坎地沙坦酯与依那普利对高血压病患者尿微量白蛋白的影响

目的比较坎地沙坦酯与依那普利对原发性高血压病人的血压及尿微量白蛋白的影响。方法原发性高血压伴尿微量白蛋白患者71例随机分为两组:口服坎地沙坦酯8～16mg/d(A组,35例);口服依那普利10～20mg/d(B组,36例),疗程12周。分别测量两组治疗前后血压、尿微量白蛋白、血肌酐、尿肌酐并计算内生肌酐清除率。结果两组治疗后血压及尿微量白蛋白均显著下降(P<0.01),组间比较,差异无统计学意义(P>0.05);两组治疗前后血肌酐、计算内生肌酐清除率均无明显变化(P>0.05)。结论坎地沙坦酯不仅能有效降低血压,而且能降低尿微量白蛋白,与依那普利疗效相似。     

3种药物(氨氯地平,坎地沙坦,咪达普利)小剂量联合治疗明显减少高血压糖尿病患者的尿微量白蛋白释出

目的 探讨3种药物,包括钙拮抗剂(左旋氨氯地平),血管紧张素转换酶抑制剂(ACEI)(咪达普利)和血管紧张素受体拮抗剂(ARB)(坎地沙坦)联合治疗方案对2型糖尿病高血压患者尿微量蛋白的影响.方法 高血压2型糖尿病伴尿微量蛋白阳性门诊或住院病人160例,按就诊顺序随机分4组:分别用坎地沙坦(4 mg/d) 左旋氨氯地平(2.5 mg/d)、坎地沙坦(4 mg/d) 咪达普利(5 mg/d,n=40)、咪达普利(5 mg/d) 左旋氨氯地平(2.5mg/d,n=40)和左旋氨氯地平(2.5 mg/d) 坎地沙坦(4 mg/d) 咪达普利治疗(5 mg,n=40),疗程3月.观察治疗前后血压、尿微量白蛋白变化.结果 4组血压均较治疗前明显降低(P<0.05),但治疗后4组间血压比较,差异无统计学意义;尿微量白蛋白4组均较治疗前减少(P<0.01),3种药联合治疗组比2种药联合治疗组下降更明显[坎地沙坦 左旋氨氯地平组:治疗前(40.5±9.6)mg/L比治疗后(25.2±6.2)mg/L;坎地沙坦 咪达普利组:治疗前(41.3±10.8)mg/L比治疗后(20.2±6.3)mg/Li咪达普利 左旋氨氯地平组:治疗前(43.3±10.4)mg/L比治疗后(20.6±6.4)mg/L;左旋氨氯地平 坎地沙坦 咪达普利联合组:治疗前(41.7±10.2)mg/L比治疗后(15.6±6.3)mg/L;P<0.05].结论 小剂量坎地沙坦、咪达普利及左旋氨氯地平联合应用在有效降压的同时,能改善2型糖尿病高血压患者早期肾损害,提示有早期肾损害者应尽早联合降压治疗.     

3种药物(氨氯地平,坎地沙坦,咪达普利)小剂量联合治疗明显减少高血压糖尿病患者的尿微量白蛋白释出

目的探讨3种药物,包括钙拮抗剂(左旋氨氯地平),血管紧张素转换酶抑制剂(ACEI)(咪达普利)和血管紧张素受体拮抗剂(ARB)(坎地沙坦)联合治疗方案对2型糖尿病高血压患者尿微量蛋白的影响。方法高血压2型糖尿病伴尿微量蛋白阳性门诊或住院病人160例,按就诊顺序随机分4组:分别用坎地沙坦(4 mg/d)+左旋氨氯地平(2.5 mg/d)、坎地沙坦(4 mg/d)+咪达普利(5 mg/d,n=40)、咪达普利(5 mg/d)+左旋氨氯地平(2.5mg/d,n=40)和左旋氨氯地平(2.5 mg/d)+坎地沙坦(4 mg/d)+咪达普利治疗(5 mg,n=40),疗程3月。观察治疗前后血压、尿微量白蛋白变化。结果 4组血压均较治疗前明显降低(P<0.05),但治疗后4组间血压比较,差异无统计学意义;尿微量白蛋白4组均较治疗前减少(P<0.01),3种药联合治疗组比2种药联合治疗组下降更明显[坎地沙坦+左旋氨氯地平组:治疗前(40.5±9.6)mg/L 比治疗后(25.2±6.2)mg/L;坎地沙坦+咪达普利组:治疗前(41.3±10.8)mg/L 比治疗后(20.2±6.3)mg/L;咪达普利+左旋氨氯地平组:治疗...     

坎地沙坦酯与依那普利对高血压病患者尿微量白蛋白的影响

目的 比较坎地沙坦酯与依那普利对原发性高血压病人的血压及尿微量白蛋白的影响.方法 原发性高血压伴尿微量白蛋白患者71例随机分为两组:口服坎地沙坦酯8～16 mg/d(A组,35例);口服依那普利10～20 mg/d(B组,36例),疗程12周.分别测量两组治疗前后血压、尿微量白蛋白、血肌酐、尿肌酐并计算内生肌酐清除率.结果 两组治疗后血压及尿微量白蛋白均显著下降(P＜0.01),组问比较,差异无统计学意义(P＞0.05);两组治疗前后血肌酐、计算内生肌酐清除率均无明显变化(P＞0.05).结论 坎地沙坦酯不仅能有效降低血压,而且能降低尿微量白蛋白,与依那普利疗效相似.     

苯那普利与伊贝沙坦联合用药对高血压患者尿蛋白,血肌酐清除率,血肌酐的影响

目的观察苯那普利、伊贝沙坦及两药联用对原发性高血压患者微量白蛋白尿的影响.方法采用随机、单盲、病例对照设计,82例原发性高血压伴微量白蛋白尿的患者,随机接受苯那普利10 mg/d(n＝25)、伊贝沙坦300 mg/d(n＝28)或苯那普利5 mg/d联用伊贝沙坦150 mg/d(联用组n＝29)治疗18周,比较治疗前后及同期各组间的收缩压(SBP)、舒张压(DBP)、尿白蛋白排泄率(UAER)、肌酐清除率(CCr)、血清肌酐(SCr).为达到血压<140/90 mm Hg的控制目标,可以加用吲达帕胺和/或倍他乐克.结果 (1)SBP、DBP同期各组无显著差别,治疗前后比较各组均下降显著(P<0.001);(2)UAER治疗后各组均显著下降(苯那普利组下降18.8%,伊贝沙坦组下降18.5%,联用组下降46.8%,P<0.001),两单药组分别与联用组比较差别显著(苯那普利组P＝0.022,伊贝沙坦组P＝0.025),联用组较单药组下降幅度总体增加28.2%.(3)联合用药组治疗后血肌酐上升(85.9±16.1 vs 94.6±14.5)μmol/L,肌酐清除率下降(85.3±5.8 vs 78.3±4.1)mL/min.结论对原发性高血压伴微量白蛋白尿的患者,苯那普利、伊贝沙坦减少微量白蛋白尿的作用相当,两药联用则作用明显加强.联合用药组血肌酐浓度上升,肌酐清除率下降,可能提示肾小球内压下降,其长期预后意义有待观察.     

坎地沙坦与氨氯地平对高血压左室肥厚患者心功能和尿微量白蛋白的疗效观察

目的探讨坎地沙坦和氨氯地平对高血压患者左室肥厚和尿微量白蛋白的疗效。方法对83例门诊原发性高血压(1级、2级)并左室肥厚患者随机分为坎地沙坦组(42例)和氨氯地平组(41例),分别予以坎地沙坦和氨氯地平治疗。于受试前、后分别测定血压及二维彩色B超,检测室间隔(IVS)、左室后壁厚度(LVPW)、左室舒张末内径(LVDd)、E/A、左室射血分数(EF)和左室重量指数(LVMI),同时测定尿微量白蛋白、血清尿素氮和肌酐。结果两组在受试2周后与治疗前相比,血压均开始明显下降(P<0.01),两组降压疗效相比差异无统计学意义。两组24周测IVS、LVPW、LVDd和LVMI,较治疗前明显降低(P<0.01),EF和E/A升高(P<0.01),24周后坎地沙坦组优于氨氯地平组(P<0.05)。两组治疗4周后尿微量白蛋白都有明显下降(P<0.01)。坎地沙坦组随用药时间的延长,尿微量白蛋白不断降低,24周后明显优于氨氯地平组(P<0.01)。两组治疗前后血清尿素氮和肌酐无明显变化(P>0.05)。结论坎地沙坦和氨氯地平都有良好的降压作用,并且能逆转左室肥厚、降低尿微量白蛋白,但坎地沙坦的保护作用优于氨氯地平。     

苯那普利与伊贝沙坦联合用药对高血压患者尿蛋白，血肌酐清除率，血肌酐的影响

目的　观察苯那普利、伊贝沙坦及两药联用对原发性高血压患者微量白蛋白尿的影响。方法采用随机、单盲、病例对照设计 ,82例原发性高血压伴微量白蛋白尿的患者 ,随机接受苯那普利 10mg/d(n =2 5 )、伊贝沙坦 30 0mg/d(n =2 8)或苯那普利 5mg/d联用伊贝沙坦 15 0mg/d(联用组 :n =2 9)治疗 18周 ,比较治疗前后及同期各组间的收缩压 (SBP)、舒张压 (DBP)、尿白蛋白排泄率(UAER)、肌酐清除率 (CCr)、血清肌酐 (SCr)。为达到血压 <14 0 / 90mmHg的控制目标 ,可以加用吲达帕胺和 /或倍他乐克。结果 (1)SBP、DBP同期各组无显著差别 ,治疗前后比较各组均下降显著(P <0 0 0 1) ;(2 )UAER治疗后各组均显著下降 (苯那普利组下降 18.8% ,伊贝沙坦组下降 18 5 % ,联用组下降 4 6 .8% ,P <0 0 0 1) ,两单药组分别与联用组比较差别显著 (苯那普利组 :P =0 0 2 2 ,伊贝沙坦组 :P =0 0 2 5 ) ,联用组较单药组下降幅度总体增加 2 8.2 %。 (3)联合用药组治疗后血肌酐上升(85 .9± 16 .1vs 94 .6± 14 .5 ) μmol/L ,肌酐清除率下降 (85 .3± 5 .8vs 78.3± 4 .1)mL/min。结论对原发性高血压伴微量白蛋白尿的患者 ,苯那普利、伊贝沙坦减少微量白蛋白尿的作用相当 ,两药联用则作用明显加强。联合用药组血肌酐浓度上升 ,肌     

坎地沙坦和苯那普利治疗高血压病的对照研究

目的评价坎地沙坦同苯那普利治疗高血压病的疗效及其对血脂、肾功能的影响及副作用。方法坎地沙坦组59例给予坎地沙坦剂量816 mg/d,苯那普利组56例服用苯那普利,剂量1020 mg/d,均治疗6周。治疗前后所有参与者测血压和测定胆固醇、三酰甘油、肾功能。结果监测血压显示坎地沙坦组降压与苯那普利组无差异,对胆固醇、三酰甘油没有影响,有降低尿酸的作用,与苯那普利组相比,咳嗽发生率低,并能改善肾功能及保护内皮细胞功能。结论坎地沙坦同苯那普利治疗轻、中度高血压病安全、有效,对血脂、肾功能无影响。坎地沙坦有降低尿酸的作用,咳嗽发生率低。     

睡前服用坎地沙坦对高血压患者血压晨峰及尿微量白蛋白的影响

目的观察睡前服用坎地沙坦对高血压患者血压晨峰的影响及尿微量白蛋白的变化。方法选择162例存在血压晨峰的高血压患者,随机分为对照组54例、上午服药组54例和睡前服药组54例。对照组患者给予氢氯噻嗪25mg睡前(18:00~21:00),上午服药组上午给予坎地沙坦4~8mg(08:00~10:00),睡前服药组睡前给予坎地沙坦4~8mg(18:00~21:00)。3组患者均在服药4周后再次行24h动态血压监测,并记录昼间、夜间及晨起血压,并测量3组患者治疗前后尿微量白蛋白的变化。结果与对照组和上午服药组比较,睡前服药组治疗后血压晨峰明显降低[(19.6±2.3)mm Hg vs(38.5±4.8)mm Hg和(32.2±3.6)mm Hg,1 mm Hg=0.133kPa,P<0.05],尿微量白蛋白明显降低[(35.2±6.1)mg/L vs(60.6±12.1)mg/L和(54.3±8.3)mg/L,P<0.05]。结论睡前服用坎地沙坦可以有效改善患者的血压晨峰现象,并有效降低尿微量白蛋白,减少早期肾损害的发生。     

氯沙坦对原发性高血压患者内皮功能及肾功能的影响

目的:观察氯沙坦对原发性高血压患者血一氧化氮(NO)、内皮素(ET)、血尿微球蛋白(β2MG)、尿微量白蛋白的影响。方法:将60例患者分为A组(氯沙坦组n=30)和B组(福辛普利组n=30),进行血NO、ET、β2MG、尿微量白蛋白及血肌酐等检查。2组治疗前后相互比较。结果:2组治疗前后血NO、ET、β2MG、尿微量白蛋白均有显著性差异(P<0.05)。而血尿素氮、肌酐治疗前后差异无显著性(P>0.05)。A组B组组间比较差异无显著性(P>0.05)。结论:氯沙坦同福辛普利相类似,均具有血管内皮及肾脏保护作用。     

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.