血清和肽素水平与急性缺血性卒中患者转归的相关性

目的 探讨血清和肽素水平与急性缺血性卒中患者转归的关系.方法 纳入发病24 h内的首次缺血性卒中患者,应用酶联免疫吸附法检测血清和肽素水平,应用美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评估基线卒中严重程度.在发病后90 d时应用改良Rankin量表(modified Rankin Scale,mRS)评分评价转归,0～2分定义为转归良好.年龄和性别相匹配的健康体检者作为对照者.结果 共纳入连续86例发病24 h内首次缺血性卒中患者和50名年龄和性别相匹配的健康体检者作为对照者.急性缺血性卒中患者发病24 h、7d和14 d血清和肽素水平分别为(7.81±0.66) pmol/L、(4.78±1.76) pmol/L和(2.82±1.42) pmol/L,均显著高于对照组[(1.67±0.56) pmol/L;P均＜0.05].86例患者中,74例(86.05％)转归良好,12例(13.95％)转归不良.转归不良组年龄[(67.64 ±9.62)岁对(61.12±7.31)岁;t=-3.420,P=0.020]、NIHSS评分[(14.16±4.22)分对(6.96±2.04)分;t=-8.26 3,P＜ 0.001]、基线收缩压[(166.06±13.42)mmHg对(154.12±11.69)mmHg;t=5.216,P=0.037;1mmHg=0.133 kPa]、空腹血糖[(8.79±2.98) mmol/L对(6.92±2.24) mmol/L;t=2.076,P=0.041]、C反应蛋白[(7.02±1.72) mg/L对(4.07±1.58) mg/L;t=-1.724,P=0.019]、24 h时和肽素水平[(9.67±2.28)p mol/L对(6.88±2.82)pmol/L;t=13.962,P＜ 0.001]、7d时和肽素水平[(8.22±2.14) pmol/L对(2.97±2.04)pmol/L;t=20.564,P＜0.001]、14 d时和肽素水平[(4.77±1.86)p mol/L对(2.02±0.76) pmol/L;t=8.428,P=0.032]以及心房颤动(33.33％对8.11％;x2=4.986,P=0.036)、大动脉粥样硬化性卒中(41.67％对21.62％;x2 =6.729,P=0.038)、心源性栓塞(33.33％对8.11％;x2=4.986,P=0.036)的患者构成比均显著高于转归良好组,小动脉闭塞性卒中的患者构成比显著低于转归良好组(16.67％对70.27％;x2=16.972,P=0.041).多变量logistic回归分析显示,血清24 h(优势比2.424,95％可信区间1.920 ～ 3.562;P＜0.001)和7d(优势比2.326,95％可信区间1.768 ～3.482;P＜0.001)时和肽素水平以及基线NIHSS评分(优势比2.146,95％可信区间1.616～3.268;P＜0.001)是转归不良的独立危险因素.结论 基线血清和肽素水平增高是急性缺血性卒中患者90 d时转归不良的独立预测因素.     

血清尿酸浓度对急性缺血性卒中患者短期转归的影响:回顾性病例系列研究

目的 探讨血清尿酸浓度对急性缺血性卒中患者短期转归的影响.方法 选取就诊的缺血性卒中患者,根据出院时改良Rankin量表(modified Rankin Scale,mRS)评分将患者分为转归良好组(mRS评分0～2分)和转归不良组(mRS评分3～6分),比较两组基线美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分、血清尿酸(serum uric acid,SUA)水平以及其他人口统计学和临床资料.结果 共纳入311例急性缺血性卒中患者,转归良好组185例,转归不良组126例.转归不良组基线NIHSS评分(中位数,四分位间距)[7(4 ～11)分对3(2 ～4)分;Z=9.858,P=0.001]、既往2型糖尿病(29.4％对14.1％;x2=10.877,P=0.001)和TIA史(27.8％对17.8％;x2=4.335,P=0.037)患者构成比显著性高于转归良好组,而SUA水平[(331.984±118.995) mmol/L对(363.276±100.743) mmol/L;t=2.497,P=0.013]和NIHSS评分＜9分的患者构成比(63.5％对96.8％;x2 =59.562,P=0.000)显著性低于转归良好组.SUA较低四分位数组基线NIHSS评分和出院mRS评分更高(P均＜0.01).多变量logistic回归分析显示,SUA增高为急性缺血性卒中患者短期转归的独立保护因素(优势比0.997,95％可信区间0.995 ～0.999;P =0.016).结论 SUA增高是急性缺血性卒中患者短期转归的独立保护因素.     

依那普利叶酸对伴有H型高血压的急性缺血性卒中患者转归的影响

目的 探讨依那普利叶酸片对伴有H型高血压的急性缺血性卒中患者转归的影响.方法 前瞻性连续纳入伴有H型高血压的急性缺血性卒中患者,随机分为依那普利叶酸治疗组和依那普利治疗组.依那普利叶酸治疗组给予马来酸依那普利叶酸片(10 mg/0.8 mg,1次/d);依那普利治疗组给予马来酸依那普利片(10 mg,1次/d).收集所有患者的人口学特征以及基线临床资料.应用改良Rankin量表(modified Rankin Sacle,mRS)评估患者出院和90 d时的转归情况,转归良好定义为mRS评分0～2分,转归不良定义为mRS评分＞2分.结果 共纳入248例患者,其中男性占66.5％,平均高半胱氨酸(homocysteine,Hcy)水平为(18.513±9.700) μmol/L.依那普利叶酸组和依那普利组分别为123例和125例,2组人口统计学、基线临床资料均无显著差异,转归不良的患者比例亦无显著差异(16.3％对18.4％;x2=0.198,P=0.738).将2组所有病例分为转归良好组和转归不良组,其中转归良好组205例(82.7％),转归不良组43例(17.3％).转归良好组平均年龄显著小于转归不良组[(69.22±11.12)岁对(75.88±9.26)岁;t=-4.826,P＜ 0.001],基线收缩压[(139.88±19.23)mmHg对(144.28±17.92) mmHg,l mmHg =0.133 kPa;t =2.138,P=0.033]和美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分[(2.454±2.340)分对(13.605±6.415)分;t=-27.081,P＜0.001]以及大动脉粥样硬化性卒中的患者构成比(58.50％对74.4％;x2=5.901,P=0.015)均显著低于转归不良组,但Hcy水平[(18.524±10.339) μmol/L对(18.298±6.105) μmol/L;t=0.013,P=0.989]和接受依那普利叶酸治疗的患者比例(50.2％对46.5％;x2 =0.198,P=0.738)无显著差异.多变量logistic回归分析显示,大动脉粥样硬化性卒中(优势比1.025,95％可信区间1.002～1.049;P =0.006)和基线NIHSS评分(优势比2.4,95％可信区间1.734 ～3.322;P ＜0.001)是转归不良的独立危险因素.结论 Hcy水平不是伴有H型高血压的急性缺血性卒中患者转归不良的独立危险因素.与依那普利比较,依那普利叶酸不能显著改善伴有H型高血压的急性缺血性卒中患者的转归.     

心房颤动对静脉溶栓治疗急性缺血性卒中转归的影响

目的 探讨心房颤动(atrial fibrillation,AF)对急性缺血性卒中患者静脉溶栓后临床转归和出血性转化(hemorrhagic transformation,HT)的影响.方法 回顾性纳入接受静脉重组组织型纤溶酶原激活剂溶栓治疗的急性缺血性卒中患者.90 d时改良Rankin量表评分0～2分定义为转归良好.采用多变量logistic回归分析确定AF与静脉溶栓后临床转归的相关性.结果 共纳入160例接受静脉溶栓治疗的急性缺血性卒中患者,其中67例(41.88％)合并AF.与非AF组相比,AF组年龄更大[中位数和四分位数间距:77(71 ～83)岁对69(59 ～78)岁;Z=4.142,P＜0.001],基线美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NHISS)评分更高[11(6～17)分对7(4 ～14)分;Z=2.623,P=0.009].AF组溶栓后24 h[3.0(1.0～4.5)分对2.0(0～6.0)分;Z=-0.312,P=0.775]和7 d[4.0(2.0～5.0)分对5.0(2.0～8.0)分;Z=1.574,P=0.115]时NIHSS评分较基线降低值以及90 d时转归良好患者比例(38.81％对25.82％;x2 =3.063,P=0.080)与非AF组差异均无统计学意义,但24 h内HT(14.93％对5.38％;x2=4.179,P=0.041)和90 d内死亡(16.42％对6.45％;x2 =4.073,P=0.044)患者比例显著高于非AF组.多变量logistic回归分析显不,AF与90 d时临床转归[优势比(odds ratio,OR0.95,95％可信区间(confidence interval,CI)0.381～2.366;P=0.912]、24 h内HT(OR1.992,95％ CI 0.580 ～6.369;P=0.285)以及90 d内死亡(OR 2.483,95％ CI0.727～8.586;P=0.146)均无独立相关性.结论 AF不是影响急性缺血性卒中患者静脉溶栓后90 d时临床转归和24 h内HT的独立危险因素.     

急性缺血性卒中机械取栓后出血性转化和临床转归的影响因素

目的 探讨急性缺血性卒中患者机械取栓治疗后出血性转化(hemorrhagic transformation,HT)和转归不良的危险因素.方法 回顾性纳入接受机械取栓治疗的急性缺血性卒中患者,收集患者的人口统计学、血管危险因素和其他临床资料,应用改良Rankin量表(modified Rankin Scale,mRS)评价发病90d时临床转归,转归良好定义为mRS评分0～2分.根据HT情况将患者分为HT组和非HT组,根据mRS评分将患者分为转归良好组和转归不良组.应用多变量logistic回归分析确定HT和转归不良的独立危险因素.结果 共纳入48例接受机械取栓治疗的急性缺血性卒中患者,男性25例(52.1％),平均年龄(64.77 ±9.14)岁,平均美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分(17.70 ±3.77)分.22例(45.8％)发生HT,其中9例为有症状HT;24例(50.0％)转归良好.HT组男性比例显著低于非HT组(30.4％对72.0％;x2=8.293,P=0.004),而糖尿病(65.2％对36.0％;x2=4.090,P=0.043)和心房颤动(78.3％对44.0％;x2=5.880,P=0.015)的患者比例以及基线空腹血糖水平[(8.514±4.400) mmol/L对(6.354±1.472) mmol/L;t =2.319,P=0.025]则显著高于非HT组.多变量logistic回归分析显示,心房颤动[优势比(odds ratio,OR)6.136,95％可信区间(confidence interval,CI)1.617～23.291;P=0.042]是机械取栓后发生HT的危险因素.转归良好组基线NIHSS评分[(16.050±4.865)分对(19.210±4.423)分;=2.354,P =0.023]以及糖尿病(29.2％对70.8％;x2=8.333,P=0.004)、前循环卒中(62.5％对87.5％;x2 =4.000,P =0.046)、大脑中动脉闭塞(29.2％对75.0％;x2=10.101,P=0.002)和脑实质血肿(4.1％对33.3％;P=0.011)患者比例显著低于转归不良组,而心房颤动(75.0％对45.8％;x2=4.269,P=0.039)和椎基底动脉闭塞(37.5％对12.5％;x2=10.113,P=0.006)患者比例显著高于转归不良组.多变量logistic回归分析显示,糖尿病(OR5.898,95％ CI 1.699～20.479;P=0.005)、基线NIHSS评分(OR1.167,95％ CI 1.011 ～1.347;P=0.035)和脑实质血肿(OR 1.295,95％ CI 1.099 ～ 1.875;P =0.028)是转归不良的独立危险因素.结论 心房颤动是急性缺血性卒中患者机械取栓治疗后HT风险的独立预测因素.糖尿病、基线NIHSS评分较高和并发脑实质血肿是转归不良的独立预测因素.因此,在对急性缺血性卒中患者开展机械取栓治疗前应充分评估其HT和转归不良风险.     

血浆纤维连接蛋白与急性缺血性卒中患者出血性转化的相关性

目的 探讨血浆纤维连接蛋白(fibronectin,Fn)水平与急性缺血性卒中患者出血性转化(hemorrhagic transformation,HT)的关系.方法 前瞻性纳入发病72 h内、基线MRI(包括梯度回波序列)未见出血且未行溶栓治疗的急性缺血性卒中患者,在发病7～10d后复查MRI,根据有无出血分为HT组和非HT组,比较两组患者血浆Fn水平.采用logistic回归分析探讨HT的预测因素.结果 共纳入78例急性缺血性卒中患者,其中11例(14.10％)发生HT.HT组心房颤动(36.4％对9.0％,P=0.012)和心源性栓塞(36.4％对6.0％,P=0.002)比例显著性高于非HT组,基线平均收缩压[( 182.09 ±20.73)mm Hg(1 mm Hg=0.133 kPa)对(161.25±26.40)mm Hg,P=0.015]、平均舒张压[ (98.00±11.26) mm Hg对(86.60±15.21)mm Hg,P=0.020]和血浆Fn浓度[(4 835.04±756.30)μg/L对(3 849.44±1 289.18) μg/L,P=0.016]均显著性高于非HT组.多变量logistic回归分析显示,血浆Fn浓度[优势比(odds ratio,OR)1.001,95％可信区间(confidence interval,CI)1.000 ～1.001,P=0.017]和心房颤动(OR 13.408,95％ CI 1.963 ～ 91.592;P=0.008)是急性缺血性卒中患者发生HT的独立预测因素.结论 HT患者血浆Fn水平显著增高,血浆Fn水平可作为急性缺血性卒中发病后非溶栓性HT的独立预测因素.     

合并非瓣膜性心房颤动的急性缺血性卒中患者出血性转化和转归的影响因素

目的 探讨合并非瓣膜性心房颤动(non-valvular atrial fibrillation,NVAF)的急性缺血性卒中患者出血性转化(hemorrhagic transformation,HT)风险以及溶栓治疗后3个月时的转归及其影响因素.方法 回顾性纳入连续的合并NVAF的急性缺血性卒中患者,收集其人口统计学、血管危险因素以及其他临床资料.采用改良Rankin量表(modified Rankin Scale,mRS)评价发病3个月时的转归,mRS评分≤2分定义为转归良好,＞2分定义为转归不良.结果 共纳入合并NVAF的急性缺血性卒中患者119例,其中男性63例(52.9％),女性56例(47.1％);平均年龄(72.1±10.0)岁;45例(37.81％)接受重组组织型纤溶酶原激活剂(recombinant tissue plasminogen activator,rtPA)溶栓治疗,55例(46.2％)转归良好,27例(22.7％)合并HT.与转归不良组相比,转归良好组平均年龄较小(P =0.028),合并缺血性心脏病以及发病至治疗时间＞4.5h的患者构成比较低(P均＜0.05),基线收缩压和舒张压以及美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分较低(P均＜0.05),而接受rtPA静脉溶栓的患者比例较高(P=0.019).多变量logistic回归分析显示,合并缺血性心脏病[优势比(odds ratio,OR)4.572,95％可信区间(confidence interval,CI)1.392～15.014;P=0.012]、治疗前收缩压(OR 1.028,95％ CI1.007 ～1.049;P=0.009)、基线NIHSS评分(OR 1.058,95％ CI1.002～1.117;P=0.042)是转归不良的独立危险因素,而rtPA静脉溶栓治疗(OR 0.264,95％ CI0.102 ～0.683;P=0.006)是转归不良的独立保护因素.HT组基线收缩压、空腹血糖和NIHSS评分以及既往卒中或短暂性脑缺血发作(transient ischemic attack,TIA)史患者构成比均显著性高于非HT组(P均＜0.05).多变量logistic回归分析显示,基线NIHSS评分(OR 1.147,95％ CI1.068 ～1.231;P＜0.001)、基线收缩压(OR 1.951,95％ CI1.921～1.982;P=0.002)和血糖水平(OR 1.191,95％ CI1.095 ～ 1.294;P＜0.001)为HT的独立危险因素.与非溶栓组相比,溶栓组平均年龄较低(P=0.021),基线收缩压、空腹血糖和NIHSS评分以及合并高脂血症、既往卒中或TIA史以及入院前使用抗高血压药的患者比例较高(P均＜ 0.05),合并缺血性心脏病的患者比例较低(P=0.035),但转归良好的患者比例更高(P=0.019).结论 合并缺血性心脏病、治疗前收缩压和基线NIHSS评分高是转归不良的独立危险因素,而rtPA静脉溶栓治疗是转归不良的独立保护因素;基线NIHSS评分、基线收缩压和血糖水平高为HT的独立危险因素.对于合并NVAF的急性缺血性卒中患者,如无明显溶栓禁忌证,则能从静脉溶栓治疗中获益,且不会增高HT风险,但应适当控制患者的血压和血糖水平.     

血糖变异性与重症急性卒中患者3个月内死亡风险的相关性

目的 探讨血糖变异性对重症急性卒中患者3个月内死亡风险的影响.方法 回顾性分析河北大学附属医院神经重症监护室收治的重症急性卒中患者的临床资料.根据3个月内转归将患者分为存活组和死亡组,比较2组基线美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分、急性生理与慢性健康评分Ⅱ(Acute Physiology and Chronic Health Evaluation Ⅱ,APACHEⅡ)、平均血糖、血糖标准差、平均血糖波动幅度、平均血糖变异系数以及其他临床资料,应用多变量logistic回归分析确定3个月内死亡风险的独立预测因素.结果 共纳入176例重症急性卒中患者,其中缺血性卒中124例(70.4％),脑出血52例(29.6％);27例(15.3％)在3个月内死亡.死亡组基线NIHSS评分[(22.5±2.3)分对(17.1±2.7)分;t=8.974,P＜0.001]、APACHEⅡ评分[(17.5±5.1)分对(6.8±7.1)分;t=13.136,P＜0.001]、血糖标准差[(3.6±2.2) mmol/L对(1.4±1.1) mmol/L;t =9.246,P＜0.001]、平均血糖波动幅度[(6.3±3.5)mmol/L对(3.8 ±2.1)mmol/L;t=5.989,P＜0.001]和平均血糖变异系数[(43.3±l3.1)％对(22.8±11.3)％;t=8.593,P＜0.001]均显著高于存活组,但平均血糖水平无显著差异[(13.5±1.7)mmol/L对(12.6±1.5) mmol/L;t=0.990,P=0.323].多变量logistic回归分析显示,基线APACHEⅡ评分[优势比(odds ratio,OR)2.911,95％可信区间(confidence interval,CI)1.962 ～ 4.560;P＜0.001]、NIHSS评分(OR 12.436,95％ CI5.071 ～30.495;P＜0.001)、血糖标准差(OR 4.302,95％ CI 1.855 ～9.973;P=0.001)、平均血糖波动幅度(OR 7.231,95％CI1.585 ～ 32.992;P=0.011)和平均血糖变异系数(OR 3.408,95％ CIl.363～8.522;P=0.009)是重症急性卒中患者3个月内死亡的独立预测因素.结论 血糖变异性是重症急性卒中患者3个月内死亡风险的独立预测因素,血糖波动范围大提示转归不良,其预测价值与基线APACHEⅡ评分相当.相比之下,平均血糖水平与患者转归无显著相关性.     

血清尿酸、胆红素水平与急性缺血性卒中患者近期转归的相关性

目的：探讨基线尿酸水平及胆红素水平与急性缺血性卒中患者短期转归的关系。方法收集缺血性卒中患者的临床资料,包括入院时血清尿酸和胆红素水平、美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale, NIHSS)评分、出院时或第14天时改良 Rankin 量表(modified Rankin Scale, mRS)评分(0~2分定义为转归良好,>2分定义为转归不良)。结果共纳入急性缺血性卒中患者162例,转归良好组114例,转归不良组48例。2组之间糖尿病(51．75%对75．00%;χ2=7．526,P =0．006)、既往卒中或短暂性脑缺血发作( transient ischemic attack, TIA)史(18．42%对50．00%;χ2=17．790, P <0．001)的患者构成比以及基线舒张压[(87．061±12．245)mmHg 对(82．375±10．949)mmHg,1 mmHg =0．133 kPa;t =2．293,P =0．023]、高密度脂蛋白胆固醇[(1．604±0．299)mmol/L 对(1．265±0．206)mmol/L; t =3．227, P =0．002]、空腹血糖[(2．875±0．438)mmol/L 对(8．160±0．592)mmol/L; t =-4．761, P <0．001)]、尿酸[(289．365±77．168)μmol/L 对(248．206±66．206)μmol/L; t =3．111, P =0．002]、总胆红素[(14．673±2．213)μmol/L 对(10．395±2．714)μmol/L; t =3．779, P <0．001]、直接胆红素[(6．036±1．392)μmol/L 对(4．956±1．379)μmol/L; t =2．088, P =0．038]、间接胆红素[(8．634±2．307)μmol/L 对(5．439±1．223)μmol/L;t =4．219,P <0．001]水平存在显著差异。多变量 logistic回归分析显示,既往卒中或 TIA 史[优势比(odds ratio, OR)3．751,95%可信区间(confidence interval, CI)1．395~10．091;P =0．009]和基线 NIHSS 评分(OR 2．723,95% CI 1．093~6．783;P =0．031)是缺血性卒中转归不良的独立危险因素,而尿酸(OR 0．357,95% CI 0．141~0．900;P =0．029)、高密度脂蛋白胆固醇(OR 0．262,95% CI 0．079~0．870;P =0．029)和间接胆红素(OR 0．117,95% CI 0．025~0．539;P =0．006)与转归良好独立相关。结论基线尿酸和间接胆红素水平增高是急性缺血性卒中患者转归良好的有利因素。     

血清透明质酸水平与急性自发性脑出血患者转归的相关性

目的 探讨脑出血患者血清透明质酸水平与临床转归的相关性.方法 纳入明确诊断为急性自发性脑出血的患者,记录基线临床资料,在入院24 h内检测血清透明质酸水平,在发病3个月后采用改良Rankin量表评价临床转归,分为转归良好组(0～2分)和转归不良组(＞2分),对2组临床资料进行比较和分析.结果 共纳入321例患者,转归良好组184例,转归不良组137例.转归良好组年龄[(46.3±8.6)岁对(62.4± 10.5)岁;t=3.761,P=0.025]、体质指数[(24.1±5.3)kg/m2对(27.8±6.1)kg/m2;t=6.193,P=0.013]、血肿体积[(59.7±9.7)ml对(89.2±14.9)ml;=6.278,P＜0.001]、基线格拉斯哥昏迷量表(Glasgow Coma Scale,GCS)评分[(6.3±1.5)分对(3.9±0.7)分;t=9.121,P＜0.001]、基线美国国立卫生研究院卒中量表(National Institutes of Health Stroke Scale,NIHSS)评分[(9.6±1.5)分对(16.3±4.5)分;=9.989,P＜0.001]和血清透明质酸水平[(376.2 ±22.9)ng/ml对(876.1±19.6)ng/ml;t=19.681,P＜0.001]与转归不良组存在显著统计学差异.多变量logistic回归分析显示,透明质酸[优势比(odds ratio,OR)4.396,95％可信区间(confidence interval,CI)1.912～6.897;P ＜0.001]、血肿体积(OR2.328,95％ CI 1.912 ～3.843;P=0.013)、NIHSS评分(OR2.662,95％ CI 1.127 ～2.976;P=0.023)和GCS评分(OR 0.879,95％ CI 0.097～0.969;P =0.046)是影响脑出血患者转归的独立因素.结论 基线血清透明质酸水平增高是急性自发性脑出血患者转归不良的独立预测因素.     

胰岛素瘤的解剖分布特点分析

目的胰岛素瘤是最常见的胰腺神经内分泌肿瘤，因其临床表现多样，导致诊断困难。影像学诊断尤其是超声内镜(EUS)在胰岛素瘤的诊断中起着重要作用，拥有较高的敏感性和特异性。本研究拟通过明确胰岛素瘤的解剖分布特点，以期有助于提高影像学的诊断准确率和降低漏诊率，尤其是在教育和培训实践中对于EUS的学习者更具有指导价值。 方法回顾性分析解放军总医院第一医学中心病案资料数据库1993年1月至2019年11月经外科手术、病理确诊为胰岛素瘤的患者的临床资料，检索方法采取搜索术后病理诊断为"胰岛素瘤"的病例，通过查阅病例的方法，提取出胰岛素瘤的大小和解剖分布等数据，进一步分析其特点。 结果共检索到确诊为胰岛素瘤的患者116例，其中，男45例、女71例，年龄13～76岁，平均年龄(44.4±14.85)岁。胰岛素瘤单发110例(94.8%)、多发6例(5.2%)。位置分布：头颈部46例(39.7%)，单发45例、多发1例；体尾部68例(58.6%)，单发65例、多发3例；全胰腺多发2例(1.7%)。病变大小特点：最大径0.4～3.4 cm，平均大小(1.53±0.58)cm。≤1 cm 29例、>1 cm而≤1.5 cm41例、>1.5 cm而≤2.0 cm28例，≤3 cm 15例，>3 cm 3例。年龄与肿瘤的大小相关，≤44岁患者肿瘤平均大小为(1.36±0.51)cm、>44岁患者肿瘤平均大小为(1.70±0.60)cm，P<0.05。头颈部的肿瘤大于体尾部的肿瘤，头颈部肿瘤平均大小(1.66±0.63)cm，体尾部(1.42±0.52)cm，P<0.05。 结论胰岛素瘤在胰腺体尾部较头颈部更好发；绝大多数单发，但可以全胰腺多发；多数小于1.5 cm，肿瘤的大小与患者年龄和肿瘤的解剖分布相关。     

Pathogenesis of carcinoma of the papilla of Vater

Most adenomas and carcinomas of the small intestine and extrahepatic bile ducts arise in the region of the papilla of Vater. In familial adenomatous polyposis (FAP) it is the main location for carcinomas after proctocolectomy. In many cases symptoms due to stenosis lead to diagnosis at an early tumor stage. In about 80%, curative intended resection is possible. Operability is the most relevant prognostic factor. Most ampullary carcinomas resp. carcinomas of the papilla of Vater develop from adenomatous or flat dysplastic precursor lesions. They can be sited in the ampulloduodenal part of the papilla of Vater, which is lined by intestinal mucosa. They also can develop in deeper parts of the ampulla, which are lined by pancreaticobiliary duct mucosa. Intestinal-type adenocarcinoma and pancreaticobiliary-type adenocarcinoma represent the main histological types of ampullary carcinoma. Furthermore, there exist unusual types and undifferentiated carcinomas. Many carcinomas of intestinal type express the immunohistochemical marker profile of intestinal mucosa (keratin 7?, keratin 20+, MUC2+). Carcinomas of pancreaticobiliary type usually show the immunohistochemical profile of pancreaticobiliary duct mucosa (keratin 7+, keratin 20?, MUC2?). Even poorly differentiated carcinomas, as well as unusual histological types, may conserve the marker profile of the mucosa they developed from. These findings underline the concept of histogenetically different carcinomas of the papilla of Vater which develop either from intestinal- or from pancreaticobiliary-type mucosa of the papilla of Vater. Molecular alterations in ampullary carcinomas are similar to those of colorectal as well as pancreatic carcinomas, although they appear at different frequencies. In future studies, molecular alterations in ampullary carcinomas should be correlated closely with the different histologic tumor types. Consequently, the histologic classification should reflect the histogenesis of ampullary tumors from the two different types of papillary mucosa.     

Demonstration of the mechanism of action of biguanides

Summary Palmitic acid oxidation in rat diaphragm homogenate is depressed by biguanide concentrations that are still incapable of inhibiting oxidative phosphorylation. Glucose oxidation is not directly effected by the same biguanide concentrations: however, the inhibitory effect of palmitic acid on glucose oxidation is partly removed by biguanides. Inhibition of fatty acid oxidation, which accounts for most of the metabolic effects caused by these drugs, can be regarded as the fundamental mechanism of action of biguanides. There is some evidence suggesting that these drugs might interact with carnitine, thus preventing long-chain fatty acids from being transported across the mitochondrial membrane to the site of oxidation. Traduzione a cura degli AA.     

Lack of correlation of degree of villous atrophy with severity of clinical presentation of coeliac disease

BACKGROUND AND AIM: Both the clinical presentation and the degree of mucosal damage in coeliac disease vary greatly. In view of conflicting information as to whether the mode of presentation correlates with the degree of villous atrophy, we reviewed a large cohort of patients with coeliac disease. PATIENTS AND METHODS: We correlated mode of presentation (classical, diarrhoea predominant or atypical/silent) with histology of duodenal biopsies and examined their trends over time. RESULTS: The cohort consisted of 499 adults, mean age 44.1 years, 68% females. The majority had silent coeliac disease (56%) and total villous atrophy (65%). There was no correlation of mode of presentation with the degree of villous atrophy (p=0.25). Sixty-eight percent of females and 58% of males had a severe villous atrophy (p=0.052). There was a significant trend over time for a greater proportion of patients presenting as atypical/silent coeliac disease and having partial villous atrophy, though the majority still had total villous atrophy. CONCLUSIONS: Among our patients the degree of villous atrophy in duodenal biopsies did not correlate with the mode of presentation, indicating that factors other than the degree of villous atrophy must account for diarrhoea in coeliac disease.     

血吸虫童虫生长发育及其机制的研究进展

血吸虫童虫是宿主免疫系统攻击的重要靶标,包括皮肤型、肺型和肝门型童虫。宿主分子对童虫生长发育具有重要作用。童虫生长发育机制包括免疫调节、信号转导、性别发育及凋亡等。肌动蛋白、组织蛋白酶、烯醇化酶和葡萄糖基转移酶等分子为血吸虫童虫生长发育的重要分子。本文对血吸虫童虫生长发育及其机制的研究进展做一综述。     

氯硝柳胺悬浮剂的毒性评价

目的评价氯硝柳胺悬浮剂的毒性，为现场大规模应用灭螺提供依据。方法按照中华人民共和国国家标准GB 15670-1995《农药登记毒理学试验方法》和鱼类毒性试验方法进行。结果经口、经皮肤的LDso雌、雄性大鼠均>5 000 mg/kg，经呼吸道的LCso雌、雄性大鼠均>5 000mg/m3，该药经口、经皮肤、经呼吸道毒性均属微毒类药物；兔眼用药后，观察期内无不良反应，对眼无刺激性；皮肤用药后对皮肤无刺激性。与氯硝柳胺原药、氯硝柳胺乙醇胺盐原药和氯硝柳胺乙醇胺盐可湿性粉剂相比，氯硝柳胺悬浮剂对鱼急性毒性最低。结论氯硝柳胺悬浮剂属微毒类药物，对鱼的毒性低于其乙醇胺盐可湿性粉剂，适合于现场应用。     

124例耐多药结核分枝杆菌基因突变特征分析

目的对临床分离的耐多药结核分枝杆菌相关基因的突变特征进行分析。方法对124例耐多药结核分枝杆菌以及50株敏感株的耐药相关基因(包括异烟肼inh A、kat G、oxyR-ahp C间隔区以及利福平rpo B)进行序列测定,分析其基因突变情况。结果异烟肼耐药inh A基因突变率为14.5%;kat G基因突变率为70.2%(87/124),主要位于315位;oxyR-ahp C间隔区突变率为15.3%;inh A、kat G两种基因同时突变率75.0%,三种基因同时突变率为89.5%。利福平rpo B基因突变的检出率高达95.2%,突变主要发生在531、526、516位点。结论我省耐多药菌异烟肼耐药相关基因最常见突变为kat G 315、inh A C-T(-15)、axyR-ahp C间隔区(-10)C-T,利福平为rpo B531、526、516。结合MDR-TB耐药相关基因的特征分析,可以建立一种快速、准确、特异的适合于我省的检测结核菌耐多药性的新方法。     

Assessment of quality of life of parents of children with juvenile chronic arthritis

The aim of the study was to assess the quality of life (QOL) and the psychological status of parents of children with juvenile chronic arthritis (JCA). The QOL, anxiety and depression of the parents of 28 children with JCA were evaluated and compared to those of the parents of 28 healthy children. Mothers of JCA children and mothers of healthy children reported similar QOL. The reported anxiety and depression levels were similar for mothers and fathers in both groups. The parents of children with pauciarticular-type JCA reported lower QOL and higher levels of anxiety and depression than the parents of children with other types, namely polyarticular and systemic JCA. These findings may be explained by the fact that the pauciarticular patients had shorter disease duration and were less frequently seen in the outpatient clinic. The QOL of mothers of children with JCA was found to be slightly impaired in the group of children with pauciarticular JCA. Future larger studies are needed to confirm these results, as the number of subjects in the three groups was rather low. Received: 26 September 2001 / Accepted: 8 February 2002     

Numerical Simulation of the Effect of Rate of Change of Glucose on Measurement Error of Continuous Glucose Monitors

Background

A 5-day in-patient study designed to assess the accuracy of the FreeStyle Navigator® Continuous Glucose Monitoring System revealed that the level of accuracy of the continuous sensor measurements was dependent on the rate of glucose change. When the absolute rate of change was less than 1 mg•dl⁻¹•min⁻¹ (75% of the time), the median absolute relative difference (ARD) was 8.5%, with 85% of all points falling within the A zone of the Clarke error grid. When the absolute rate of change was greater than 2 mg•dl⁻¹•min⁻¹ (8% of the time), the median ARD was 17.5%, with 59% of all points falling within the Clarke A zone.

Method

Numerical simulations were performed to investigate effects of the rate of change of glucose on sensor measurement error. This approach enabled physiologically relevant distributions of glucose values to be reordered to explore the effect of different glucose rate-of-change distributions on apparent sensor accuracy.

Results

The physiological lag between blood and interstitial fluid glucose levels is sufficient to account for the observed difference in sensor accuracy between periods of stable glucose and periods of rapidly changing glucose.

Conclusions

The role of physiological lag on the apparent decrease in sensor accuracy at high glucose rates of change has implications for clinical study design, regulatory review of continuous glucose sensors, and development of performance standards for this new technology. This work demonstrates the difficulty in comparing accuracy measures between different clinical studies and highlights the need for studies to include both relevant glucose distributions and relevant glucose rate-of-change distributions.     

Study of constancy of hydrogen-consuming flora of human colon

The constancy of the hydrogen consuming flora of the human colon was studied in 15 healthy subjects via two measurements obtained 18 to 36 months apart. Hydrogen disappearance rate and the major products of H₂-consuming bacteria, methane and sulfide, were measured during incubation of fecal homogenates with excess hydrogen and sulfate. In 11/15, the hydrogen consumption rate and the predominant hydrogen-consuming pathway (methanogenesis, sulfate reduction, or neither) remained constant. However, major shifts in these pathways were observed in four subjects, with two losing and two gaining the ability to produce methane. Methanogenesis was associated with the highest hydrogen consumption rate. This study demonstrates that clinically unrecognizable, major alterations of the colonic flora occur in healthy subjects. Understanding of the factors responsible for these alterations might allow for therapeutic manipulation of the colonic flora.Supported in part by the Department of Veterans Affairs and NIDDKD RO1 DK 13309-25.