANG S K,CHEN S E,et al.Heme oxygenase-1mediates BAY11-7085induced ferroptosis[J].Cancer Letters,2018,416:124-137.[20]BUCCARELLI M,MARCONI M,PACIONI S,et al.Inhibition ofautophagy increases susceptibility of glioblastoma stem cells totemozolomide by igniting ferroptosis[J].Cell Death&Disease,2018,9(8):841.[21]HOU W,XIE Y C,SONG X X,et al.Autophagy promotesferroptosis by degradation of ferritin[J].Autophagy,2016,12(8):1425-1428.[22]GAO M H,MONIAN P,PAN Q H,et al.Ferroptosis is anautophagic cell death process[J].Cell Research,2016,26(9):1021-1032.[23]NISHIZAWA H,MATSUMOTO M,SHINDO T,et al.Ferroptosis iscontrolled by the coordinated transcriptional regulation ofglutathione and labile iron metabolism by the transcription factorBACH1[J].Journal of Biological Chemistry,2020,295(1):69-82.[24]BROWN C W,AMANTE J J,CHHOY P,et al.Prominin2drivesferroptosis resistance by stimulating iron export[J].Developmental Cell,2019,51(5):575-586.[25]CASARES D,ESCRIBÁP V,ROSSELLÓC A.Membrane lipidcomposition:effect on membrane and organelle structure,functionand compartmentalization and therapeutic avenues[J].International Journal of Molecular Sciences,2019,20(9):2167. [26]CHENG J,FAN Y Q,LIU B H,et al.ACSL4suppresses glioma cellsproliferation via activating ferroptosis[J].Oncology Reports,2020,43(1):147-158.[27]LATUNDE-DADA G O.Ferroptosis:role of lipid peroxidation,ironand ferritinophagy[J].Biochimica et Biophysica Acta(BBA)-General Subjects,2017,1861(8):1893-1900.[28]KAGAN V E,MAO G W,QU F,et al.Oxidized arachidonic andadrenic PEs navigate cells to ferroptosis[J].Nature ChemicalBiology,2017,13(1):81-90.[29]YAN B,AI Y W,SUN Q,et al.Membrane damage during ferroptosisis caused by oxidation of phospholipids catalyzed by theoxidoreductases POR and CYB5R1[J].Molecular Cell,2021,81(2):355-369.[30]KOPPULA P,ZHUANG L,GAN B Y.Cystine transporter SLC7A11/xCT in cancer:ferroptosis,nutrient dependency,and cancertherapy[J].Protein&Cell,2021,12(8):599-620.[31]SEIBT T M,PRONETH B,CONRAD M.Role of GPX4inferroptosis and its pharmacological implication[J].Free RadicalBiology and Medicine,2019,133:144-152.[32]BAJIC V P,VAN NESTE C,OBRADOVIC M,et al.Glutathioneredox homeostasis and its relation to cardiovascular disease[J].Oxidative Medicine and Cellular Longevity,2019,2019:5028181. [33]CAO J Y,DIXON S J.Mechanisms of ferroptosis[J].Cellular andMolecular Life Sciences,2016,73(11):2195-2209.[34]PRONETH B,CONRAD M.Ferroptosis and necroinflammation,ayet poorly explored link[J].Cell Death and Differentiation,2019,26(1):14-24.[35]DOLL S,FREITAS F P,SHAH R,et al.FSP1is a glutathione-independent ferroptosis susuker[J].Nature,2019,575(7784):693-698.[36]BERSUKER K,HENDRICKS J M,LI Z P,et al.The CoQoxidoreductase FSP1acts parallel to GPX4ppressor[J].Nature,2019,575(7784):688-692.[37]LEI G,Z HUANG L,GAN B Y.Targeting ferroptosis as avulnerability in cancer[J].Nature Reviews Cancer,2022,22(7):381-396.[38]ZHENG J S,CONRAD M.The metabolic underpinnings offerroptosis[J].Cell Metabolism,2020,32(6):920-937. [39]KRAFT V A N,BEZJIAN C T,PFEIFFER S,et al.GTP cyclohydrolase1/tetrahydrobiopterin counteract ferroptosis through lipid remodeling[J].ACS Central Science,2020,6(1):41-53.[40]SOULA M,WEBER R A,ZILKA O,et al.Metabolic determinants ofcancer cell sensitivity to canonical ferroptosis inducers[J].Nature Chemical Biology,2020,16(12):1351-1360.[41]DEHART D N,FANG D A,HESLOP K,et al.Opening of voltagedependent anion channels promotes reactive oxygen speciesgeneration,mitochondrial dysfunction and cell death in cancercells[J].Biochemical Pharmacology,2018,148:155-162. [42]BATTAGLIA A M,CHIRILLO R,AVERSA I,et al.Ferroptosis andcancer:mitochondria meet the iron maiden cell death[J].Cells,2020,9(6):1505.[43]SHIN D,LEE J,YOU J H,et al.Dihydrolipoamide dehydrogenaseregulates cystine deprivation-induced ferroptosis in head andneck cancer[J].Redox Biology,2020,30:101418.[44]WOLF D,LEY K.Immunity and inflammation in atherosclerosis[J].Circulation Research,2019,124(2):315-327.[45]MARCHIO P,GUERRA-OJEDA S,VILA J M,et al.Targeting earlyatherosclerosis:a focus on oxidative stress and inflammation[J].Oxidative Medicine and Cellular Longevity,2019,2019:8563845. [46]BAI T,LI M X,LIU Y F,et al.Inhibition of ferroptosis alleviatesatherosclerosis through attenuating lipid peroxidation andendothelial dysfunction in mouse aortic endothelial cell[J].FreeRadical Biology and Medicine,2020,160:92-102.[47]OMIYA S,HIKOSO S,IMANISHI Y,et al.Downregulation of ferritinheavy chain increases labile iron pool,oxidative stress and celldeath in cardiomyocytes[J].Journal of Molecular and CellularCardiology,2009,46(1):59-66.[48]PARK T J,PARK J H,LEE G S,et al.Quantitative proteomicanalyses reveal that GPX4downregulation during myocardialinfarction contributes to ferroptosis in cardiomyocytes[J].CellDeath&Disease,2019,10(11):835.[49]IBÁÑEZ B,HEUSCH G,OVIZE M,et al.Evolving therapies formyocardial ischemia/reperfusion injury[J].Journal of theAmerican College of Cardiology,2015,65(14):1454-1471. [50]CADENAS S.ROS and redox signaling in myocardial ischemia-reperfusion injury and cardioprotection[J].Free Radical Biologyand Medicine,2018,117:76-89.[51]YAN H F,TUO Q Z,YIN Q Z,et al.The pathological role offerroptosis in ischemia/reperfusion-related injury[J].ZoologicalResearch,2020,41(3):220-230.[52]FENG Y S,MADUNGWE N B,IMAM ALIAGAN A D,et al.Liproxstatin-1protects the mouse myocardium against ischemia/reperfusion injury by decreasing VDAC1levels and restoringGPX4levels[J].Biochemical and Biophysical ResearchCommunications,2019,520(3):606-611.[53]DABKOWSKI E R,WILLIAMSON C L,HOLLANDER J M.Mitochondria-specific transgenic overexpression of phospholipidhydroperoxide glutathione peroxidase(GPx4)attenuates ischemia/reperfusion-associated cardiac dysfunction[J].Free RadicalBiology and Medicine,2008,45(6):855-865.[54]GAO M H,MONIAN P,QUADRI N,et al.Glutaminolysis andtransferrin regulate ferroptosis[J].Molecular Cell,2015,59(2):298-308.[55]DE COUTO G,OUZOUNIAN M,LIU P P.Early detection ofmyocardial dysfunction and heart failure[J].Nature ReviewsCardiology,2010,7(6):334-344.[56]CHEN X Q,XU S D,ZHAO C X,et al.Role of TLR4/NADPHoxidase4pathway in promoting cell death through autophagyand ferroptosis during heart failure[J].Biochemical andBiophysical Research Communications,2019,516(1):37-43. [57]FANG X X,WANG H,HAN D,et al.Ferroptosis as a target forprotection against cardiomyopathy[J].Proceedings of theNational Academy of Sciences of the United States of America,2019,116(7):2672-2680.(收稿日期:2022-07-23)(本文编辑邹丽)。
独刺鱼际穴治疗支气管哮喘急性发作验案
Advances in Clinical Medicine 临床医学进展, 2023, 13(10), 15435-15439Published Online October 2023 in Hans. https:///journal/acmhttps:///10.12677/acm.2023.13102158独刺鱼际穴治疗支气管哮喘急性发作验案葛楠1，李俐2*1福建中医药大学针灸学院，福建福州2福建中医药大学附属第二人民医院针灸科，福建福州收稿日期：2023年8月28日；录用日期：2023年9月21日；发布日期：2023年10月8日摘要近年来支气管哮喘的全球患病率、死亡率呈上升趋势，而支气管扩张剂等哮喘防治药物易产生免疫抑制、产生耐药性、增加呼吸道感染风险之弊端，使得哮喘的治疗陷入两难。
故探寻支气管哮喘急性发作期时低毒副作用且高效的治疗方法意义重大。
本文通过介绍独刺鱼际穴治疗支气管哮喘急性发作验案2则，阐释独刺鱼际穴对于哮喘急性发作时的临床效能，该法疗效显著、不良反应少，远期随访疗效佳，以期对临床诊疗哮喘有所裨益。
关键词鱼际穴，支气管哮喘，验案Treatment of Acute Attack of BronchialAsthma by Acupuncture Onlyat the Yuji PointNan Ge1, Li Li2*1School of Acupuncture and Moxibustion, Fujian University of Traditional Chinese Medicine, Fuzhou Fujian2Department of Acupuncture and Moxibustion, The Second Affiliated People’s Hospital of Fujian University of Traditional Chinese Medicine, Fuzhou FujianReceived: Aug. 28th, 2023; accepted: Sep. 21st, 2023; published: Oct. 8th, 2023AbstractIn recent years, the global prevalence and mortality of bronchial asthma are on the rise. Howev-er, anti-asthma drugs such as bronchodilator asthma are prone to produce immunosuppression,*通讯作者。
血清内脂素、脂联素和C-反应蛋白与冠状动脉病变的相关性
血清内脂素、脂联素和C-反应蛋白与冠状动脉病变的相关性焦路阳;袁彬;袁晓梅;孙浩杰;袁宇【期刊名称】《新乡医学院学报》【年(卷),期】2012(029)008【摘要】目的探讨血清内脂素(Visfantin)、脂联素(APN)和C-反应蛋白(CRP)与冠状动脉病变的关系.方法 70例经冠状动脉造影确诊的冠状动脉粥样硬化性心脏病(冠心病)患者作为观察组,并根据血管病变情况分为单支病变组、双支病变组、多支病变组,另选20例健康体检者作为对照组,采用酶联免疫吸附试验测定血清Visfantin、APN、CRP水平,比较不同程度病变者血清Visfantin、APN、CRP的差异及其与冠状动脉病变的相关性.结果观察组血清Visfantin、CRP水平均显著高于对照组(P＜0.01),APN水平显著于低于对照组(P＜0.01).双支病变组和多支病变组血清CRP、Visfantin水平及Gensini积分均明显高于单支病变组(P＜0.05)；多支病变组血清Visfantin、CRP水平及Gensini积分显著高于双支病变组(P＜0.05).双支病变组和多支病变组的APN水平均低于单支病变组(P＜0.05),但双支病变组和多支病变组比较差异无统计学意义(P＞0.05).血清Visfantin与CRP(r=0.929,P＜0.001)、Gensini 积分(r=0.777,P＜0.001)呈正相关,与APN(r=-0.351,P＜0.001)呈负相关；APN与CRP(r=-0.873,P＜0.001)、Gensini积分(r=-0.740,P＜0.001)呈负相关；CRP与Gensini积分呈正相关(r=0.692,P＜0.001).结论血清Visfantin、APN、CRP均可能是冠心病的危险因素,对评估冠状动脉病变程度有重要价值.%Objective To discuss the relationships of serum visfatin,adiponectin(APN) and C-reactive protein(CRP) with coronary artery disease. Methods Seventy patients with coronary heart disease who wereconfirmed by coronary angiogra-phy were selected as observation group, and according to the number of vascular lesion, the patients were divided into three subgroup:single-vessel disease group,double-vessel disease group and muti-vessel disease group. In addition,20 healthy people were selected as control group. Serum visfatin, APN and CRP levels were measured by enzyme-linked immunosorbent assay. The differences of them in different severity of coronary artery disease patients and the the relationships of serum visfatin, APN and CRP with coronary artery disease were analyzed. Results Compared with the control group,serum visfatin and CRP levels were significantly increased (P<0.01) ,APN level was significantly decreased in observation group(P <0.01). Serum visfatin, CRP levels and Gensini points in double or multi-vessel disease group were significantly higher than in single-vessel disease group(P <0. 05) ;and the indexes in multi-vessel disease group were significantly higher than in double-vessel disease group (P<0.05). Serum APN level in double or multi-vessel disease group was higher than single-vessel disease group(P <0. 05). However, there was no significant difference in serum APN between double-vessel disease group and multi-vessel disease group (P>0. 05). Multiple correlation analysis showed that serum visfatin level was positively correlated with the serum level of CRP (r = 0. 929, P < 0. 001) and Genisini points ( r = 0. 777, P < 0. 001 ) , negatively correlated with the serum level of APN ( r = -0. 351 ,P <0. 001). Serum APN level was negatively correlated with the serum level of CRP (r = - 0. 873 ,P <0. 001) and Genisini points ( r = - 0. 740, P < 0. 001) . Serum CRP level waspositively correlated with Genisini points ( r = 0. 692, P < 0. 001) . Conclusion Visfatin, APN and CRP levels may be risk factors for coronary heart disease. They all have significant value to evaluate degree of coronary artery disease.【总页数】3页(P600-602)【作者】焦路阳;袁彬;袁晓梅;孙浩杰;袁宇【作者单位】新乡医学院第一附属医院检验科,河南卫辉 453100;新乡医学院第一附属医院神经内二科,河南卫辉 453100;新乡医学院第一附属医院呼吸内科,河南卫辉 453100;新乡医学院第一附属医院核医学科,河南卫辉 453100;新乡医学院第一附属医院心血管内二科,河南卫辉 453100【正文语种】中文【中图分类】R543.3【相关文献】1.血清内脂素、脂联素和C-反应蛋白在2型糖尿病肾病发生发展中作用的研究 [J], 毕进2.冠状动脉病变程度及Gemini积分与血清脂联素和高敏C反应蛋白的相关性 [J], 杨萌;王显良;王荦楠;蔡瑞艳3.血清C-反应蛋白(CRP)、内脂素、脂联素在2型糖尿病肾病不同时期的变化 [J], 潘苗;张黎;张晓虹;梁蕴谊4.血清内脂素、超敏C反应蛋白与冠状动脉病变的相关性分析 [J], 何全利;刘伟5.血清脂联素和超敏C反应蛋白水平与冠心病患者冠状动脉病变不稳定性及狭窄程度的相关性分析 [J], 杨美霞;李凌;刘刚琼因版权原因，仅展示原文概要，查看原文内容请购买。
The metabolic syndrome—a new worldwide definition
The metabolic syndrome (visceral obesity, dyslipidaemia, hyperglycaemia, and hypertension), has become one of the major public-health challenges worldwide.1There has been growing interest in this constellation of closely related cardiovascular risk factors. Although the association of several of these risk factors has been known for more than 80years,2the clustering received scant attention until 1988 when Reaven described syndrome X: insulin resistance, hyperglycaemia, hypertension, low HDL-cholesterol, and raised VLDL-triglycerides.3Surpris-ingly, he omitted obesity, now seen by many as an essential component, especially visceral obesity.1Various names were subsequently proposed, the most popular being metabolic syndrome.1The cause of the syndrome remains obscure. Reaven proposed that insulin resistance played a causative role,3 but this remains uncertain. Lemieux et al suggested visceral obesity and the hypertriglyceridaemic waist phenotype as a central component,4but this too has been contested. Several different factors are probably involved, many related to changes in lifestyle.1The ultimate importance of metabolic syndrome is that it helps identify individuals at high risk of both type 2 diabetes and cardiovascular disease (CVD). Several expert groups have therefore attempted to produce diagnostic criteria. The first attempt was by a WHO diabetes group in 1999, which proposed a definition that could be modified as more information became available.5The criteria had insulin resistance or its surrogates, impaired glucose tolerance or diabetes, as essential components, together with at least two of: raised blood pressure, hyper-triglyceridaemia and/or low HDL-cholesterol, obesity (as measured by waist/hip ratio or body-mass index), and microalbuminuria. The European Group for the Study of Insulin Resistance6then produced a modification of the WHO criteria excluding people with diabetes and requiring hyperinsulinaemia to be present. Waist circumference was the measure of obesity, with different cutoffs for the other variables.A fresh approach came from the US National Cholesterol Education Program: Adult Treatment Panel III in 2001, with a focus on cardiovascular disease risk.7The specific remit was to facilitate clinical diagnosis of high-risk individuals. It was less glucocentric than the definition from WHO and the European Group for the Study of Insulin Resistance, requiring the presence of any three of five components: central obesity, raised blood pressure, raised triglycerides, low HDL-cholesterol, and fasting hyperglycaemia.The different definitions inevitably led to substantial confusion and absence of comparability between studies. One difficulty has been that the conceptual framework used to underpin the metabolic syndrome (and hence drive definitions) has not been agreed on. Opinions have varied as to whether the metabolic syndrome should be defined to mainly indicate insulin resistance, the metabolic consequences of obesity, risk for CVD, or simply a collection of statistically related factors. Prevalence figures for the syndrome have been similar in any given population regardless of which definition is used, but different individuals are identified.8What matters, of course, is which produces the best prediction of subsequent diabetes and CVD. Thus Adult Treatment Panel III was superior to WHO in the San Antonio Study, but WHO gave better prediction of CVD in Finnish men.9,10 Another problem with the WHO and the Adult Treatment Panel definitions has been their applicability to different ethnic groups, especially as relates to obesity cutoffs.11For example, the risk of type 2 diabetes is apparent at much lower levels of adiposity in Asian populations than in European populations.12With current metabolic syndrome definitions, particularly Adult Treatment Panel III, suspiciously low prevalence figures in Asian populations resulted,12 suggesting the need for ethnic-specific cutoffs, at least for obesity.The International Diabetes Federation (IDF) felt there was a strong need for one practical definition that would be useful in any country for the identification of people at high risk of CVD, but also diabetes. This definition would also allow comparative long-term studies, which could then be used, if necessary, to refine the definition on the basis of solid endpoints. As a result, an IDF consensus group met in 2004, with representatives from the organisations that had generated the previous definitions and members from all IDF regions. Their recommenda-tions are now available.13There was consensus that the components identified by Adult Treatment Panel III were a sensible starting point. It was also agreed that diabetes and insulin resistance had been overemphasised as core measurements in the earlierThe metabolic syndrome—a new worldwide definitiondefinitions. Measurement of insulin resistance was deemed impractical, although it is clear that several metabolic syndrome components, especially waist circumference and triglycerides, are highly correlated with insulin sensitivity.4Central obesity, as assessed by waist circumference, was agreed as essential (panel), because of the strength of the evidence linking waist circumference with cardiovascular disease and the other metabolic syndrome components,and the likelihood that central obesity is an early step in the aetiological cascade leading to full metabolic syndrome. The waist circumference cutoff selected was the same as that used by European Group for the Study of Insulin Resistance, and lower than the main Adult Treatment Panel III recommendations, because most available data suggest an increase in other cardiovascular disease risk factors in Europids (white people of European origin, regardless of where they live in the world) when the waist circumference rises above 94 cm in men and 80cm in women.1Ethnic-specific waist circumference cutoffs have been incorporated into the definition (table),and have been based on available data linking waist circumference to other components of the metabolic syndrome in different populations.12,14,15The levels of the other variables were as described by Adult Treatment Panel III, except that the most recent diagnostic level from the American Diabetes Association for impaired fasting glucose (5·6 mmol/L [100 mg/dL]) was used.16Although this new definition will still miss substantial numbers of people with impaired glucose tolerance (because an oral glucose-tolerance test is not required), it retains the simplicity of the instrument.The consensus group also recommended additional criteria that should be part of further research into metabolic syndrome, including: tomographic assessment of visceral adiposity and liver fat, biomarkers of adipose tissue (adiponectin, leptin), apolipoprotein B, LDL particle size, formal measurement of insulin resistance and an oral glucose-tolerance test, endothelial dysfunction, urinary albumin, inflammatory markers (C-reactive protein,tumour necrosis factor ␣, interleukin 6), and thrombotic markers (plasminogen activator inhibitor type 1,fibrinogen). These factors should be combined with assessment of CVD outcome and development of diabetes so better predictors can be developed.Researchers and clinicians should use the new criteria for the identification of high-risk individuals and for research studies. Preventive measures are obviously needed in the people identified. Mounting evidence suggests that lifestyle modification with weight loss and increased physical activity will be beneficial, although specific studies in metabolic syndrome are needed. TherePanel:International Diabetes Federation: metabolic syndrome definitionCentral obesityWaist circumference*—ethnicity specific (see table 1)Plus any two:Raised triglyceridesϾ150 mg/dL (1·7 mmol/L)Specific treatment for this lipid abnormality Reduced HDL-cholesterolϽ40 mg/dL (1·03 mmol/L) in men Ͻ50 mg/dL (1·29 mmol/L) in womenSpecific treatment for this lipid abnormality Raised blood pressure Systolic у130 mm Hg Diastolic у85 mm HgTreatment of previously diagnosed hypertension Raised fasting plasma glucose†Fasting plasma glucose у100 mg/dL (5·6 mmol/L)Previously diagnosed type 2 diabetesIf above 5·6 mmol/L or 100 mg/dL, oral glucose tolerance test is strongly recommended,but is not necessary to define presence of syndrome*If body-mass index is over 30 kg/m 2, central obesity can be assumed and waist circumference does not need to be measured. †In clinical practice, impaired glucose tolerance is also acceptable, but all reports of prevalence of metabolic syndrome should use only fasting plasma glucose and presence of previously diagnosed diabetes to define hyperglycaemia. Prevalences also incorporating 2-h glucose results can be added as supplementary findings.are suggestions from the Finnish Diabetes Prevention Study that individuals with metabolic syndrome show less development of diabetes with lifestyle advice.17In many people, however, pharmacological intervention will be needed. There is no specific treatment for the metabolic syndrome so individual abnormalities will have to be attended to.Again, long-term studies will help establish whether existing or newer agents, such as agonists for the peroxisome-proliferator-activated ␣/␥receptors or cannabinoid-1 receptor blockers,18could be of specific benefit.Recently, the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD) have published a provocative discussion paper on the syndrome.19They raise several interesting questions, based on a critique of the earlier WHO and Adult Treatment Panel III criteria: 1) is it indeed a syndrome, particularly as the precise cause is unknown, 2) does it serve a useful purpose, and 3) is it labelling (and medicalising) people unnecessarily? Additionally, it has been suggested in an editorial that recognition of the metabolic syndrome has been largely driven by industry to create new markets.20A major part of the ADA/EASD19stance is based on pure semantics, but the IDF (and the cardiovascular community) feel strongly that this clustering of closely related risk factors for CVD and type 2 diabetes is indeed a very good basis for calling this a syndrome. Many examples exist of conditions being given a name even when the precise underlying cause or causes, are unknown (eg, type 2 diabetes). The IDF feels that it serves a useful purpose to focus on people, in both the community and clinical settings, who are at high risk of developing CVD and type 2 diabetes, particularly using the new IDF criteria proposed above.Indeed, the ADA has just reinvented and redefined the condition of “prediabetes” for people who only have a 50% chance of developing diabetes.20We also emphasise most strongly in our longer article13that treatment must be focused on lifestyle change—and on the individual components if the former fails. This is a far cry from a condition claimed to be invented by industry.21The metabolic syndrome concept has been around for over 80years.1The burgeoning epidemic of type 2 diabetes and CVD worldwide, particularly in the developing world seem adequate reasons for identifying and treating people with the syndrome.We would stress that the new IDF criteria are not the final word, but hopefully will help identify people at increased risk, and through further research will lead to more accurate predictive indices.*K George M M Alberti, Paul Zimmet, Jonathan Shaw, for the IDF Epidemiology Task Force Consensus Group Department of Endocrinology and Metabolism, St Marys Hospital, London W2 1NY, UK (KGMMA); and International Diabetes Institute, Melbourne, Victoria, Australia (PZ, JS)George.Alberti@The International Diabetes Federation Consensus Group was supported by an unrestricted educational grant from AstraZeneca. KGMMA receives consultancy fees from AstraZeneca, GlaxoSmithKline, Novartis, and Servier. PZ has received consultancy fees from Novartis, GlaxoSmithKline, Bristol Myer Squibb, Bayer AG, Abbott, and Merck, and has received payment for speaking from E Merck, Sanofi-Aventis, AstraZeneca, Kissei, and Fournier. JS has received consultant fees from Merck, Eli Lilly, and Novo Nordisk.1Eckel RH, Grundy SM, Zimmet PZ. The metabolic syndrome. Lancet2005;365: 1415–28.2Kylin E. Studien ueber das Hypertonie-Hyperglyka “mie-Hyperurika”miesyndrom. Zentralblatt fuer Innere Medizin1923; 44: 105–27.3Reaven G. Role of insulin resistance in human disease. Diabetes1988; 37: 1595–607.4Lemieux I, Pascot A, Couillard C, et al. Hypertriglyceridemic waist: a marker of the atherogenic metabolic triad (hyperinsulinemia; hyperapolipoprotein B; small, dense LDL) in men? Circulation2000; 102: 179–84.5Alberti K, Zimmet P. Definition, diagnosis and classification of diabetes mellitus and its complications. Part 1: diagnosis and classification ofdiabetes mellitus provisional report of a WHO consultation. Diabet Med1998; 15: 539–53.6Balkau B, Charles MA. Comment on the provisional report from the WHO consultation. European Group for the Study of Insulin Resistance (EGIR).Diabet Med1999; 16: 442–43.7Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, AndTreatment of High Blood Cholesterol In Adults (Adult Treatment Panel III).JAMA2001; 285: 2486–97.8Cameron AJ, Shaw JE, Zimmet PZ. The metabolic syndrome: prevalence in worldwide populations. Endocrinol Metab Clin North Am 2004; 33: 351–76. 9Stern MP, Williams K, Gonzalez-Villalpando C, Hunt KJ, Haffner SM. Does the metabolic syndrome improve identification of individuals at risk oftype 2 diabetes and/or cardiovascular disease? Diabetes Care2004; 27:2676–81.10Lakka HM, Laaksonen DE, Lakka TA, et al. The metabolic syndrome and total and cardiovascular disease mortality in middle-aged men.JAMA2002; 288: 2709–16.11WHO expert consultation. Appropriate body-mass index for Asian populations and its implications for policy and intervention strategies.Lancet2004; 363: 157–63.12Tan CE, Ma S, Wai D, Chew SK, Tai ES. Can we apply the National Cholesterol Education Program Adult Treatment Panel definition of themetabolic syndrome to Asians? Diabetes Care2004; 27: 1182–86.13International Diabetes Federation. The IDF consensus worldwide definition of the metabolic syndrome. April 14, 2005:/webdata/ docs/Metac_syndrome_def.pdf (accessed June 10, 2005).14Snehalatha C, Viswanathan V, Ramachandran A. Cutoff values for normal anthropometric variables in asian Indian adults. Diabetes Care2003; 26:1380–84.15Examination Committee of Criteria for ‘Obesity Disease’ in Japan; Japan Society for the Study of Obesity.New criteria for ‘obesity disease’ in Japan.Circ J2002; 66: 987–92.16Genuth S, Alberti KG, Bennett P, et al. Follow-up report on the diagnosis of diabetes mellitus. Diabetes Care2003; 26: 3160–67.17Lindstrom J, Louheranta A, Mannelin M, for the Finnish Diabetes Prevention Study Group. The Finnish Diabetes Prevention Study (DPS):lifestyle intervention and 3-year results on diet and physical activity.Diabetes Care2003; 26: 3230–36.18Van Gaal LF, Rissanen AM, Scheen AJ, for the RIO-Europe Study Group.Effects of the cannabinoid-1 receptor blocker rimonabant on weight reduction and cardiovascular risk factors in overweight patients: 1-year experience from the RIO-Europe study. Lancet 2005; 365: 1389–97.19Kahn R, Buse J, Ferrannini E, Stern M. The metabolic syndrome: time for a critical appraisal: joint statement from the American Diabetes Association and the European Association for the Study of Diabetes. Diabetes Care2005; 28:2289-304. [Also Diabetologia 2005; published online Aug 4.DOI:10.1007/s00125-005-1876-2]20Zimmet P, Shaw J, Alberti KG. Preventing type 2 diabetes and the dysmetabolic syndrome in the real world: a realistic view. Diabet Med 2003; 20:693–702.21Gale EAM. Editorial: the myth of the metabolic syndrome. Diabetologia 2005; 10: 1873–75.Last year I joined the research advisory board of the drug company GlaxoSmithKline and get paid for that work. I was asked to write this article by The Lancet and my fee for writing will be diverted to a charity. You need to know these things before you read on.A ward round can reveal that many patients are taking ten or more drugs. A scan of a newspaper identified no fewer than six stories suggesting therapeutic breakthroughs. Therapeutic interventions, central to the practice of medicine, have spilled over into daily news—ranging from the adoption of fluoxetine as a drug for well-being in the 1990s to the pursuit of cardiovascular disease prevention resulting in 2003 for calls for a “polypill” for the entire population.1Yet despite this enthusiasm for drugs from doctors and patients,paradoxically the reputation of the drug industry is at an all time low—the industry is often portrayed as aiming for profit above all else. And it is not just the moral highgrounders who are voicing concern. Read this, fromthe business section of a major newspaper: “most drug failures are a by-product of the way the industry is structured: it develops drugs as fast as possible and employs an army of salesmen to sell like crazy before the patent expires. It ignores the fact that the side-effects of a drug are often not known until it has been taken by hundreds of thousands of patients.”2If this picture is correct, is industry alone to blame or are the medical profession and academia complicit in helping industry pursue profit above all else? This question is the theme of a report by Carl Elliott.3Let us get one thing straight: the drug industry works within a system that demands it makes a profit to satisfy shareholders. Indeed it has a fiduciary duty to do so. The best way to make a lot of money is to invent a drug that produces a dramatically beneficial clinical effect, is far more effective than any existing options, and has few unwanted effects. Unfortunately most drugs fall short of this ideal. Does this stop doctors from prescribing them,or patients’ groups from demanding availability for all?Clearly not. Even if we consider novel drugs rather than me-too products, recent examples provide some insights:the interferons for multiple sclerosis, drugs for dementia,and the inhibitors of cyclo-oxygenase 2 (COX-2).Interferon was potentially an exciting scientific advance and seemed to produce detectable biological effects in patients with multiple sclerosis. However, you needed an MRI to detect the change and the extent to which structural changes translated into clinical benefit,and improvement in quality of life, was unclear. In 2000,the UK National Institute for Clinical Excellence 4released an early statement that “on the basis of a very careful consideration of the evidence their [the interferons]modest clinical benefit appears to be outweighed by their very high cost”. The outcry was immediate, loud, and successful. Doctors, nurses, carers, and a patients’ group lobbied Government and the drug was made available within the UK National Health Service (NHS), albeit withDeveloping an open relationship with the drug industryPublished online July 7, 2005DOI:10.1016/S0140-6736(05)66835-3See Correspondencepage 1077See Department of Errorpage 1078。
_Q波_的鉴别与诊断
对于不够标准的又该怎样诊断呢 ? 没有 局限性的电静止 、纤维化或其他成分代 等位性 Q波 ,导致误诊 。至今 ,常规心电
出现 Q 波的又没有症状 、有了症状而没 替心肌 、室间隔肥厚及自主神经或间接 图是临床上应用最广的一项无创性检查
有 Q 波等无 Q 波的 M I呢 ? 因此 ,在传 刺激等有关 [3 ] ,但不是 M I导致的病理性 技术 ,是诊断 M I心律失常的重要手段之
(ACS)的提出与应用 ,心电图作为无创 波都恢复正常 。那么此时与心电图的正 说 ,坏死性变化是不能恢复的 ,但在某些
的 M I判断与排除是快捷 、方便 、实用 ,具 常变异 ,或称位置性 Q 波如何区分 ? 非 急性心肌缺血情况下 ,确可发现一些暂
有其他检查不可替代的重要作用 。ACS M I疾病所导致的 Q波及等位性 Q波 ,人 时性 Q波 。当严重缺血使得细胞内大量
JOURNAL OF PRACTICAL ELECTROCARD IOLOGY JS (2009) Vol118No12
157
于坏死 ,一旦恢复血供 ,有可能又恢复除 联 R波的递增不良 ,即 V1 ～V5 导联的 R 位置的改变 。位置性 Q 波不属于病理性 极性能 。这便是可逆 Q波出现的原因 。 波振幅丢失了逐渐增高的趋势 ;胸导联 Q波 ,其不是因 M I或其他器质性疾病引
不够诊断为传统病理 Q 波的条件 , 皮病 、淀粉样变性 、原发性或转移性心脏 现及必要的心脏超声 、头胸导联心电图
或者心电ห้องสมุดไป่ตู้上根本没有出现 Q 波 ,系部 肿瘤 、肥厚性心肌病 、左心室肥厚 、右心 等无创性检查 ,进一步还可做冠状动脉
分 M I的梗死面积小 ,心电图上没有出现 室肥厚 、肺气肿 、肺源性心脏病 、大量心 造影等有创性检查 。作为临床心电图检
冠状动脉周围脂肪组织与动脉粥样硬化的关系生物学到影像学进展
•综述"冠状动脉周围脂肪组织与动脉粥样硬化的关系：生物学到影像学进展韩婷婷,穆癑,洪叶,黄明刚【摘要$近年来，冠状动脉周围脂肪组织(PCAT)已经成为心血管疾病中具有独特生物学意义的诊断指标之一。
在生理解剖中PCAT是最接近血管壁的脂肪组织，它通过旁分泌途径及滋养血管分泌机制形成的促炎信号，调节血管周围炎症及血管重构，从而影响冠状动脉粥样硬化发展的进程。
动脉粥样硬化形成是心脑血管疾病发生的病理学基础。
因此，PCAT无论数量还是质量都是决定心脏代谢风险的关键因素，在心血管诊断与治疗方面具有重要的临床意义。
本文就PCAT在冠状动脉粥样硬化斑块形成及演变过程中所发生的生物学行为及影像学研究现状与进展进行综述。
【关键词$冠状动脉周围脂肪组织；病理生理；动脉粥样硬化；易损斑块；体层摄影术，X线计算机:PET【中图分类号$R543.3；R814.42【文献标志码】DOI：10.13609/ki.10000313.2021.05.022据相关统计显示&1',随着国民经济水平的提高，人们生活质量的改善，心血管疾病已成为我国城乡居民死亡的首要原因，且死亡呈年轻化趋势。
动脉粥样硬化斑块是导致心血管疾病的病理学基础，其中易损斑块的破裂、血栓形成是引发心血管疾病甚至主要不良心血管事件(major adverse cardiovascular events, MACE)的重要因素，因此早期检测出易损斑块并给予及时有效的临床干预，可大大降低MACE的发生。
冠状动脉周围脂肪组织(pericoronary adipose tissue,PCAT)是指冠状动脉三大主要分支血管外膜周围的脂肪组织，属于心外膜脂肪(epicardial adipose tissue,EAT)的组成部分。
PCAT由多种细胞类型组成，被认为是一种代谢活跃的内分泌器官，通过旁分泌及滋养血管分泌机制形成的促炎信号影响冠状动脉粥样硬化发展的进程，在心血管疾病的发病机制中起着至关重要的影响作用。
冠状动脉内注射替罗非班治疗无再流现象28例临床观察
伴随完全性右束支传导阻滞的急性心肌梗死的心功能衰竭发生率为45%左右,明显高于不伴右束支传导阻滞的急性心肌梗死[4,5]。
本组从K illip分级和左室射血分数两方面分析表明,合并完全性右束支传导阻滞的急性前壁及前间壁心肌梗死患者其心功能明显比对照组差。
急性前壁及前间壁心肌梗死合并完全性右束支传导阻滞患者院内病死率(25.9%)高于单纯急性心肌梗死患者(9.9%)[1]。
住院死因主要为泵功能衰竭和恶性室性心律失常[5,6]。
国外文献报道,心肌梗死合并右束支传导阻滞往往可预测患者病情的突然恶化[7],急性心肌梗死伴随新发右束支传导阻滞患者在住院期间多有低左室射血分数、高住院率以及远期病死率亦增高[8]。
而且右束支传导阻滞可能造成下壁心肌梗死的心电图表现假阴性[9],故临床上易误诊、漏诊。
选择性冠状动脉搭桥术后,如果发生右束支传导阻滞,提示手术期间有心肌坏死,所以对诊断手术期间新发生的缺血事件很有价值[10]。
本组样本量较小,还需进一步观察、总结,但初步结果表明,伴随有新出现的完全性右束支传导阻滞的急性心肌梗死多累及前壁或前间壁,标志着梗死面积大、严重心律失常发生率高、心功能受损严重,以及住院病死率高。
可作为急性心肌梗死患者病情恶化(泵衰竭、恶性心律失常)的一个很有价值的预测指标。
参考文献:[1] 邹彤,魏智民,刘得平,等.急性心肌梗死合并新发完全性右束支传导阻滞的临床意义[J].心电学杂志,2001,20(2):67269.[2] Newby KH,Pisano E,Krucoff MW,et al.Incidence and clinicalrelevance of t he occurrence of bundle2branch block in patient streated wit h t hrombolytic t herapy[J].Circulation,1996,94(10):242422428.[3] 杨钧国,李治安.现代心电图学[M].北京:科学出版社,1997.2262227.[4] Melgarejo MA,Galcera TJ,Garcia Alberola A,et al.Incidence,clinical characteristics,and prognostic significance ofright bundle branch block in acute myocardial infarction[J].Circulation,1997,96(4):113921144.[5] Hod H,G oldbourt U,behar S.Bundle branch block in acute Qwave inferior wall myocardial infarction[J].Eur Heart J,1995,16(4):4712477.[6] Moreno AM,Alberola A G,Tomes J G,et al.Incidence andprognostic significance of right bundle branch block in patient swit h acute myocardial infarction receiving t hrombolytic t herapy[J].Int J Cardiol,1997,61(2):1352141.[7] Madias J E,Bravidis D,Attari M.Posterior myocardialinfarction and complete right bundle branch block[J].Chest,2002,122(5):186021864.[8] Brilakis ES,Wright RS,kopecky SL,et al.Bundle branch blockas a predictor of long2term survival after acute myocardialinfarction[J].Am J Cardiol,2001,88(3):2052209.[9] Gussak I,Zhou SH,Rautaharju P,et al.Right bundle branchblock as a cause of false2negative ECG classification of inferiormyocardial infarction[J].J Electrocardiol,1999,32(3):2792 284.[10] Rainald S,Thomas W,Nermin S,et al.Significance of rightbundle branch block in t he diagnosis of myocardial ischemia inpatient s undergoing coronary artery bypass grafting[J].Eur JCardiot horac Surg,2000,18(2):1872193.收稿日期:2006201216 修回日期:2006207216 编辑:张桂琴冠状动脉内注射替罗非班治疗无再流现象28例临床观察洪云飞,李 易,李建美,杨 锋,卢竟前(云南省第二人民医院心脏中心内科,云南昆明650021)关键词:血管成形术,经腔,经皮冠状动脉;替罗非班3中图分类号:R541.4文献标识码:B文章编号:10042583X(2006)2121558202 经皮冠状动脉介入术(PCI)中发生慢血流和无再流现象是介入治疗的难题,在急性冠状动脉综合征的介入治疗中更容易发生,且对患者的预后有重要影响[1]。
硝苯地平英文介绍
NIFEDIPINEHISTORY AND BACKGROUNDHypertension, elevated blood pressure indicated by systolic or diastolic pressures exceeding 140 mmHg or 90 mmHg, respectively, is becoming an increasingly important medical problem as the general population becomes older and more overweight. A recent summary of research in the area of hypertension indicates that 50 million Americans and as many as one billion people globally suffer from hypertension.More importantly, the treatment of hypertension is becoming more complicated as the population ages, because many patients will take drugs to treat conditions such as diabetes, rheumatoid arthritis, atherosclerosis, and so on. As such, there is a continuing evolution of treatment regimens for hypertension . In general terms, once a patient is diagnosed with hypertension, the only treatment methods are diet, exercise, and drug intervention. Although the former options can lead to some reduction in blood pressure, most patients are treated with a mono or dual drug treatment regimen. Typically, the drugs for either therapy are drawn from he diuretics, b-blockers, angiotensin- converting enzyme (ACE) inhibitors, angiotensin II antagonists, and/or calcium channel blockers. In some cases, two of the drugs are sold in a single pill. Other treatment drugs include aldosterone-receptor blockers, combined a- and b-blockers, a1-blockers, central a2-agonists, and direct vasodilators. The actual drug treatment plan depends on factors such as age, cardiac health, other health issues, and how severe the hypertension is.In addition, renin-angiotensin inhibitors are expected to become members of the treatment arsenal within the next two years. The calcium channel blockers (CCBs) are an important class of hypertension drugs incorporating three distinctive compound subtypes. Nifedipine ,first discovered in the 1960s at Bayer, remains the prototypical representative of the dihydropyridine variant of the calcium channel blockers. Verapamil and diltiazem are representatives of the other two major structural types of calcium channel blockers used for the treatment of hypertension.As mentioned before, nifedipine was the firs t marketed dihydropyridine CCB. Initially, the drug indication was exclusively for angina, but the more recently developed extended release (ER) formulations are used off-label primarily for hypertension (Bayer, 2004). The extended-release tablets use a cellulose coat that extends their release time. The half- life of the ER formulation is reported as 7 h, whereas the immediate-release formulation has a half-life of 2 h (Bayer).SYNTHESIS OF NIFEDIPINEThe preparation of nifedipine and other simple symmetric analogs is very straightfor-ward (Scheme 11.1). 4-Aryldihydropyridine-3,5-dicarboxylates are isolable intermediatesin the well-known Hantzsch pyridine synthesis (Bossert et al., 1981; Eisner and Kuthan, 1972; Stout and Meyers, 1982). This reaction, in its most simple form, is a one-pot reaction of an aryl aldehyde, acetoacetic acid alkyl ester, and ammonia heated in refluxing methanol for a few hours. If side reactions or by-products become troublesome, a stepwise process works as well. The original preparation of nifedipine uses 2-nitrobenzaldehyde, acetoacetic acid methyl ester, methanol, and ammonia (Bossert and Vater, 1969). The mixture is heated for several hours, cooled back down, and the product is filtered off as a yellow crystalline material.CLINICAL PHARMACOLOGYNifedipine is a calcium ion influx inhibitor (slow-channel blocker or calcium ion antagonist) and inhibits the transmembrane influx of calcium ions into cardiac muscle and smooth muscle. The contractile processes of cardiac muscle and vascular smooth muscle are dependent upon the movement of extracellular calcium ions into these cells through specific ion channels. Nifedipine selectively inhibits calcium ion influx across the cell membrane of cardiac muscle and vascular smooth muscle without altering serum calcium concentrations.Mechanism of ActionA) AnginaThe precise mechanisms by which inhibition of calcium influx relieves angina has not been fully determined, but includes at least the following two mechanisms:1) Relaxation and Prevention of Coronary Artery SpasmNifedipine dilates the main coronary arteries and coronary arterioles, both in normal and ischemic regions, and is a potent inhibitor of coronary artery spasm, whether spontaneous orergonovine-induced. This property increases myocardial oxygen delivery in patients with coronary artery spasm, and is responsible for the effectiveness of nifedipine in vasospastic (Prinzmetal's or variant) angina. Whether this effect plays any role in classical angina is not clear, but studies of exercise tolerance have not shown an increase in the maximum exercise rate-pressure product, a widely accepted measure of oxygen utilization. This suggests that, in general, relief of spasm or dilation of coronary arteries is not an important factor in classical angina.2) Reduction of Oxygen UtilizationNifedipine regularly reduces arterial pressure at rest and at a given level of exercise by dilating peripheral arterioles and reducing the total peripheral vascular resistance (afterload) against which the heart works. This unloading of the heart reduces myocardial energy consumption and oxygen requirements, and probably accounts for the effectiveness of nifedipine in chronic stable angina.B) HypertensionThe mechanism by which nifedipine reduces arterial blood pressure involves peripheral arterial vasodilatation and the resulting reduction in peripheral vascular resistance. The increasedperipheral vascular resistance that is an underlying cause of hypertension results from an increase in active tension in the vascular smooth muscle. Studies have demonstrated that the increase in active tension reflects an increase in cytosolic free calcium.Nifedipine is a peripheral arterial vasodilator which acts directly on vascular smooth muscle. The binding of nifedipine to voltage-dependent and possibly receptor-operated channels in vascular smooth muscle results in an inhibition of calcium influx through these channels. Stores of intracellular calcium in vascular smooth muscle are limited and thus dependent upon the influx of extracellular calcium for contraction to occur. The reduction in calcium influx by nifedipine causes arterial vasodilation and decreased peripheral vascular resistance which results in reduced arterial blood pressure.PHARMACOKINETICS AND METABOLISMNifedipine is completely absorbed after oral administration. Plasma drug concentrations rise at a gradual, controlled rate after a nifedipine extended-release tablet dose and reach a plateau at approximately six hours after the first dose. For subsequent doses, relatively constant plasma concentrations at this plateau are maintained with minimal fluctuations over the 24-hour dosing interval. About a four-fold higher fluctuation index (ratio of peak to trough plasma concentration) was observed with the conventional immediate-release nifedipine capsule at t.i.d. dosing than with once daily nifedipine extended-release tablet. At steady-state the bioavailability of the nifedipine extended-release tablet is 86% relative to nifedipine capsules. Administration of the nifedipine extended-release tablet in the presence of food slightly alters the early rate of drug absorption, but does not influence the extent of drug bioavailability. Markedly reduced GI retention time over prolonged periods (i.e., short bowel syndrome), however, may influence the pharmacokinetic profile of the drug which could potentially result in lower plasma concentrations. Pharmacokinetics of nifedipine extended-release tablets are linear over the dose range of 30 to 180 mg in that plasma drug concentrations are proportional to dose administered. There was no evidence of dose dumping either in the presence or absence of food for over 150 subjects in pharmacokinetic studies.Nifedipine is extensively metabolized to highly water-soluble, inactive metabolites accounting for 60 to 80% of the dose excreted in the urine. The elimination half-life of nifedipine is approximately two hours. Only traces (less than 0.1% of the dose) of unchanged form can be detected in the urine. The remainder is excreted in the feces in metabolized form, most likely as a result of biliary excretion. Thus, the pharmacokinetics of nifedipine are not significantly influenced by the degree of renal impairment. Patients in hemodialysis or chronic ambulatory peritoneal dialysis have not reported significantly altered pharmacokinetics of nifedipine. Since hepatic biotransformation is the predominant route for the disposition of nifedipine, the pharmacokinetics may be altered in patients with chronic liver disease. Patients with hepatic impairment (liver cirrhosis) have a longer disposition half-life and higher bioavailability of nifedipine than healthy volunteers. The degree of serum protein binding of nifedipine is high (90 to 98%). Protein binding may be greatly reduced in patients with renal or hepatic impairment.。
2016-原发性醛固酮增多症诊断治疗的专家共识
如患者因冠心病或心律失常等原因长期服用 β 受体 4. 检测技术及单位换算:目前常用免疫测定技术
阻滞剂,临床医师根据患者情况决定是否停药。 (6) 检测血浆肾素活性( PRA) 或 DRC,前者是通过测定血
如血压控制不佳,建议使用 α 受体阻滞剂及非二氢吡 管紧张素Ⅰ产生的速率来反映 PRA,而后者则通过放
中华内分泌代谢杂志 2016 年 3 月第 32 卷第 3 期 Chin J Endocrinol Metab, March 2016, Vol. 32, No. 3
·189·
表 2 在筛查及确诊试验中可用于控制血压且对肾素血管紧张素系统影响较小的药物
药物名称
分类
常用剂量
注意事项
维拉帕米缓释片 肼屈嗪 哌唑嗪 多沙唑嗪 特拉唑嗪
1. 筛查前准备:(1)尽量将血钾纠正至正常范围。 (2) 维持正常钠盐摄入。 (3) 停用对 ARR 影响较大药 物至少 4 周:包括醛固酮受体拮抗剂( 安体舒通、依普 利酮)、保钾利尿剂( 阿米洛利、氨苯喋啶)、排钾利尿 剂(氢氯噻嗪、呋塞米) 及甘草提炼物。 (4) 血管紧张 素转 换 酶 抑 制 剂 ( ACEI ) 、 血 管 紧 张 素 受 体 拮 抗 剂 (ARB) 、钙离子拮抗剂( CCB) 类等药物可升高肾素活 性,降低醛固酮,导致 ARR 假阴性,因此 ARR 阴性不 能排除原醛症,需停用上述药至少 2 周再次进行检测; 但如服药时肾素活性<1 ng·ml-1 ·h-1 或低于正常检 测下限同时合并 ARR 升高,考虑原醛症可能大,可维 持原有药物治疗。 (5) 由于 β 受体阻滞剂、中枢 α2 受
急性缺血性脑卒中后吞咽障碍发病率及影响因素分析
-论著.急性缺血性脑卒中后吞咽障碍发病率及影响因素分析曹猛，宋学梅，梁丽，麦静慧，吴亚男，朱丽娜，张晓梅摘要：目的探讨急性缺血性脑卒中后吞咽障碍发病率、危险因素及预后，为采取干预措施提供参考％方法对急性缺血性脑卒中患者在入院48h内，采用洼田饮水试验结合容积一黏度吞咽测试完成吞咽功能评估，收集年龄、性别、既往史、卒中部位、肌力、Barthel指数、美国国立卫生研究院脑卒中量表（NIHSS）评分等资料，并随访患者出院后1、3个月的预后情况%结果共纳入542例患者，吞咽障碍发病率为37.3%；Logistic回归分析显示，NIHSS评分、年龄、肌力及Barthel指数是吞咽障碍的影响因素（P< 0.05,P<0.01）；吞咽障碍患者与吞咽正常患者出院后死亡率、肺部感染率及改良Rankin评分比较，差异有统计学意义（均P<0.01）%结论急性缺血性脑卒中后吞咽障碍发病率较高，日常生活自理能力、神经功能、年龄及肌力是影响因素，吞咽障碍的发生显著影响患者预后；需系统和针对性开展吞咽障碍筛查，早期进行护理干预，以改善预后%关键词：脑卒中；吞咽障碍；吞咽功能；洼田饮水试验；容积一黏度吞咽测试；肌力；自理能力；预后中图分类号.R473.74；R743.3文献标识码：A DOI：10.3870/j.issn.1001-4152.202102.024Prevalence and risk factors of dysphagia among acute ischemic stroke patients Cao Meng$Song Xuemei$Liang Li$Mai Jinghui$ Wu Yanan$Zhu Lina,Zhang Xiaomei.Department of Neurology,Nan f ang Hospital,Southern Medical University,Guangzhou510515,ChinaAbstract:Objective To study the incidence,risk factors and prognosis of dysphagia after acute ischemic stroke,and to provide reference for targeted interventions.Methods Patients with acute ischemic stroke were consecutively enrolled and assessed for swallowing function by Water-Swallow Test and Volume-Viscosity Swallow Test within48h of hospitalization.Age ,gender ,medical history,location of the stroke lesion ,muscle strength,Barthel Index(BI),and National Institute of Health Stroke Scale(NIHSS) score were collected and follow-ups were performed at1and3months after discharge.Results A total of542patients were enrolled inthisstudy Theincidenceofdysphagia was373%Logisticregression analysisshowedthat NIHSS score age muscle strength and BI were independent risk factors for dysphagia(P<0.05,P<0.01).There were significant differences in mortality, incidenceofpulmonaryinfectionandtheModifiedRankinScale(mRS)scorebetweenthedysphagiaandnon-dysphagiapatientsaf-ter discharge(P<0.01for all).Conclusion Dysphagia after acute ischemic stroke is prevalent,and is affected by performance in activitiesofdailyliving neurologicalfunction ageand musclestrength Dysphagiawouldimpedetherecoveryafteracuteischemic stroke sosystematicandtargetedscreeningandearlyinterventionshouldbeconductedtoimprovetheprognosisKeywords：stroke；dysphagia；swallowing function；Water-Swallow Test；Volume-Viscosity Swallow Test；muscle strength；self-care ability；prognosis卒中后吞咽障碍是世界卫生组织认可的一种疾病⑴，与营养不良、脱水、误吸等并发症显著相关,导致患者预后不良及病死率高[25]（据文献报道,卒中后吞咽障碍发病率为19%〜81%[6],可能与研究人员选择的评估方法和诊断标准有关因为临床对吞咽障碍的诊断和评估手段缺乏统一的规范,导致吞咽障碍发病率的结果差别较大。
(完整版)医学影像检查方法、部位中英文对照
头部急诊平扫Emergent Head Scan头部急诊增强Emergent Head Enhanced Scan 头部平扫Head Routine Scan头部增强Head Enhanced Scan眼部平扫Orbits Routine Scan眼部增强Orbits Enhanced Scan内耳平扫Inner Ear Routine Scan内耳增强Inner Ear Enhanced Scan乳突平扫Mastoid Routine Scan乳突增强Mastoid Enhanced Scan蝶鞍平扫Sella Routine Scan蝶鞍增强Sella Enhanced Scan鼻窦轴位平扫Sinus Axial Routine Scan鼻窦轴位增强Sinus Axial Enhanced Scan鼻窦冠位平扫Sinus Coronal Scan鼻窦冠位增强Sinus Coronal Enhanced Scan 鼻咽平扫Nasopharynx Routine Scan鼻咽增强Nasopharynx Enhanced Scan腮腺平扫Parotid Routine Scan腮腺增强Parotid Enhanced Scan喉平扫Larynx Routine Scan喉增强Larynx Enhanced Scan甲状腺平扫Hypothyroid Routine Scan甲状腺增强Hypothyroid Enhanced Scan颈部平扫Neck Routine Scan颈部增强Neck Enhanced Scan肺栓塞扫描Lung Embolism Scan胸腺平扫Thymus Routine Scan胸腺增强Thymus Enhanced Scan胸骨平扫Sternum Routine Scan胸骨增强Sternum Enhanced Scan胸部平扫Chest Routine Scan胸部薄层扫描High Resolution Chest Scan胸部增强Chest Enhanced Scan胸部穿刺Chest Puncture Scan轴扫胸部穿刺Axial Chest Punture Scan上腹部平扫Upper-Abdomen Routine Scan中腹部平扫Mid-Abdomen Routine Scan上腹部增强Upper-Abdomen Routine Enhanced Scan 中腹部增强Mid-Abdomen Routine Scan腹部穿刺Abdomen Puncture Scan轴扫腹部穿刺Axial Abdomen Puncture Scan颈椎平扫C-spine Routine Scan胸椎平扫T-spine Routine Scan腰椎平扫L-spine Routine Scan盆腔平扫Pelvis Routine Scan盆腔增强Pelvis Enhanced Scan骶髂关节平扫SI Joint Scan肩关节平扫Shoulder Joint Scan上肢软组织平扫Upper Extremities Soft Tissue Scan上肢软组织增强 Upper Extremities Soft Tissue Enhanced 肘关节平扫 Elbow Joint Routine Scan腕关节平扫Wrist Joint Routine Scan手部平扫Hand Routine Scan髋关节平扫Hip Joint Routine Scan膝关节平扫Knee Joint Routine Scan踝关节平扫Ankle Joint Routine Scan下肢软组织平扫Lower Extremities Soft Tissue Scan下肢软组织增强 Lower Extremities Soft Tissue Enhanced 足部平扫 Foot Routine Scan血管造影和三维成像头部血管造影Head CT Angiography颈部血管造影Neck CT Angiography心脏冠脉造影Coronal Artery Angiography心脏冠脉钙化积分Cardiac Calcium Scoring Scan胸部血管造影Chest CT Angiography腹部血管造影Abdomen CT Angiography上肢血管造影Upper Extremities CT Angiography下肢血管造影Lower Extremities CT Angiography医界资讯网五官三维成像3D Facial Scan胃三维3D Stomach CT Scan结肠三维3D Colon CT Scan颈椎三维3D C-Spine胸椎三维3D T-Spine腰椎三维3D L-Spine肩关节三维3D Shoulder Joint肘关节三维3D Elbow Joint腕关节三维3D Wrist Joint髋关节三维3D Hip Joint膝关节三维3D Knee Joint踝关节三维3D Ankle Joint检查名称英文对照头部平扫Head Routine Scan头部常规增强Head Routine Enhanced Scan头部动态增强Head Dynamic Enhanced Scan垂体平扫Sella Routine Scan垂体增强Sella Enhanced Scan鼻咽部平扫Nasopharynx Routine Scan鼻咽部增强Nasopharynx Enhanced Scan眼眶部平扫Orbits Routine Scan眼眶部增强Orbits Enhanced Scan内听道平扫Inner Ear Routine Scan颈部平扫Neck Routine Scan颈部普通增强Neck Enhanced Scan颈部动态增强Neck Dynamic Enhanced Scan上腹部平扫Upper Abdomen Scan上腹部普通增强Upper Abdomen Routine Enhanced 上腹部动态增强Upper Abdomen Dynamic Enhanced 中腹部平扫Mid-Abdomen Scan中腹部普通增强Mid-Abdomen Routine Enhanced中腹部动态增强Mid-Abdomen Dynamic Enhanced肾脏平扫Kidney Routine Scan肾上腺平扫Adrenal Routine Scan肾脏普通增强Kidney Routine Enhanced Scan肾脏动态增强Kidney Dynamic Enhanced Scan胰胆管造影MRCP尿路造影MRU腹和盆腔联合扫描Abdomen & Pelvis Scan医界资讯网颈椎平扫C-spine Scan颈椎增强C-spine Enhanced Scan胸椎平扫T-spine Scan胸椎增强T-spine Enhanced Scan腰椎平扫L-spine Scan腰椎增强L-spine Enhanced Scan胸腰段平扫T&L Spine Scan胸腰段增强T&L Spine Enhanced Scan胸部平扫Chest Scan胸部普通增强Chest Routine Enhanced Scan胸部动态增强Chest Dynamic Enhanced Scan女性盆腔平扫Female Pelvis Scan女性盆腔普通增强Female Pelvis Routine Enhanced女性盆腔动态增强Female Pelvis Dynamic Enhanced男性盆腔平扫Male Pelvis Scan男性盆腔普通增强Male Pelvis Routine Enhanced男性盆腔动态增强Male Pelvis Dynamic Enhanced肩关节平扫Shoulder Joint Scan肘关节平扫Elbow Joint Scan腕关节平扫Wrist Joint Scan手部平扫Hand Scan上肢软组织平扫Upper Soft Tissue Scan上肢软组织普通增强 Upper Soft Tissue Routine Enhanced 上肢软组织动态增强 Upper Soft Tissue Dynamic Enhanced骶髂关节平扫Sacrum Ilium Joint Scan髋关节平扫Hip Joint Scan膝关节平扫Knee Joint Routine Scan踝关节平扫Ankle Joint Routine Scan足部平扫 Foot Routine Scan下肢软组织平扫Lower Soft Tissue Scan下肢软组织普通增强 Lower Soft Tissue Routine Enhanced 下肢软组织动态增强 Lower Soft Tissue Dynamic Enhanced头颅正侧位Skull PA & LAT鼻窦Sinus PA左侧乳突Left Mastoid Process医界资讯网右侧乳突Right Mastoid Process鼻骨侧位Nasal Bones LAT颈椎正侧位C-Spine PA & LAT颈椎双斜位C-Spine Dual Oblique胸椎正侧位T-Spine PA & LAT腰椎正侧位L-Spine PA & LAT骶尾正侧位Saccrum/Coccyx AP & LAT胸部正侧位（成人）Chest PA & LAT (Adult)胸部正侧位（儿童）Chest PA & LAT (Pediatrics)骨盆（成人）Pelvis PA (Adult)骨盆（儿童）Pelvis PA (Pediatrics)腹部（成人）Abdomen ( Adult)腹部（儿童）Abdomen (Pediatircs)左侧肩关节Left Shoulder Joint右侧肩关节Right Shoulder Joint左侧肱骨正侧位Left Humerus AP & LAT右侧肱骨正侧位Right Humerus AP & LAT左侧尺桡骨正侧位Left Forearm AP & LAT右侧尺桡骨正侧位Right Forearm AP & LAT左侧肘关节正侧位Left Elbow Joint AP & LAT右侧肘关节正侧位Right Elbow Joint AP & LAT左手正斜位Left Hand AP & Oblique右手正斜位Right Hand AP & Oblique左侧腕关节正侧位Left Wrist Joint AP & LAT右侧腕关节正侧位Right Wrist Joint AP & LAT双腕关节正位（成人）Dual Wrist Joint AP (Adult)双腕关节正位（儿童）Dual Wrist Joint AP (Pediatrics) 左侧股骨正侧位Left Femur AP & LAT右侧股骨正侧位Right Femur AP & LAT左侧膝关节正侧位Left Knee Joint AP & LAT右侧膝关节正侧位Right Knee Joint AP & LAT左侧胫腓骨正侧位Left Tibia Fibula AP & LAT右侧胫腓骨正侧位Right Tibia Fibula AP & LAT左侧踝关节正侧位Left Ankle Joint AP & LAT右侧踝关节正侧位Right Ankle Joint AP & LAT左侧足部正侧位Left Foot AP & LAT右侧足部正侧位Right Foot AP & LAT足跟侧位Calcaneus LAT胸部正位Chest PA胸部正侧位Chest PA & LAT心脏三位片Heart胸部斜位Chest OBL胸骨侧位Sternum LAT胸锁骨关节像Sternum Calvicle Joint PA锁骨正位Calvicle PA肩关节正位Shoulder Joint AP头颅正位Skull AP头颅正侧Skull AP & LAT颈椎正位C-spine AP颈椎张口位C-spine Open Mouth颈椎正侧位C-spine AP & LAT颈椎正侧双斜位C-spine AP & LAT & Dual OBL颈椎六位像C-spine 6 position颈椎正侧双斜张口位 C-spine AP & LAT & Dual OBL Open Mouth 颈胸段正侧位 C-T-spine AP & LAT 胸椎正侧 T-spine AP & LAT胸腰段正侧位T-L-spine AP & LAT腰椎正侧位L-spine AP & LAT腰椎正侧双斜L-spine AP & LAT & Dual OBL腰椎双斜L-spine Dual OBL腰椎六位像L-spine 6 position腰椎过伸过屈位L-spine Lordotic Kyphotic Position腰骶椎正侧位L-S-spine AP & LAT骶尾椎正侧位Saccrum/Coccyx AP & LAT尾椎侧位像Coccyx LAT骶髂关节正位Sacrum Ilium Joint AP骶髂关节切线位Sacrum Ilium Joint Tangential Position骨盆正位Pelvis AP耻骨坐骨正位Pubis Ischium AP腹部平片Abdomen AP上肢Upper Extremities下肢Lower Extremities华氏位Waltz Position下颌骨正侧位Mandible PA_LAT头颅正侧位Skull PA_LAT颧弓切线位Zygomatic小儿胸片Chest膝关节造影Knee Joint Contrast肩关节造影Shoulder Joint Contrast椎管造影Spinal ContrastTMJ 造影TMJ contrast腮腺造影Parotid Contrast静脉肾盂造影IVP逆行尿路造影Contrary Urethral Contrast子宫造影Uterus ContrastT 管造影T-tube Cholangiography五官造影Facial Contrast窦道造影Contrast Fistulography瘤腔造影Tumor Cavity Contrast异物定位Orientation胆系造影CholecystographyERCP ERCP上消化道造影Upper Gastrointestinal Contrast全消化道造影Full Gastrointestinal Contrast钡灌肠造影Barium Contrast of Colon小肠低张造影Small Bowel Enema结肠低张造影Hypotonic Colon Contrast食道造影Contrast Esophagography下肢静脉造影Lower Vein Angiography上肢静脉造影Upper Vein Angiography下肢动脉造影Lower Artery Angiography上肢动脉造影Upper Artery Angiography脑血管造影Cerebrovascular Angiograhy主动脉弓胸腹主动脉造影Aorta Angiography肾静脉取血Kidney Vein Blood Sampling右心、左心造影 Right and Left Ventricular Angiography心肌活检 Myocardiam Centesis and Sampling冠状动脉造影Coronary Arteriography腔静脉取血Vena cava sampling心导管检查 ( 微导管同 )(进口仪器） Cardiac catheterization 经皮球囊扩张 Percutaneous balloon dilatating予激综合症心内膜检测 Endocardial investigation of preexcitation syndrome 希氏束电图 Electrocardiogram of bundle of His心脏临时起搏Cardiac temporary pacing埋置永久心脏起搏器 Cardioc permanent pacemaker implanting 体肢动脉系统介入治疗 Transartery interventional therapy支气管动脉介入治疗 Bronchus artery interventional therapy肺动脉介入治疗 Pulmonary artery interventional therapy头臂动脉介入治疗 Brachiocephalic artery interventional therapy静脉介入治疗 Veinous interventional therapy冠状动脉介入治疗 (球囊成形 ) Coronary Artery interventional therapy (balloon angioplasty)冠状动脉介入治疗(腔内旋磨 ) Coronary Artery interventional therapy (rotablating) 冠状动脉介入治疗(腔内支架 ) Coronary Artery interventional therapy (stent implantaion)主动脉介入治疗Aorta interventional therapy肾动脉介入治疗Renal artery interventional therapy心脏瓣膜成形术Heart valvuloplasty房间隔缺损封堵术Atrial septal defect closer室间隔缺损封堵术Ventricular septal defect closer动脉导管封堵术Patent doctus arteriosus closer冠状动脉瘘封堵术Coronary artery fistula closer冠状动脉腔内超声Intracoronary ultrasound非冠状动脉血管内支架置入治疗 Stenting therapy of non-coronary artery 经皮清除血管内异物 Transluminal eyewinker clearing经皮放置静脉滤器Transluminal filter implantaion上肢 MRA Upper Extremities MRA下肢 MRA Lower Extremities MRA心脏大血管造影Heart MR Angiography胸主动脉造影T-Artery MR Angiography腹主动脉造影Abd-Artery MR Angiography头部血管造影Head MR Angiography颈部血管造影Head MR Angiography盆腔血管造影Pelvis MR Angiography。
原发性醛固酮增多症(中英文
• 原醛症病人一般服用安体舒通1周后，尿 钾减少、血钾上升、血浆CO2结合力下 降，肌无力、四肢麻木等症状改善，夜 尿减少，约半数病人血压有下降趋势。
原醛的筛查
• 立，卧位的血ARR=ALDO/PRA。各种文 献对比值报道不一，>25可疑， > 50可能 性大。
• 如果同时运用下述标准:ALDO/PRA>30, ALDO>20ng/dl, 其诊断原醛的灵敏性为 90%，特异性为91% 。
原醛的确诊
FST
氟氢可的松0.1mg q6h，共4天 ➢测定立位ALDO>60pg/dl，立位PRA ＜1.0ng/ml ➢尿钠的排泄>3 mmol/kg/天 ➢血K正常。 ➢服药4天后10Am的血浆皮质醇必须低于7Am 的
皮质醇
盐负荷试验
• 静脉和口服 • 静脉：生理盐水2L，4小时内静注完，测
定血ALDO >5ng/dl，PA确诊。 • 口服：高钠饮食3天（300mmol钠/d），
测定24小时尿ALDO >10µg/d， PA确诊
盐负荷试验
• 高钠试验正常人及高血压病人血钾无明 显变化，原醛症患者血钾可降至3．5毫 摩尔/升以下
Schimenbach, Best Pract Res Clin Endocrinol Metab. 2006 Sep;20(3):369-84
机制
肾上腺皮质病变Aldo↑储NA排K 血容量↑ PRA↓
自主性
低K
BP↑
临床特点
1.BP↑ : 血容量↑,平滑肌内NA↑,Aldo增加血 管对NAR的反应. 最早最常见,病程进展, BP逐渐↑,轻中度.以DBP ↑为主 伴头晕,头痛.
type I) • FH type II (APA or IHA)
X线检查技术中英文词汇
X 线检查技术中英文•air bronchogram 支气管影像•ankle joint 踝关节•ankylosis of joint 关节强直•arches of foot 足弓•biligrafin 胆影葡胺•bone age 骨龄•bone canaliculi 骨小管•bone cortex 骨皮质•bone deformity 骨骼变形•bone destruction 骨质破坏•bone lacuna 骨陷窝•bone lamella 骨板•bony articular surface 骨关节面•bursa 滑膜囊•calcification 钙化•carpal bones 腕骨•cavity 空洞•chondral calcification 软骨钙化•compact bone and spongy bone 密质骨和松质骨•degeneration of joint 关节退行性变•destruction of joint 关节破坏•diaphysis 骨干•digital subtraction angiography, DSA 数字减影血管造影•dislocation of joint 关节脱位•dual photon absorptiometry, DPA 双光子吸收法•dual X-ray energy absorptiometry, DXA 双能X 线吸收法•elbow joint 肘关节•encapsulated effusion 包裹性积液•end plate 终板•epiphyseal line 骨骺线•epiphyseal plate 骨骺板•epiphysis 骨骺•exudation 渗出•fibrotic lesion 纤维性病变•filling defect 充盈缺损•free pleural effusion 游离性胸腔积液•haemosiderosis 含钱血黄素沉着•Hafersian system 哈弗系统•haversian lamella 哈氏骨板•hilar dance 肺门舞蹈•hip joint 髋关节•hydropneumothorax 液气胸• hydroxyapatite crystal 羟基磷灰石结晶• hyperostosis/osteosclerosis 骨质增生硬化• intercondyloid eminence 髁间隆起•interlobar effusion 叶间积液•intermediate lamella 骨间板•internal and external circumfereutial lamella 内、外环骨板•interstitial pulmonary oedema 间质性肺水肿• intervertebral disc 椎间盘• intervertebral foramen 椎间孔• intervertenral space 椎间隙• intra-alveolar pulmonary oedema 肺泡性肺水肿• joint 关节• joint capsule 关节囊• joint cartilage 关节软骨•joint cavity 关节腔•joint space 关节间隙• knee joint 膝关节•lamellar bone 层板骨• left atrial enlargement 左心房增大• left ventricular enlargement 左心室增大• ligament 韧带•localized pleural effusion 局限性胸腔积液•looser zone 假骨折线• mass 肿块• medullary space 骨髓腔•metacarpal bones 掌骨• metaphysis 干骺端• metatarsal bones 跖骨• niche 龛影• obstructive atelectasis 阻塞性肺不张• obstructive emphysema 阻塞性肺气肿•oral cholecystography 口服胆囊造影• ossifcation 骨化•ossification centre 骨化中心•osteoblast 成骨细胞•osteoclast 破骨细胞•osteocyte 骨细胞•osteomalacia 骨质软化•osteonecrosis 骨质坏死•osteoporosis 骨质疏松•periosteal proliferation 骨膜增生• periosteal reaction 骨膜反应•periosteum and intermal periosteum 骨膜和骨内膜•phalanges of fingers 指骨•phalanges of toes 趾骨•pleural thickening,adhesion and calaification 胸膜增厚、粘连及钙化•pleural tumor 胸膜肿瘤•pneumothorax 气胸•proliferative lesion 增殖性病变•pulmonary hilar enlargement 肺门增大•pulmonary arterial hypertension 肺动脉高压•pulmonary arterial pleonaemia 肺充血•pulmonary hypertension 肺高压•pulmonary oligaemia 肺少血•pulmonary venous hypertension 肺静脉高压•pulmonary venous pleonaemia 肺淤血•quantitative computed tomography, QCT 定量CT 法•right atrial enlargement 右心房增大•right ventricular enlargement 右心室增大•sequestrum 死骨•shoulder joint 肩关节•soft tissue mass 软组织肿胀•soft tissue swelling 软组织肿胀•subpulmonary effusion 肺下积液•swelling of joint 关节肿胀•tarsal bones 跗骨•tibia tuberosity 胫骨粗隆•trabecula 骨小梁•Volkmann canal 福尔克曼管•woven bone 非层板骨•wrist 腕关节•abestosis 石棉肺•acquired immunodeficiency syndrome, AIDS 艾滋病•actinomycosis 放线菌病•acute military tuberculosis 急性粟粒型肺结核•agenesis and hypoplasia of the lung 肺不发育和肺发育不全•allergic pneumonia 过敏性肺炎•aluminum pneumoconiosis 铝尘肺•amyloidosis of lung 肺淀粉样变性•angiogram sign 血管造影征•anthracosis 炭黑尘肺•aspergillosis 曲菌病•bronchiectasis 支气管扩张•bronchogenic cyst 支气管囊肿•bronchopneumonia 支气管肺炎•broncho-pulmonary sequestration 支气管肺隔离症•butterfly sign 蝶翼征•cement pneumoconiosis 水泥尘肺•chronic bronchitis 慢性支气管炎•chronic pneumonia 慢性肺炎• coalworker pneumoconiosis 煤工尘肺• congenital bronchial cysts 先天性支气管囊肿•contusion of lung 肺挫伤•cryptococcosis 隐球菌病• cylindrical bronchiectasis 柱状支扩•dermoid cyst 皮样囊肿• diaphragmatic eventeration 膈膨升• diaphragmatic hermia 膈疝•electric welder pneumoconiosis 电焊工尘肺• esophageal cyst 食管囊肿•foreign body of chest 胸部异物•foundry worker pneumoconiosis 铸工尘肺• Goodpasture syndrome 肺- 肾综合征•graphite pneumoconiosis 石墨尘肺• halo sign 晕轮征• hamartoma 错构瘤•hematogenous pulmonary tuberculosis 血行播散型肺结核（II 型）• Hodgkin lymphoma 霍奇金淋巴瘤•Hodgkin disease, HD 霍奇金病•honeycomb lung 蜂窝状肺• hydropneumothorax 液气胸• inflammatory pseudotumor 炎性假瘤• interstitial pneumonia 间质性肺炎•intrathoracic goiter 胸内甲状腺• kaolin pneumoconiosis 陶工尘肺• Kaposi sarcoma 卡波济肉瘤•laceration and hematoma of lung 肺撕裂伤与肺血肿•laceration of trachea and bronchus 气管及支气管裂伤•lipoma 脂肪瘤•lobar pneumonia 大叶性肺炎•Loffler syndroma 吕弗留综合征•lung abscess 肺脓肿•lymphangioma 淋巴管瘤•lymphoma 淋巴瘤•mediastinal emphysema 纵隔气肿•mediastinal hematorma 纵隔血肿•mediastinal tumor 纵隔肿瘤•mediastinitis 纵隔炎•mesothelial cyst 间皮囊肿•mesothelioma of pleura 胸膜间皮瘤•metastatic tumor of pleura 胸膜转移瘤•mica pneumoconiosis 云母尘肺•neurogenic neoplasms 神经源性肿瘤• non Hodgkin lymphoma, NHL 非霍奇金淋巴瘤•pleural thickening, adhesion and calcification 胸膜肥厚粘连和钙化• pleuro-peritoneal hiatus hernia 胸腹裂孔疝• pneumocomosis 尘肺• pneumomediastinum 纵隔气肿• pneumothorax 气胸• primary complex 原发综合征• primary tuberculosis 原发性肺结核（I 型）•pulmonary alveolar microlithiasis 肺泡微石症•pulmonary alveolar proteinosis 肺泡蛋白沉积症•pulmonary arterio-venous fistula 肺动静脉瘘•pulmonary arterio-venous malformation,PA VM 肺动静脉畸形•pulmonary connective tissue diseases 肺结缔组织疾病•pulmonary edema 肺水肿•pulmonary emboli 肺梗塞•pulmonary infarcts 肺梗死•pulmonary sequestration 肺隔离症•pulmonary tuberculosis 肺结核•pyothorax 化脓性胸膜炎•radiation pneumonitis 放射性肺炎•rheumatoid disease of the lung 肺类风湿性病• saccular bronchiectasis 囊状支扩• sarcoidosis 结节病• secondary pulmonary tuberculosis 继发性肺结核（III 型）• seminoma 精原细胞瘤• silicosis 矽肺•staphylococal pneumonia 葡萄球菌肺炎•subacute or chronic hematogenous pulmonary tuberculosis 亚急性或慢性血行播散型肺结核• systemic lupus erythomatosis, SLE 系统性红斑狼疮•talc pneumoconiosis 滑石尘肺•teratoma 畸胎瘤•thymoma 胸腺瘤• tramline sign 轨道征• traumatic diaphragmatic hernia 外伤性隔疝•tuberculosis of intrathoracic lymph nodes 胸内淋巴结结核•tuberculosis pleuritis 结核性胸膜炎• varicose bronchiectasis 静脉曲张型支扩• Wegner granuloma 韦格氏肉芽肿• 下肢静脉造影: Lower Vein Angiography• 上肢静脉造影: Upper Vein Angiography• 下肢动脉造影: Lower Artery Angiography• 上肢动脉造影: Upper Artery Angiography• 脑血管造影: Cerebrovascular Angiograhy• 主动脉弓胸腹主动脉造影: Aorta Angiography• 肾静脉取血: Kidney Vein Blood Sampling• 右心、左心造影: Right and Left Ventricular Angiography• 心肌活检: Myocardiam Centesis and Sampling• 冠状动脉造影: Coronary Arteriography• 腔静脉取血: Vena cava sampling• 心导管检查（微导管同）（进口仪器）: Cardiac catheterization• 经皮球囊扩张: Percutaneous balloon dilatating• 予激综合症心内膜检测: Endocardial investigation of preexcitation syndrome• 希氏束电图: Electrocardiogram of bundle of His• 心脏临时起搏: Cardiac temporary pacing• 埋置永久心脏起搏器: Cardioc permanent pacemaker implanting• 体肢动脉系统介入治疗: Transartery interventional therapy• 支气管动脉介入治疗: Bronchus artery interventional therapy• 肺动脉介入治疗: Pulmonary artery interventional therapy• 头臂动脉介入治疗: Brachiocephalic artery interventional therapy• 静脉介入治疗: Veinous interventional therapy• 冠状动脉介入治疗（球囊成形）: Coronary Artery interventional therapy （balloon angioplasty ）• 冠状动脉介入治疗（腔内旋磨）: Coronary Artery interventional therapy （rotablating ）• 冠状动脉介入治疗（腔内支架）: Coronary Artery interventional therapy （stent implantaion ）• 主动脉介入治疗: Aorta interventional therapy• 肾动脉介入治疗: Renal artery interventional therapy• 心脏瓣膜成形术: Heart valvuloplasty• 房间隔缺损封堵术: Atrial septal defect closer• 室间隔缺损封堵术: Ventricular septal defect closer• 动脉导管封堵术: Patent doctus arteriosus closer• 冠状动脉瘘封堵术: Coronary artery fistula closer• 冠状动脉腔内超声: Intracoronary ultrasound• 非冠状动脉血管内支架置入治疗: Stenting therapy of non-coronary artery• 经皮清除血管内异物: Transluminal eyewinker clearing• 经皮放置静脉滤器: Transluminal filter implantaion。
肾小球滤过率估算公式在糖尿病患者中的应用
肾小球滤过率估算公式在糖尿病患者中的应用吴楠【摘要】Diabetic kidney disease (DKD) is the most common microvascular complications of diabetes and the main cause of chronic kidney disease and end-stage renal disease (ESRD). Because of its incidence of occult, poor prognosis and high cost, it is essential to raising awareness of DKD, making a reasonable assessment of golmerular filtration rate (GFR) and taking effective intervention to prevent disease progression as early as possible, which is also important for preventing serious complications of the kidney. Many clinicians have recognized the importance of stratifying chronic kidney disease (CKD)in diabetic subjests. This article reviews recent literature of application of equations to estimate GFR in patients with diabetes to wake a general review.%糖尿病肾脏疾病(diabetic kidney disease,DKD)是糖尿病最常见的微血管并发症,是慢性肾脏疾病及终末期肾病(end-stage renal disease,ESRD)的首因,其发病隐匿且预后不佳,治疗费用极为昂贵.提高对DKD的早期认识,对GFR进行合理性评估,早期采取有力干预手段能预防疾病恶化.目前越来越多的临床医师认识到进行慢性肾脏疾病(chronic kidney disease,CKD)分期的重要性,但目前尚未确立适合于糖尿病患者的肾小球滤过率(glomerular filtration rate,GFR)评估公式.本文回顾近年来的文献资料,就GFR估算公式在糖尿病患者中的应用做一系统综述.【期刊名称】《复旦学报（医学版）》【年(卷),期】2011(038)003【总页数】6页(P275-280)【关键词】糖尿病;糖尿病肾脏疾病;肾小球滤过率;评估公式【作者】吴楠【作者单位】复旦大学附属华山医院内分泌科,上海,200040【正文语种】中文【中图分类】R587.1糖尿病是慢性肾脏疾病(chronic kidney disease,CKD)的主要病因之一,也是终末期肾脏疾病(end-stage renal disease,ESRD)接受肾脏替代治疗的首因[1]。
骨质疏松症与腰椎间盘突出症共病调查及影响因素分析
·4375··专题研究·共病问题·骨质疏松症与腰椎间盘突出症共病调查及影响因素分析韩涛1，孙凯1，孙传睿1，章轶立2，谢雁鸣3，申浩4，王旭1，齐保玉1，朱立国1*，魏戌1*【摘要】 背景 骨质疏松症（OP）和腰椎间盘突出症（LDH）是骨科临床中十分常见的两种疾病，二者关系密切，常合并发病。
随着社会老龄化的不断加剧，其给中老年人带来了严重的困扰。
目的 基于北京市社区中老年人群横断面调查研究，分析OP 与LDH 的共病发生情况及相关影响因素，为临床有效防治该类疾病提供参考。
方法 2017年11月至2018年7月选取北京市朝阳区和丰台区10个社区的1 540例社区居民为研究对象，有完整的信息记录和骨量筛查数据，现场采集居民的一般资料、骨折史、跌倒史、遗传病史、骨密度、EuroQol 健康指数等数据，筛选符合OP 诊断的患者，以其是否并发LDH 分为并发LDH 组与未并发LDH 组。
采用多因素Logistic 回归分析探讨OP 并发LDH 的影响因素。
结果 共纳入521例OP 患者，其中是否并发LDH 信息记录缺失1例；并发LDH 组80例，未并发LDH 组440例。
多因素Logistic 回归分析结果显示，将年龄、体质指数（BMI）作为校正因素，跌倒史〔OR=1.96，95%CI （1.02，3.78），P =0.044〕、骨折史〔OR=1.80，95%CI （1.04，3.12），P =0.035〕以及疼痛/不舒适〔OR=2.43，95%CI （1.41，4.18），P =0.001〕可能是OP 并发LDH 的影响因素。
结论 OP 和LDH 共病情况普遍存在，跌倒、骨折以及疼痛/不舒适可能是OP 并发LDH 的影响因素。
【关键词】 骨质疏松症；骨质疏松；腰椎间盘突出症；横断面研究；共病；影响因素分析【中图分类号】 R 681 【文献标识码】 A DOI：10.12114/j.issn.1007-9572.2022.0584韩涛，孙凯，孙传睿，等. 骨质疏松症与腰椎间盘突出症共病调查及影响因素分析［J］. 中国全科医学，2022，25（35）：4375-4380.［］HAN T，SUN K，SUN C R，et al. Prevalence and associated factors of lumbar disc herniation in osteoporosis：a cross-sectional survey［J］. Chinese General Practice，2022，25（35）：4375-4380.Prevalence and Associated Factors of Lumbar Disc Herniation in Osteoporosis ：a Cross-sectional Survey HAN Tao 1，SUN Kai 1，SUN Chuanrui 1，ZHANG Yili 2，XIE Yanming 3，SHEN Hao 4，WANG Xu 1，QI Baoyu 1，ZHU Liguo 1*，WEI Xu 1*1.Wangjing Hospital of CACMS ，Beijing 100102，China2.School of Chinese Medicine ，School of Integrated Chinese and Western Medicine ，Nanjing University of Chinese Medicine ，Nanjing 210023，China3.Institute of Basic Research In Clinical Medicine ，China Academy of Chinese Medical Sciences ，Beijing 100700，China4.Fengtai Changxindian Community Health Center ，Beijing 100072，China*Corresponding authors ：WEI Xu ，Researcher ，Professor ，Doctoral supervisor ；E-mail ：ZHU Liguo ，Chief physician ，Professor ，Doctoral supervisor ；E-mail ：HAN Tao and SUN Kai are co-first authors【Abstract 】 Background Osteoporosis（OP） and lumbar disc herniation（LDH） are two common orthopedic diseases encountered clinically，which are closely related and often coexisted，causing great suffering to middle-aged and elderly people along with the accelerated process of population aging. Objective To perform a cross-sectional survey on the prevalence and associated factors of LDH in OP in community-dwelling middle-aged and elderly people in Beijing，providing a reference for clinical prevention and treatment of this disease. Methods From November 2017 to July 2018，1 540 residents with complete demographics and bone mass measurement data who lived in 10 communities in Chaoyang District and Fengtai District of Beijing基金项目：国家重点研发计划（2021YFC1712800）；国家中医药传承创新团队项目（ZYYCXTD-C-202003）；中国中医科学院科技创新工程（CI2021A02013）；中国中医科学院优秀青年人才（创新类）培养专项（ZZ13-YQ-039）1.100102 北京市，中国中医科学院望京医院2.210023 江苏省南京市，南京中医药大学中医学院·中西医结合学院3.100700 北京市，中国中医科学院中医临床基础医学研究所4. 100072 北京市丰台区长辛店镇社区卫生服务中心*韩涛、孙凯为共同第一作者本文数字出版日期：2022-09-29扫描二维码查看原文·4376·E-mail:******************.cn骨质疏松症（osteoporosis，OP）与腰椎间盘突出症（lumbar disc herniation，LDH）是临床常见的骨科疾病。
阻塞性睡眠呼吸暂停低通气综合征患者血红蛋白增多发生率及其临床意义研究
·论著·阻塞性睡眠呼吸暂停低通气综合征患者血红蛋白增多发生率及其临床意义研究赵彬吉1，郭竞宇1，周佳瑾1，牟兰雪1，母桃娟2，张开艳2，吕云辉1*【摘要】 背景 阻塞性睡眠呼吸暂停低通气综合征（OSAHS）可引起红细胞和血红蛋白（HGB）增多，但对于OSAHS 患者HGB 增多发生率及其对临床合并症的预测价值尚无公认的结论。
目的 探讨OSAHS 患者HGB 增多发生率、相关影响因素以及其对肺动脉高压和Ⅱ型呼吸衰竭的预测作用。
方法 选取2018—2020年在云南省第一人民医院睡眠医学中心住院的1 035例OSAHS 患者为研究对象；采用倾向性评分匹配均衡基线资料，HGB 增多者纳入HGB 增多组（n=145），与之年龄、性别、体质指数（BMI）匹配的HGB 未增高者纳入HGB 正常组（n=145）；比较两组间多导睡眠监测（PSG）参数、临床检测指标和合并症发生率的差异。
采用Spearman 秩相关分析、多重线性回归分析探究HGB 的影响因素；采用受试者工作特征（ROC）曲线评估HGB 预测OSAHS 发生肺动脉高压和Ⅱ型呼吸衰竭的价值。
结果 OSAHS 患者HGB 增多发生率为16.8%（174/1 035），其中男性患者HGB 增多发生率25.7%（157/610）高于女性患者4.0%（17/425）（P<0.05），呼吸暂停低通气指数（AHI）重度的OSAHS 患者HGB 和HGB 增多发生率均高于中度和轻度患者（P<0.05）。
HGB 增多组的OSAHS 患者AHI、最长呼吸暂停持续时间（maxAT）、血氧饱和度小于90%的时间占总监测时间的百分比（TS90%）、红细胞计数（RBC）、HGB、血细胞比容（HCT）、平均HGB 浓度（MCHC）、天冬氨酸氨基转移酶（AST）、丙氨酸氨基转移酶（ALT）、血清尿酸（UA）、总胆固醇（TC）、三酰甘油（TG）、甲状腺素（T 4）、三碘甲状腺原氨酸（T 3）、动脉血二氧化碳分压（PaCO 2）水平高于HGB 正常组，平均血氧饱和度（MSpO 2）、最低血氧饱和度（LSpO 2）、动脉血氧分压（PaO 2）均低于HGB 正常组（P<0.05）；HGB 增多组合并高尿酸血症、蛋白尿、高碳酸血症的发生率高于HGB 正常组，合并甲状腺功能减退的发生率低于HGB 正常组（P<0.05）。
- 1、下载文档前请自行甄别文档内容的完整性，平台不提供额外的编辑、内容补充、找答案等附加服务。
- 2、"仅部分预览"的文档,不可在线预览部分如存在完整性等问题,可反馈申请退款(可完整预览的文档不适用该条件!)。
- 3、如文档侵犯您的权益，请联系客服反馈,我们会尽快为您处理(人工客服工作时间：9:00-18:30)。
P Widimsky MD DrSc FESC1, B Stellova MD1, L Groch MD2, M Aschermann MD DrSc FESC1, M Branny MD3, M Zelizko MD CSc4, J Stasek MD PhD1, P Formanek MD5; on behalf of the PRAGUE Study Group Investigators P Widimsky, B Stellova, L Groch, et al; on behalf of the PRAGUE Study Grouቤተ መጻሕፍቲ ባይዱ Investigators. Prevalence of normal coronary angiography in the acute phase of suspected ST-elevation myocardial infarction: Experience from the PRAGUE studies. Can J Cardiol 2006;22(13):1147-1152.
La prévalence de coronarographies normales pendant la phase aiguë d’une présomption d’infarctus du myocarde avec surélévation du segment ST : L’expérience des études PRAGUE
CLINICAL STUDIES
Prevalence of normal coronary angiography in the acute phase of suspected ST-elevation myocardial infarction: Experience from the PRAGUE studies
BACKGROUND: Acute ST-elevation myocardial infarction in patients with normal coronary arteries has previously been described, but coronary angiography in these patients was performed after the acute phase of the infarction. It is possible that these patients did not have normal angiograms during the acute phase (transient coronary thrombosis or spasm were usually suspected to be the cause). Information on the prevalence of truly normal coronary angiograms during the acute phase of a suspected ST-elevation myocardial infarction is lacking. PATIENTS AND METHODS: The PRimary Angioplasty in patients transferred from General community hospitals to specialized PTCA Units with or without Emergency thrombolysis-1 (PRAGUE-1) and PRAGUE-2 studies enrolled 1150 patients with ST-elevation acute myocardial infarction, in whom 625 coronary angiograms were performed within 2 h of the initial electrocardiogram. A simultaneous registry included an additional 379 coronary angiograms performed during the ST-elevation phase of a suspected myocardial infarction. Thus, a total of 1004 angiograms were retrospectively analyzed. A normal coronary angiogram was defined as one with the absence of any visible angiographic signs of atherosclerosis, thrombosis or spontaneous spasm. RESULTS: Normal coronary angiograms were obtained for 26 patients (2.6%). Among these, the diagnosis at discharge was a small myocardial infarction in seven patients (0.7%), acute (peri)myocarditis in five patients, dilated cardiomyopathy in four patients, hypertension with left ventricular hypertrophy in three patients, pulmonary embolism in two patients and misinterpretation of the electrocardiogram (ie, no cardiac disease) in five patients. Seven patients with small infarctions underwent angiography within 30 min to 90 min of complete relief of the signs of acute ischemia, and thus, angiograms during pain were not taken. None of the 898 patients catheterized during ongoing symptoms of ischemia had a normal coronary angiogram. Spontaneous coronary spasm as the only cause (without underlying coronary atherosclerosis) for the evolving infarction was not seen among these 898 patients. Thus, the causes of the seven small infarcts in patients with normal angiograms remain uncertain. CONCLUSIONS: The observed prevalence of normal coronary angiography in patients presenting with acute chest pain and ST elevations was 2.6%. Most of these cases were misdiagnoses, not infarctions. A normal angiogram during a biochemically confirmed infarction is extremely rare (0.7%) and was not seen during the ongoing symptoms of ischemia.