2种方案治疗2型糖尿病伴血脂紊乱的成本-效果分析

目的:比较2种药物方案治疗2型糖尿病伴血脂紊乱的近期疗效和经济学效果。方法:将102例伴有血脂紊乱的2型糖尿病患者随机均分成2组,分别以二甲双胍片(A组)、二甲双胍片+阿托伐他汀钙片(B组)治疗,2组疗程均为12周。观察疗效并运用药物经济学方法评价2组的成本-效果。结果:A、B组降血糖降血脂的总体有效率分别为3.9%和68.6%,成本-效果比分别为739.4和48.1。结论:与A方案比较,B方案因其良好的成本-效果,更适合于2型糖尿病伴血脂紊乱患者的治疗。     

格列吡嗪、活血降糖胶囊及两者联用治疗2型糖尿病的成本-效果分析

目的:比较格列吡嗪、活血降糖胶囊及两者联用治疗2型糖尿病的近期疗效和经济学效果。方法:105例患者按随机双盲法分为3组,分别给予活血降糖胶囊(A组)、格列吡嗪(B组)、活血降糖胶囊+格列吡嗪(C组)治疗,疗程均为2个月。运用药物经济学方法分析其成本-效果。结果:A、B、C组总有效率分别为74.3%、68.6%、94.3%,治疗2个月的费用分别为951.2、744.2、1097.0元。每获得1个单位效果,A、B、C组方案所需成本分别为12.8、10.8、11.6元。在B组方案的基础上,每增加1个单位效果,A、C组所追加的成本分别为36.3、13.7元。结论:C组方案治疗2型糖尿病最佳。     

国产与进口阿卡波糖片治疗2型糖尿病的成本-效果分析

目的:比较国产与进口阿卡波糖片治疗2型糖尿病的成本-效果。方法:采用已发表治疗2型糖尿病的用药资料,按其给药方案分为卡博平(A组,国产)与拜糖平(B组,进口)2组,运用药物经济学原理进行成本-效果比较。结果:2组给药方案治疗2型糖尿病均具有相同疗效,但成本间却存在显著差异。结论:国产比进口阿卡波糖具有较好的成本-效果比。     

老年2型糖尿病治疗方案的费用-效果分析

目的 观察2种不同的联合用药方案治疗老年2型糖尿病的经济效果.方法 选择老年2型糖尿病患者80例,随机分为两组,分别给予预混人胰岛素 马来酸罗格列酮、预混人胰岛素 阿卡波糖 二甲双胍进行治疗,应用药物经济学的费用-效果分析方法进行评价.结果 B方案是治疗老年2型糖尿病的理想方案.结论 应选用费用最合理、疗效最好、安全性最佳的药物治疗老年2型糖尿病.     

胰岛素类似物与口服降糖药治疗2型糖尿病成本-效果分析

目的 比较不同药物治疗方案治疗2型糖尿病的经济效果,以利糖尿病患者用药更安全、经济、有效.方法 将259例患者随机分为3组,运用药物经济学成本-效果分析方法,比较格列吡嗪控释片联合盐酸二甲双胍片(A组)、阿卡波糖口服(B组)、注射胰岛素类似物诺和锐30(C组)3种方案治疗糖尿病的疗效、直接医疗费用和间接费用,并以最小成本分析法进行药物经济学评价.结果 A组、B组、C组总有效率分别为51.16%,62.07%,88.37%,成本-效果比分别为13.85,16.76,12.20.结论 从成本-效果分析看,C组为最佳治疗方案.     

2种方案治疗口服降糖药无效2型糖尿病的最小成本分析

目的:比较2种方案治疗口服降糖药无效的2型糖尿病的药物经济学效果.方法:采用回顾性调查,利用药物经济学方法对艾塞那肽注射液联合二甲双胍缓释片(A组),甘精胰岛素注射液联合二甲双胍缓释片(B组)治疗口服降糖药无效的2型糖尿病的方案进行分析.结果:A组和B组的总有效率分别为86.96%和83.72%,差异无统计学意义(P>0.05).A组和B组的药物成本分别为3 032.7元,623.4元,B组的药物成本低于A组.结论:2种治疗方案均能将血糖控制在相对理想的范围内,但B方案治疗2型糖尿病的经济效果较优.     

2型糖尿病不同口服药物治疗方案的经济学评价

目的:评价2型糖尿病不同口服药物治疗方案的疗效及经济成本。方法:运用药物经济学成本-效果分析法,对不同药物治疗2型糖尿病的疗效及成本进行分析比较。结果:二甲双胍组、罗格列酮组、伏格列波糖组、阿卡波糖组的成本-效果比(E1/C)和(E2/C)分别为4.23、2.01、1.38、0.95和2.58、0.63、0.42、0.40。结论:用二甲双胍治疗2型糖尿病的方案要优于其他口服药物治疗方案。     

两种方案治疗2型糖尿病的成本-效果分析

目的 探讨不同方案治疗2型糖尿病的疗效与经济效果.方法 50例2型糖尿病患者随机分成两组.A组25例,用盐酸二甲双胍肠溶胶囊(商品名:君力达),0.5,po,tid;B组25例,用盐酸二甲双胍薄膜片,0.5,po,tid.疗程20～60d.运用药物经济学的成本-效果分析方法 进行评价.结果 A、B两组的成本-效果(C/E)1.73、0.21.结论 B方案为较佳治疗方案.     

2种方案治疗口服降糖药无效2型糖尿病的数据包络分析

目的:比较2种方案治疗口服降糖药无效2型糖尿病的药物经济学效果。方法:利用数据包络分析法,对预混胰岛素注射液联合二甲双胍片(A组,n=30)、甘精胰岛素注射液联合二甲双胍片(B组,n=28)2种方案治疗口服降糖药无效的2型糖尿病进行分析。在随访过程中根据血糖波动特点调整每位患者给药剂量。每位患者每3个月随访1次,共随访5次。结果:两组患者的临床疗效指标空腹血糖、餐后2 h血糖、糖化血红蛋白差异无统计学意义(P>0.05),质量调整生命年(QALYs)A组高于B组。结论:2种治疗方案均能将血糖控制在相对理想的范围内,但A方案治疗口服降糖药无效2型糖尿病的投入产出达到最优,B组投入偏高且临床疗效和QALYs有待提高。     

格列美脲联合用于Ⅱ型糖尿病治疗的药物经济学评价

目的运用药物经济学中的成本效果分析方法评价格列美脲联合用于Ⅱ型糖尿病治疗的短期药物经济学效果,为Ⅱ型糖尿病病人选择治疗药物提供依据。方法采用回顾性分析法,选取80例病人,以血糖值为健康效果测量指标,运用成本效果分析方法评价口服降糖药三种给药方案(A组:格列美脲+二甲双胍缓释片;B组:格列美脲+阿卡波糖;C组:格列美脲+罗格列酮)治疗Ⅱ型糖尿病的药物经济学效果,并进行敏感性分析。结果3种方案的有效率分别为83.3%、86.7%、96.7%,C方案疗效要优于A、B方案。使平均血糖下降一个百分点,三方案费用分别为15.29元、27.29元和34.14元。结论3种治疗方案都能将血糖控制在理想范围,从药物经济学的角度分析,格列美脲+二甲双胍方案为佳;格列美脲+罗格列酮疗效最好,但成本效果比最高。     

2型糖尿病患者口服降糖药的成本效果分析

目的：分析比较7种治疗2型糖尿病（DM）药物的成本效果。方法：将705例2型DM患者分成7组,运用药物经济学成本效果分析（CEA）方法,对7组口服降糖药[A组：马来酸罗格列酮（文迪雅）;B组：盐酸二甲双胍;C组：格列齐特（达美康）;D组：格列美脲;E组：格列喹酮（糖适平）;F组：阿卡波糖（拜糖平）;G组：阿卡波糖（卡博平）]进行评价;并同时做敏感度分析。结果：在2型DM的治疗中,二甲双胍为疗效较好且最经济的方案。结论：二甲双胍治疗2型DM安全性最佳、疗效最好、费用最合理,值得临床推广应用。     

2型糖尿病患者口服降糖药的成本-效果分析

目的比较7种治疗2型糖尿病药物的成本-效果。方法将235例2型糖尿病患者分成7组：马来酸罗格列酮（文迪雅）组29例（A组）;二甲双胍组54例（B组）;格列齐特（达美康）组40例（C组）;格列美脲组28例（D组）;格列喹酮（糖适平）组38例（E组）;阿卡波糖（拜糖平）组25例（F组）;阿卡波糖（卡博平）组21例（G组）,运用药物经济学成本-效果分析方法,对7组口服降糖药进行评价;并且同时做了敏感性分析。结果在2型糖尿病的治疗中,二甲双胍为疗效较好且最经济的方案。结论应选用安全、有效、费用合理的药物治疗2型糖尿病。     

我院3种口服降糖药治疗2型糖尿病的成本-效果分析

目的评价我院3种口服降糖药治疗2型糖尿病的临床效果,并探讨其经济学效果。方法选择102例2型糖尿病患者随机分成3组,A组:格列美脲口服:B组:吡格列酮口服;C组:二甲双胍口服,2个月后比较临床效果并进行成本效果分析。结果3种方案的总成本分别为570.40元、596.30元、498.10元;成本效果比分别为6.42、7.07、5.21。结论C组方案为最佳方案。     

2型糖尿病合并非酒精性脂肪性肝病血浆chemerin与炎症指标的相关性

目的:探讨2型糖尿病(T2DM)合并非酒精性脂肪性肝病(NAFLD)患者血浆chemerin与炎症的关系.方法:采用酶联免疫法(ELISA)检测T2DM合并NAFLD患者(A组),T2DM不合并NAFLD患者(B组)及正常对照组(C组)血浆chemerin水平,同时测定3组血糖、血脂、糖化血红蛋白(HbAlc)、空腹胰...     

4种口服降糖药治疗2型糖尿病的成本-效果分析

目的比较4种口服降糖药治疗2型糖尿病病人的成本-效果。方法运用药物经济学成本-效果分析方法,对4种口服降糖药(A组:瑞格列奈;B组:二甲双胍;C组:格列吡嗪;D组:罗格列酮)进行评价。结果4组均可有效控制空腹血糖(P<0.05),二甲双胍、罗格列酮还可以显著降低糖化血红蛋白。结论4种治疗方案都能将血糖控制在理想范围,二甲双胍疗效较好且最经济,罗格列酮疗效最优但是价格偏高。     

2型糖尿病三种治疗方案的成本-效果分析

目的 分析三种用于2型糖尿病(T2DM)治疗方案的效果与成本的关系,以得出最合理的治疗方案.方法 利用药物经济学原理,回顾性分析198例T2DM患者的病例资料,对格列美脲、瑞格列奈、罗格列酮三种用于T2DM的药物进行药物成本-效果分析.结果 三种方案的总有效率没有显著差异,而三种方案的成本-效果比(C/E)分别为:2.99、1.43、5.76,三种方案的增量成本-效果比(△C/△E)分别为:42.15、18.32、214.74.结论 应根据患者的个体差异,选择治疗效果最好,价格最低,安全系数最高的治疗方案.     

A 50-year history of new drugs in Japan-the development and progress of anti-diabetic drugs and the epidemiological aspects of diabetes mellitus

The development and progress of antidiabetic drugs (e.g., insulin preparations and hypoglycemic drugs) are retrospectively investigated in Japan. Their influences on the treatment of diabetes mellitus (DM) and its epidemiological aspects are also discussed. 1) Insulin preparations: Insulin was introduced for DM therapy in 1925, two or three years after its discovery in Canada. The preparations were raw extracts of bovine or porcine pancreas. These did not prevail widely in Japan because of the low incidence of DM before World Wan II. After the war, a shortage of mammalian materials compelled the use of fish pancreatic tissues such as bonito and/or tuna for insulin production. Insulin infection, so-called regular insulin, was first promoted in the 6th "Pharmacopoeia Japonica" (JP6) in 1951 and has been maintained to the present edition (JP14, 2001). Although depot-type insulin preparations were developed in the USA and Europe during the war, the introduction of those preparations to Japan was delayed until 1951, when Protamine zinc insulin appeared. Globin zinc insulin and Isophane insulin were introduced for clinical use in 1952 and 1955, respectively. These were also adopted for JP7 (1961). Biphasic-type insulin, which has a rapid onset and long duration of activity, appeared in 1965. Purified preparations from bovine or porcine sources have been available since 1980, which might be a strong reason for the decrease in insulin allergy. Insulin from animal origin has been supplied for almost 60 years since its discovery. Amino acid sequences of insulins from various species of animals were determined by the pioneering studies of Sanger and his associates. Human insulin, which differs from porcine insulin by only one amino acid, was produced by Novo researchers in 1982 using a semi-synthetic method. Then the Lilly group soon succeeded in obtaining human insulin by recombinant DNA technology in the same year. Both products were introduced to Japan in 1985, and the recombinant products prevailed throughout the 1990s. Human insulin analogues (i.e., Insulin lispro and Insulin aspart) appeared in 2001. These are applied for after-meal glycosmia owing to their ultrarapid onset of activity. Self-injection by DM patients was legalized in 1981. To make the infection technique sure and easy, cartridge (pen-type) and disposable kit-type needles were devised in the 1990s. 2) Oral hypoglycemic drugs: Instead of the exclusive parenteral usage of insulins, there was also demand for oral dosage forms. The first of the sulfonyrlurea (SU) group, BZ-55, was used for DM clinically in 1955 in Germany. But it was soon withdrawn because of its antibacterial action. This led to the development of various SU groups. Tolbutamide (1956), chlorpropamide (1959), acetohexamide (1964) and tolazamide (1961) were introduced to Japan as first-generation SUs. Then glyclopyramide (Kyorin, 1965), glybenclamide (1971), gliclazide (1984) and glimepiride (1999) appeared as the second-generation SUs. These were used orally for Type 2 diabetes. Biguanide (BG) group, phenformin HC1 (1959), metformin HC1 (1961) and buformin HC1 (1961) had also been in use by oral treatment of Type 2 diabetes. SU appears to act by increasing the sensitivity of b-cells, which secrete insulin. BG probably exerts by increasing glucose transport across the membranes of target organs. 3) New types of antidiabetic drugs: a-Glucosidase inhibitors (i.e., acarbose: Bayer, 1993; and voglibose: Takeda, 1994) act on hyperglycemia after meals by decreasing glucose absorption. Thiazolidinedione compounds, such as troglitazone (Sankyo, 1995) and pioglitazone HC1 (Takeda, 1994) act by increasing the insulin sensitivity of the target tissues. These are useful for Type 2 DM patients when SUs are ineffective. Nevertheless, troglitazone was discontinued in 2000 due to severe liver damage. Nateglinide (Ajinomoto Co., 1999), which is a D-phenylalanine derivative acting similar to SUs, is useful orally for after-meal hyperglycemia of Type 2 diabetes. Epalrestat (Ono Yakuhin Co., 1992) is effective for diabetic neuropathy by reducing the formation of sorbitol. These anti-DM drugs were recently studied and developed in Japan. 4) The Japan Diabetes Society proposed a guideline on diagnostic criteria and treatment of diabetes mellitus (DM) in 1999 and revised it in 2002. DM is classified as insulin-dependent DM (Type l) and non-insulin dependent DM (Type 2). Type 1, juvenile onset DM, requires insulin therapy to prevent ketosis and to sustain life. Treatment of type 2, adult onset DM, is recommended as a step-by-step method, starting with dietary-exercise therapy, followed by oral hypoglycemic drugs and then insulin therapy. DM patients with complications should have a therapy devised to match their circumstances. 5) Epidemiological aspects: The mortality rate of DM compared to the time of drug appearance was traced from 1920 to 2000. The curve goes down slowly in the time frame of World War II, but rises from 1950 to 1970. The elevation could not be suppressed by the appearance of SUs, BGs or improved insulin preparations. The curve runs flat from 1980 to 1990, which might be related to the use of purified insulin or human insulin therapy. The mortality rate of DM indicates that death by hyperglycemic coma and other deaths resulting from complications are excluded. The survey of the principal cause of death by DM during the period of 1981-1990 indicates that the death rate due to hyperglycemic coma is only 1.7% of the total deaths caused by DM. The effect of drug therapy on all of the death resulting from DM is not detected. Hospital visitation and admission rates of the DM patients have been recorded since 1952 in Japan. This curve is rising continuously, and none of the antidiabetic drugs has been able to suppress it. These data show that the antidiabetic drugs relieve DM symptoms through their effective hypoglycemic actions, but that they cannot suppress the mortality rate of DM. It is possible that none of the drugs currently available can suppress the increasing tendency of DM patients.     

盐酸小檗碱对T2DM合并高脂血症患者血清NO水平及SOD活性的影响

目的：探讨2型糖尿病（T2DM）合并高脂血症患者氧化应激水平的变化及盐酸小檗碱对患者血清一氧化氮（NO）水平和超氧化物歧化酶（SOD）活性的影响。方法：采用前瞻性随机病例对照研究,选择80例T2DM合并高脂血症的患者分为常规治疗组（A组,n=40）及小檗碱治疗组（B组,n=40）,同时选择体检健康的20例（C组,n=20）作为对照组。 A组给予口服降糖药控制血糖、钙离子拮抗剂控制血压等治疗;B组在常规治疗组的给药基础上联用盐酸小檗碱片（0.2mg,3次/d）,口服,治疗时间为3个月。检测治疗前后的血清中一氧化氮（NO）、超氧化物歧化酶（SOD）、超敏C反应蛋白（hs-CRP）、内皮素（ET-1）、丙二醛（MDA）、血清总胆固醇（TC）、甘油三酯（TG）、空腹血糖（FPG）、餐后2h血糖（2h PBG）及相关生化指标。结果：与C组比较,两组T2DM合并高脂血症患者的血清炎症因子、血脂水平升高,NO及SOD水平降低（P＜0.01）。随访治疗3个月后,A组血清2h PBG、TC、TG、hs-CRP、MDA、ET-1水平比治疗前均有明显降低,NO、SOD水平比治疗前明显升高（P＜0.05）;与同期A组比较,B组变化幅度更为显著,差异有统计学意义（P＜0.01）。结论：盐酸小檗碱显著改善了T2DM合并高脂血症患者的糖、脂代谢异常和胰岛素抵抗,降低了患者的氧化应激水平,提高了血清NO水平及SOD活性,增加了NO合成,减少了NO破坏。可见盐酸小檗碱具有较好的抗炎、抗氧化应激反应及改善血管内皮功能的作用。     

不同剂量α-硫辛酸对2型糖尿病患者尿足细胞标志蛋白及血管内皮生长因子的影响

目的:探讨不同剂量α-硫辛酸(ALA)对2型糖尿病(T2DM)患者尿足细胞标志蛋白(PCX)、血管内皮生长因子(VEGF)及尿白蛋白(UALB)的影响。方法:92例T2DM患者分为常规治疗组(DM组32例)、ALA治疗组[DM 300 mg(30例)及DM 600 mg(30例),分别给予ALA 300 mg及ALA 600 mg静脉滴注,每日一次)。另选34例正常对照者(NC组)。分别于0周及2周测定尿PCX、血VEGF、尿肌酐(Ucr)及UALB。结果:DM 300 mg组及DM 600 mg组治疗2周后VEGF、尿PCX肌酐比(UPCR)、尿白蛋白肌酐比(UACR)低于DM组(P<0.05或P<0.01),DM 600 mg组VEGF、UPCR、UACR低于DM 300 mg组(P均<0.05)。结论:ALA可通过抗氧化应激减少尿PCX的排泄,降低血VEGF,减轻足细胞的损伤和凋亡,并呈一定的剂量依赖性。     

NLR和FIB与COPD合并T2DM的相关性 #br#

摘要：目的 探究慢性阻塞性肺疾病（COPD）合并2型糖尿病（T2DM）患者的中性粒细胞/淋巴细胞比值（NLR）和 纤维蛋白原（FIB）水平及其相关性。方法 选择稳定期COPD患者120例,根据疾病情况将患者划分成A、B、C组,A 组为COPD不合并T2DM者（40例）,B组为COPD合并T2DM且无微血管病变者（40例）,C组为COPD合并T2DM有微 血管病变者（40例）。患者于清晨空腹抽取静脉血,测量白细胞、中性粒细胞及淋巴细胞计数,计算NLR。采用酶联 免疫分析法检测FIB、三酰甘油（TG）、总胆固醇（TC）、低密度脂蛋白胆固醇（LDL-C）、高密度脂蛋白胆固醇（HDLC）、超敏C-反应蛋白（hs-CRP）;并测定患者肺功能指标。结果 B、C组吸烟年限、1年内COPD急性加重住院次数、 高血压史比例均高于A组（均P＜0.05）。A、B、C组患者NLR、FIB水平依次升高,组间多重比较差异均有统计学意义 （均P＜0.05）。在稳定期COPD患者中,是否合并T2DM与吸烟年限、1年内COPD急性加重住院次数、高血压史、NLR 及FIB之间呈正相关（rs分别为0.125、0.151、0.231、0.342、0.312,均P＜0.05）。在稳定期COPD合并T2DM患者中,有 无微血管病变与吸烟年限、高血压史、NLR及FIB之间呈正相关（rs分别为0.143、0.198、0.421、0.350,均P＜0.05）。多 因素Logistic 回归分析结果显示,NLR（OR=1.644,95%CI：1.359~1.899）、FIB（OR=1.647,95%CI：1.386~1.931）升高是 稳定期 COPD 患者合并 T2DM 的危险因素;NLR（OR=1.731,95%CI：1.456~1.978）、FIB（OR=1.698,95%CI：1.543~ 1.928）升高是稳定期COPD合并T2DM患者发生微血管并发症的危险因素。结论 COPD合并T2DM及有微血管病 变与NLR、FIB相关,NLR、FIB可作为评估稳定期COPD合并T2DM病情严重程度及预后的生物学指标。