使用不同胰岛素类似物治疗老年2型糖尿病

目的用动态血糖监测方法评价两种预混胰岛素类似物治疗2型糖尿病（T2DM）时血糖漂移和低血糖发生率的差异,为临床使用提供参考。方法选取一般情况匹配且需要胰岛素治疗的老年2型糖尿病患者64例,随机分为2组。分别使用门冬胰岛素30注射液和赖脯胰岛素25注射液进行治疗。在血糖达标前提下,采用动态血糖监测的方法,评价两组患者血糖漂移和低血糖发生率的差异。结果两组患者血糖达标时,胰岛素总量无统计学差异[（38．0±6．2）w（40．0±5．1）U／d,P〉0．05]。两组平均血糖漂移幅度[（6．32±1．43）VS（6．86±1．51）mmol／L,P〉0．05]及血糖漂移系数[（1．35±0．22）VS（1．41±0．13）,P〉0．05]均无统计学差异。赖脯胰岛素25注射液低血糖事件少于门冬胰岛素30组,但差异无统计学意义（12％vs8％,P〉0．05）。结论门冬胰岛素30注射液和赖脯胰岛素25注射液治疗老年2型糖尿病,在血糖控制良好时,胰岛素总量、血糖漂移及低血糖发生率相当。     

伏格列波糖联合精蛋白锌重组赖脯胰岛素混合液25R治疗口服降糖药物血糖控制不佳老年2型糖尿病临床研究

选取2017年6月～2018年6月98例口服降糖药物血糖控制不佳老年T2DM患者,随机平分对照组给予精蛋白锌重组赖脯胰岛素混合液25R治疗,观察组给予伏格列波糖联合精蛋白锌重组赖脯胰岛素混合液25R治疗3个月后。结果观察组空腹血糖(FPG)、糖化血红蛋白(Hb A1c)、餐后2 h血糖(2hPG)低于对照组(P 0. 05)、胰岛素用量少于对照组(P 0. 05);有症状低血发生率2. 04%低于对照组16. 33%(P 0. 05)。结论伏格列波糖联合精蛋白锌重组赖脯胰岛素混合液25R治疗口服降糖药物血糖控制不佳老年T2DM患者,能提高血糖控制效果,减少胰岛素应用剂量,安全性高。     

沙格列汀联合精蛋白锌重组赖脯胰岛素混合注射液对2型糖尿病患者血糖控制及体质量指数的影响

选取2016年10月～2018年4月T2DM患者116例,随机平分为对照组采取精蛋白锌重组赖脯胰岛素混合注射液治疗,试验组采取沙格列汀联合精蛋白锌重组赖脯胰岛素混合注射液治疗,3个月。糖化血红蛋白(Hb A1c)、空腹血糖(FPG)与餐后2 h血糖(2h PG)]、体质量指数(BMI)。结果试验组治疗后Hb A1c、FPG与2h PG水平; BMI较对照组低(P0. 05)。结论联合应用沙格列汀与精蛋白锌重组赖脯胰岛素混合治疗可提高血糖控制水平,降低体质量。     

赖脯胰岛素75/25治疗2型糖尿病疗效观察

2007年2-6月，我们应用赖脯胰岛素（lispro）75／25治疗2型糖尿病（T2DM）42例，取得较好疗效。现报告如下。 临床资料：本组T2DM患者85例，男40例、女45例，年龄38～72岁，病程平均12．6a，均符合1999年WHO制定的T2DM诊断标准。患者糖化血红蛋白（HbA1c）≤正常值上限2倍，入选前均应用70／30人胰岛素（剂量〈2IU／kg，2次／d）〉2个月。随机分为观察组42例、对照组43例。两组年龄、性别、病程有可比性。     

谷赖胰岛素或赖脯胰岛素联合甘精胰岛素对糖尿病的有效性及安全性

目的 比较谷赖胰岛素和赖脯胰岛素联合甘精胰岛素对糖尿病的有效性、安全性.方法 本研究为多中心、随机、对照研究,包括4周的导人期和12周的治疗期.2007年2月至2008年6月共人选糖尿病患者484例（1型34例,2型450例）,患者糖化血红蛋白（HbA1c）为6.5％～11.0％,之前已接受连续3个月的胰岛素治疗.按3：1随机给予谷赖胰岛素（363例）或赖脯胰岛素（121例）每日3次联合甘精胰岛素每日1次治疗,比较两组治疗12周后HbA1c、血糖变化及低血糖发生情况和治疗满意度.组间数据比较采用ANOVA方法.结果 治疗12周后,谷赖胰岛素和赖脯胰岛素组HbA1c分别由8.7％±1.2％降至7.9％±1.0％及由8.8％±1.2％降至7.9％±1.0％（组内治疗前后比较,t=- 12.55、-8.88,均P＜0.05）.两组空腹血糖（FPG）分别由（8.6±2.8）mmol/L降至（7.7±2.5）mmol/L及由（8.6±2.5） mmol/L降至（7.8±2.2）mmol/L（组内治疗前后比较,t=-6.55、-2.98,均P＜0.05）.谷赖胰岛素组标准餐后2h血糖（2 h PPG）由（10.6±3.8） mmol/L降至（ 10.2±3.7） mmol/L（t=-2.07,P＜0.05）;赖脯胰岛素组2 h PPG治疗前后差异无统计学意义[由（ 10.9±4.0）mmol/L降至（10.4±3.5） mmol/L,t=-1.37,P＞0.05].治疗12周期间,谷赖胰岛素组和赖脯胰岛素组低血糖事件发生率分别为33.9％ （123/363）和34.7％ （42/121）.治疗前后谷赖胰岛素组和赖脯胰岛素组治疗满意度总评分分别由29±5升至31±5及由29±5升至31±4（组内治疗前后比较,t =6.81、4.21,均P＜0.05）.结论 谷赖胰岛素和赖脯胰岛素联合甘精胰岛素治疗糖尿病的临床疗效、安全性及治疗满意度相似.     

甘精胰岛素与精蛋白锌重组赖脯胰岛素治疗老年糖尿病疗效比较

68例老年糖尿病患者随机分为两组,甘精胰岛素联合口服药治疗组32人(1组)、精蛋白锌重组赖脯胰岛素治疗组36人(2组),比较治疗效果及不良反应发生情况。结果治疗后,两组空腹及餐后血糖、糖化血红蛋白均较前下降,体重变化不大,甘精胰岛素组低血糖发生率低于精蛋白锌重组赖脯胰岛素治疗组。结论甘精胰岛素联合口服降糖药可良好控制血糖,患者的依从性好,低血糖发生率低,可用于老年糖尿病的治疗。     

津力达颗粒联合赖脯胰岛素治疗妊娠期糖尿病的临床观察

选择2017年3月～2019年8月92例GDM患者,随机分为对照组(45例)采用赖脯胰岛素治疗,观察组(47例)采用津力达颗粒联合赖脯胰岛素治疗.结果治疗后,观察组空腹血糖(FPG)、糖化血红蛋白(HbA1c)、餐后2h血糖(2hPG)均低于对照组,(P＜0.05);观察组不良妊娠结局发生率低于对照组,(P＜0.05)...     

重组甘精胰岛素联合赖脯胰岛素治疗初诊2型糖尿病的疗效观察

60例初诊2型糖尿病患者。随机分为两组,每组30例。A组给予赖脯胰岛素三餐前皮下注射联合重组甘精胰岛素睡前皮下注射。B组通过胰岛素泵持续皮下输注胰岛素治疗。治疗14d。结果经治疗后,2组个时点血糖与治疗前比较差异有统计学意义(P﹤0.05)且2组治疗后各时点血糖﹑糖化血红蛋白﹑血糖达标时间﹑日胰岛素用量以及低血糖发生率等指标比较差异无统计学意义(P﹥0.05)但A组较B组治疗费用低,易于灵活操作。结论与胰岛素泵持续皮下输注胰岛素比较,重组甘精胰岛素联合赖脯胰岛素是强化治疗初诊2型糖尿病患者的一种理想﹑经济的方案。     

2例1型糖尿病患者使用谷赖胰岛素替代其他类似胰岛素临床比较

观察2例1型糖尿病患者应用谷赖胰岛素代替门冬胰岛素在控制血糖中的临床疗效。采用MAGE评估,提示患者在应用谷赖胰岛素后,血糖较前均明显下降,胰岛素应用总量减少,且低血糖发生次数低于门冬胰岛素。结论:对于1型糖尿病患者,谷赖胰岛素对餐时血糖控制更有效,是一种较为理想的速效胰岛素。     

门冬胰岛素30/70治疗2型糖尿病的有效性和安全性观察

目的 探讨门冬胰岛素30/70治疗2型糖尿病(T2DM)的有效性及安全性.方法 选择T2DM患者70例,随机分为观察组36例、对照组34例.观察组给予门冬胰岛素30/70强化降糖治疗方案治疗,对照组给予生物合成人胰岛素、精蛋白生物合成人胰岛素治疗.连续治疗2周后,比较两组血糖控制情况及低血糖发生率、住院天数、胰岛素用量.结果 两组治疗后空腹、三餐后2h血糖水平均明显低于治疗前(P均＜0.05),两组治疗后空腹、三餐后2h血糖水平比较无统计学意义.观察组低血糖发生率明显低于对照组(P＜0.05),住院天数、胰岛素用量两组无统计学差异.结论 门冬胰岛素30/70治疗T2DM安全、有效.     

Anti-Dia and the Dia Blood Group

Abstract. In an Austrian family the Di^a antigen was discovered by causing hemolytic disease of the newborn. No mongoloid admixture has so far been detected. No linkage to other blood groups, serum groups or red cell enzymes could be found.     

Systematic Review for the 2018 AHA/ACC/AACVPR/AAPA/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines

BackgroundThe 2013 American College of Cardiology/American Heart Association guidelines for the treatment of blood cholesterol found little evidence to support the use of nonstatin lipid-modifying medications to reduce atherosclerotic cardiovascular disease (ASCVD) events. Since publication of these guidelines, multiple randomized controlled trials evaluating nonstatin lipid-modifying medications have been published.MethodsWe performed a systematic review to assess the magnitude of benefit and/or harm from additional lipid-modifying therapies compared with statins alone in individuals with known ASCVD or at high risk of ASCVD. We included data from randomized controlled trials with a sample size of >1,000 patients and designed for follow-up >1 year. We performed a comprehensive literature search and identified 10 randomized controlled trials for intensive review, including trials evaluating ezetimibe, niacin, cholesterol-ester transfer protein inhibitors, and PCSK9 inhibitors. The prespecified primary outcome for this review was a composite of fatal cardiovascular events, nonfatal myocardial infarction, and nonfatal stroke.ResultsThe cardiovascular benefit of nonstatin lipid-modifying therapies varied significantly according to the class of medication. There was evidence for reduced ASCVD morbidity with ezetimibe and 2 PSCK9 inhibitors. Reduced ASCVD mortality rate was reported for 1 PCSK9 inhibitor. The use of ezetimibe/simvastatin versus simvastatin in IMPROVE-IT (Improved Reduction of Outcomes: Vytorin Efficacy International Trial) reduced the primary outcome by 1.8% over 7 years (hazard ratio: 0.90; 95% CI: 0.84–0.96], 7-year number needed to treat: 56). The PSCK9 inhibitor evolocumab in the FOURIER study (Further Cardiovascular Outcomes Research with PCSK9 Inhibition in Subjects with Elevated Risk) decreased the primary outcome by 1.5% over 2.2 years (hazard ratio: 0.80; 95% CI: 0.73–0.88; 2.2=year number needed to treat: 67). In ODYSSEY OUTCOMES (Evaluation of Cardiovascular Outcomes After an Acute Coronary Syndrome During Treatment With Alirocumab), alirocumab reduced the primary outcome by 1.6% over 2.8 years (hazard ratio: 0.86; 95% CI: 0.79–0.93; 2.8-year number needed to treat: 63). For ezetimibe and the PSCK9 inhibitors, rates of musculoskeletal, neurocognitive, gastrointestinal, or other adverse event risks did not differ between the treatment and control groups. For patients at high risk of ASCVD already on background statin therapy, there was minimal evidence for improved ASCVD risk or adverse events with cholesterol-ester transfer protein inhibitors. There was no evidence of benefit for the addition of niacin to statin therapy. Direct comparisons of the results of the 10 randomized controlled trials were limited by significant differences in sample size, duration of follow-up, and reported primary outcomes.ConclusionsIn a systematic review of the evidence for adding nonstatin lipid-modifying therapies to statins to reduce ASCVD risk, we found evidence of benefit for ezetimibe and PCSK9 inhibitors but not for niacin or cholesterol-ester transfer protein inhibitors.     

Evidence for Expression of the Joa Blood Group Antigen on the Gya/Hy-Active Glycoprotein

The phenotypic association between the non-assigned high-incidence antigen Jo^a and the Gy^a collection antigens Gy^a and Hy was investigated by haemagglutination studies, flow cytometric analysis, immune precipitation and immunoblotting experiments. In haemagglutination tests anti-Jo^a gave the same pattern of reactivity with erythrocytes pre-treated with pronase, trypsin, α-chymotrypsin and thiol reducing agents as did anti-Gy^a and anti-Hy. In addition, similar to that found for anti-Gy^a and anti-Hy, anti Jo^a also showed reduced binding, as determined by haemagglutination and flow cytometric analysis, to erythrocytes from patients with paroxysmal nocturnal haemoglobinuria. Immune precipitates prepared from radio-iodinated antigen-positive red cells with anti-Jo^a, anti-Gy^a and anti-Hy gave similar results – a major component of M_r 49,000–60,000 (the Gy^a/Hy-active glycoprotein) and a second component of M_r 85,000–92,000 (this may be a dimer of the Gy_a/Hy-active glycoprotein, or a coprecipitated protein). These immune precipitates, when probed with both anti-Gy^a and anti-Hy under non-reducing conditions, gave a positive immunoblotting reaction to both the M_r 49,000–60,000 and the M_r 85,000–92,000 components. These results strongly suggest that the Jo^a antigen is expressed on the same glycoprotein that carries the Gy^a and Hy antigens.     

New Variants in the ABOH Blood Group System due to Interaction of Recessive Genes Controlling the Formation of H Antigen in Erythrocytes: the ''Bombay''-Like Phenotypes OHm, OBHm and OABHm

Abstract. New variants of the ABOH blood group system are described which are similar to the 'Bombay' phenotype, but differ from it by Le(a-b+) erythrocytes and secretion of ABH and Le^a and Le^b antigens. The erythrocytes of the proposita and members of her family are group O, negative with anti-H; agglutinins if the 'Bombay' type, active also at 37°C, but weakened owing to interference by the secreted antigens, were found in the sera. The genetic background of the observed phenotypes is discussed. It appears likely that the atypical blood groups are due to a pair of recessive genes at a locus designated as Z/z and responsible for biosynthesis of H antigen in erythrocytes. The Z/z locus very probably belongs to the operator/regulator gene complex for the structural gene H , and has a position similar that of the Y/y pair in relation to A gene. The homozygous combination zz causes suppression (modification) of the H phenotype in erythrocytes. As a result, the expression of the blood groups, as determined by the structural gene A or B , is also suppressed. It is suggested that these variants (phenotypes) be given the symbols O_Hm, O^A_Hm, O^B_Hm and O^AB_Hm if the genetic information O, A, B or AB can be demonstrated only indirectly, and symbols A_Hm and B_Hm if the phenotype can be demonstrated by specific agglutination reactions.     

2011年ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS颅外颈动脉和椎动脉疾病患者处理指南

导言医疗专业人员在对与疾病检测、处理或预防中使用的药物、装置和操作相关的证据的严格评价中扮演的核心角色是十分必要的。对涉及这些疗法和操作的绝对和相对益处和风险的现有资料进行适当和严格的专业分析,可通过将资源集中于最有效的治疗策略,从而改善治疗效果、优化患者转归和合理控制成本。这些资料的一种重要应用是制定临床实践指南,后者进而能为其他各种应用,如绩效评价、合理应用标准、临床决策支持工具和质量改进工具提供依据。     

Immunochemical characterization of the new platelet alloantigen system Bra/Brb

We report the immunochemical characterization of the new platelet-specific alloantigens Bra and Brb. Bra antibodies were from mothers of children with neonatal alloimmune thrombocytopenia (NAIT), and anti-Brb was found in the serum of a polytransfused patient. By radioimmunoprecipitation, anti-Bra and anti-Brb precipitated two proteins with apparent relative molecular masses in sodium dodecyl sulphate-polyacrylamide gel electrophoresis of 155,000 and 130,000 under non-reduced conditions, and of 165,000 and 148,000 under reduced conditions. In two-dimensional polyacrylamide gel electrophoresis, the two bands moved with isoelectric points ranging from 5.2 to 5.4 and from 4.5 to 4.7, respectively. These features fulfil previously defined criteria for platelet membrane glycoproteins (GP) Ia and IIa. The results were supported by data obtained by an assay employing monoclonal antibody (mab)-specific immobilization of platelet antigens (MAIPA). By this technique, Bra and Brb antigens could be immobilized by mabs specific for the GP Ia/IIa complex (mab Gi 14) or a mab specific for the very late antigen-2 (mab 12 F1), but not by a mab specific for GP IIb/IIIa complex (mab Gi3). Furthermore, platelets from a thrombasthenic patient with complete absence of GP IIb/IIIa expressed the Brb antigen normally as shown in MAIPA; this antigen could be immunoprecipitated with anti-Brb and was identical to that of normal platelets. This confirms that the antigens of the Br system are not associated with the GP IIb/IIIa complex. By direct binding studies using mabs Gi3 and Gi14, we calculated that 51,500 +/- 3900 molecules of anti-GP IIb/IIIa and 6,470 +/- 500 molecules of anti-GP Ia/IIa were bound per platelet at saturation. Our results provide evidence for the first platelet-specific alloantigen system residing on the GP Ia. The difficulty in detecting anti-Bra and anti-Brb by direct binding assays may be related to the small number of GP Ia/IIa complexes on platelets.