特异性环氧合酶-2抑制剂西乐葆胃黏膜安全性实验研究

目的　比较特异性环氧合酶 2 (COX 2 )抑制剂西乐葆与传统非甾体抗炎药 (NSAIDs)对胃黏膜的损害。方法　分别以西乐葆、吲哚美辛复制大鼠NSAIDs性胃黏膜损伤模型 (n =8) ;以无水乙醇复制胃黏膜急性损伤模型 ,再以西乐葆灌胃 (n =8)。观察各组胃黏膜 6 酮 前列腺素F1α(6 keto PGF1α)、血栓素B2 (TXB2 )水平、损伤指数 (LI)及光镜、扫描电镜下的变化。结果　吲哚美辛组胃黏膜损害明显 (LI :13.38± 2 .0 6 ) ,6 keto PGF1α、TXB2 明显下降 (P <0 .0 1) ,抑制率分别为 81.6 %,81.8%,LI与 6 keto PGF1α、TXB2 水平呈负相关。西乐葆组 6 keto PGF1α、TXB2 无明显抑制 (P >0 .0 5 ) ,对健康胃黏膜无损害 (LI :0 ) ,但可加重乙醇诱导的胃损伤 (LI :37.19± 3.34比 19.90± 2 .2 8,P <0 .0 1)。结论　COX 1活性抑制是NSAIDs胃病的主要机制 ;特异性COX 2抑制剂西乐葆不造成健康鼠胃黏膜损伤 ,有较高的胃肠道安全性 ,但可加重原有胃损伤。     

吲哚美辛胃损伤中内皮素、一氧化氮、氧自由基的作用及其与胃动力的关系

目的 :研究吲哚美辛胃损伤中内皮素 (ET)、一氧化氮 (NO)、氧自由基的作用 ,以及胃动力对这种损伤的影响。方法 :雄性DS大鼠随机分 4组 :对照组、吲哚美辛 5mg/kg组、吲哚美辛 2 5mg/kg组、阿托品组 (阿托品 1mg/kg +吲哚美辛 2 5mg/kg)。吲哚美辛灌胃 ,灌胃前 10min阿托品皮下注射。取动脉血测ET、NO、丙二醛 (MDA)、超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶 (GSH Px)水平 ,进行胃形态学观察。结果 :5mg/kg吲哚美辛不引起胃粘膜损伤 ,各检测指标与对照组无差异 ;2 5mg/kg吲哚美辛可引起胃粘膜显著出血性损伤 ,损伤指数为 38 5 7± 12 4 7,病理损伤积分为13 36± 3 37;ET 1和MDA水平升高 (P <0 0 1) ,NO、SOD、GSH Px水平降低 (P <0 0 1,P <0 0 1,P <0 0 5 ) ;阿托品组粘膜损伤较轻 ,损伤指数为 8 71± 3 35 ,病理损伤积分为 3 77± 1 0 4,ET 1含量和对照组无差异 ,MDA水平升高 (P <0 0 5 ) ,NO、SOD含量有所下降 (P <0 0 5 ) ,GSH Px含量无变化。结论 :吲哚美辛所致胃粘膜损伤中 ,ET 1和MDA生成增加起损害作用 ,内源性NO、SOD和GSH Px可清除氧自由基 ,有保护作用 ;阿托品对吲哚美辛所致胃粘膜损伤的保护作用 ,提示胃动力增加在吲哚美辛致溃疡中有重要作用。     

前列腺素缺乏条件下促胃动力药胃复安对大鼠胃粘膜的损伤作用与可能机制

目的探讨前列腺素(prostaglandin,PG)缺乏条件下促胃动力药胃复安对大鼠胃粘膜的损伤作用与可能机制。方法 PG缺乏状态由5mg/kg吲哚美辛诱导;雄性SD大鼠随机分组:对照组;胃复安两组(30mg/kg,60mg/kg);吲哚美辛两组(5mg/kg,25mg/kg);吲哚美辛5mg/kg合用胃复安三组(10mg/kg,30mg/kg,60mg/kg);阿托品组(阿托品-吲哚美辛5mg/kg+胃复安60mg/kg),禁食24h后,生理盐水或吲哚美辛灌胃,30min后皮下注射胃复安或生理盐水,阿托品灌胃前10min皮下注射,4h后取血,处死大鼠取胃行损伤测定:放免法测血浆内皮素(Endothelin ET-1);生化法测—氧化氮(nitric oxide NO)、丙二醛(Malondialdhyde MDA)、谷胱甘肽过氧化酶(Glutathioneperoxidase GSH-Px)含量。结果吲哚美辛合用胃复安三组胃粘膜均有明显损伤,ET-1、MDA升高(p<0.05.p<0.01),NO、GSH-Px下降(p<0.05,p<0.01);吲哚美辛25ng/kg组损伤严重,ET-1、MDA升高(p<0.01),NO、GSH-Px下降(p<0.01,P<0.05);胃复安60mg/kg胃有轻微损伤,各指标无显著变化;其余各组未见明显损伤及指标变化。结论(1)PG缺乏条件下促胃动力药胃复安可引起胃黏膜出血性损伤,可能与ET-1升高、NO下降致胃黏膜微循环紊乱有关.MDA升高,GSH-Px减少可能为损伤后的继发反应结果,加剧了黏膜损伤。(32)胃动力有潜在的引起胃黏膜损伤的能力,PG缺乏增加了胃黏膜对胃高动力的敏感性。提示临床上非甾体抗炎药(NSAIDs)服用者应慎用胃动力药,因为合用可能形成或加剧胃黏膜损伤。     

胃损伤愈合过程中环氧化酶-2的表达及其作用

目的：探讨环氧化酶－2（COX－2）在胃粘膜的表达，和特异性COX－2抑制剂对胃粘膜损伤愈合的影响。方法：1、大鼠禁食24h，经胃管胃内投入0.6mol/L HCl 1ml。应用免疫印渍分析盐酸投入前、后胃粘膜COX－1和COX－2表达水平。2、盐酸投入后10min，胃内给予COX－2抑制剂NS－398，剂量为0.4mg/kg,4mg/kg和40mg/kg，盐酸投入前和盐酸投入后1h,3h,6h,12h,24h和48h，分别处死大鼠，剖腹取胃，观测胃粘膜损伤的愈合情况。结果：1、盐酸致胃粘膜损伤后，COX－2表达增加而COX－1表达无显变化。2、盐酸所致胃粘膜损伤后对照组在48h内愈合，而NS－398组呈剂量依赖性地延迟胃粘膜损伤的愈合，两组相比有显差异（P＜0．05）。结论：COX－2的表达在胃粘膜损伤愈合过程中起重要作用。     

非甾体类抗炎药胃粘膜损伤及预防实验研究

目的了解并比较不同非甾体类抗炎药(NSAID)对胃粘膜的损害及其机制,观察临床常用药物西咪替丁(泰胃美)、铝碳酸镁(胃达喜)及硫糖铝(舒克菲)对NSAID性胃粘膜损害的预防保护作用.方法分别以萘丁美酮(瑞力芬)、吲哚美辛(消炎痛)、乙酰水杨酸(阿斯匹林)复制大鼠NSAID性胃粘膜损伤模型(n=8),以光镜和扫描电镜观察损伤及预防应用西咪替丁、铝碳酸镁及硫糖铝后胃粘膜形态学改变,同时测定胃粘膜血流(GMBF),6-酮-前列环素F1α(6-kto-PGF1α),血栓素B2(TXB2)水平.结果吲哚美辛和乙酰水杨酸引起明显胃粘膜损害,平均损伤指数(LI)分别为2.13±0.46,2.06±0.71,萘丁美酮组胃粘膜损害则轻微(LI=0.38±0.52,P＜0.01).预防用药后吲哚美辛所致胃粘膜损害减轻(LI分别为1.04±0.76,1.12±0.35和0.98±0.57,与吲哚美辛组相比P＜0.01),GMBF增加(分别为2.89±0.80,3.07±0.33,3.43±0.49,与吲哚美辛组相比显著增加,P＜0.01),6-keto-PGF1α,TXB2抑制减弱.结论细胞保护性前列腺素合成抑制为NSAID性胃粘膜损伤的主要机制.萘丁美酮作为新型NSAID,有着较高的胃肠道安全性.     

大鼠胃损伤适应性作用的观察

目的　建立大鼠无水乙醇胃损伤的适应模型 ,观察大鼠胃损伤适应性保护作用。方法　采用 40 %、75 %乙醇 1ml胃饲 ,并且在 0、2、4d内予以重复刺激 ,诱发胃损伤适应模型 ,观察损伤模型胃黏膜病理形态变化。结果　对照组大鼠胃黏膜损伤指数 (UI)为 47 2 5± 2 .0 5 ;40 %乙醇处理组大鼠胃黏膜UI为 2 5 .2 5± 3 .71,较对照大鼠显著降低 (P <0 .0 5 ) ;75 %乙醇处理组大鼠胃黏膜UI为 67.40± 10 .81,较对照大鼠显著增高 (P <0 .0 5 )。提示在给予 40 %乙醇 3次刺激后 ,大鼠胃能产生适应性保护作用 ,减轻了再给予无水乙醇刺激时的胃损伤 ;而在给予 75 %乙醇 3次刺激后 ,大鼠胃不能产生适应性保护作用 ,反而加重了再给予无水乙醇刺激时的胃损伤。结论　能够促使胃产生适应性保护作用的损伤刺激有一定的程度范围     

吲哚美辛对胃黏膜细胞凋亡和增殖功能的影响

临床及实验研究显示非甾体类抗炎药(NSAIDs)可导致胃黏膜损伤，但其确切机制不明。有研究显示NSAIDs可抑制黏膜细胞DNA合成及增殖功能，同时可导致胃黏膜细胞凋亡。本研究采用吲哚美辛(IND)灌胃的方法建立急性胃黏膜损伤动物模型，选择增殖细胞核抗原(PCNA)作为反映黏膜细胞增殖功能的指标，采用脱氧核苷酰转移酶介导     

环氧合酶-1和前列腺素E2在多潘立酮对大鼠胃黏膜保护中的作用

目的　研究多潘立酮对大鼠胃黏膜损伤是否具有保护作用 ,并探讨胃黏膜细胞中环氧合酶 1(COX 1)及前列腺素 (PG)E2是否参与其中。方法　研究分为对照组和实验组。后者分别用多潘立酮 0 .5mg/kg、1mg/kg和 2mg/kg灌胃 ,3次 /d ,连续 3d。各组大鼠灌入无水乙醇后 ,肉眼观察胃黏膜损伤指数 (LI) ,光镜下观察黏膜缺损深度 ,并计算黏膜缺损深度与胃壁全层厚度百分比。放射免疫法测定各组胃黏膜PGE2的水平。免疫组织化学方法检测COX 1和COX 2蛋白表达水平并以平均吸光度值表示其强度。RT PCR检测胃黏膜COX 1和COX 2mRNA表达变化。结果　多潘立酮 1mg/kg组的LI及黏膜缺损深度与胃壁全层厚度百分比显著低于对照组 (P <0 .0 5 ) ,0 .5mg/kg组和 2mg/kg的组LI亦显著低于对照组 (P <0 .0 5 )。多潘立酮 1mg/kg组大鼠胃黏膜COX 1蛋白表达水平及PGE2水平显著高于空白对照组 (P <0 .0 1)。各实验组和对照组在胃黏膜细胞内均无COX 2蛋白表达。三个实验组COX 1mRNA表达量与对照组比较差异均有显著性 (P <0 .0 1)。各组均未检测到COX 2mRNA表达。结论　多潘立酮对胃黏膜损伤具有保护作用 ,其机制之一可能与其增加胃黏膜COX 1mRNA和COX 1蛋白表达及促进胃黏膜PGE2分泌有关。     

磷酸化丝氨酶/苏氨酸蛋白激酶B与吲哚美辛诱导胃黏膜损伤的关系探讨

目的 探讨抗凋亡信号蛋白磷酸化丝氨酸,苏氨酸蛋白激酶B(AKT)表达水平与吲哚美辛诱导胃黏膜损伤的关系.方法 采用免疫印迹法检测吲哚美辛处理后的C57BL/6小鼠胃黏膜组织和大鼠胃黏膜细胞(RGM-1)中抗凋亡信号蛋白磷酸化AKT表达水平的变化.结果 吲哚美辛处理后的小鼠胃黏膜组织呈现典型的胃溃疡病理形态变化;和对照组相比,经吲哚美辛处理后的小鼠胃黏膜组织和大鼠胃黏膜细胞RGM-1中抗凋亡信号蛋白磷酸化AKT表达水平均明显降低.结论 抗凋亡信号蛋白磷酸化AKT表达水平降低可能是吲哚美辛诱导的胃黏膜损伤的一种新的机制.     

肠三叶因子在胃黏膜应激适应性细胞保护中的作用

目的　研究肠三叶因子 (ITF ,为三叶肽家族一员 )、转化生长因子α(TGFα)及环氧合酶 2(COX 2 )在水浸束缚应激 (WRS)大鼠胃黏膜中基因表达变化 ,探讨其在胃黏膜应激适应性细胞保护中的相互关系及作用。方法　采用重复WRS制作模型 ,动态监测胃黏膜血流量 (GMBF) ,大体及光镜下观察黏膜损伤程度 (UI)及组织学变化 ,RT PCR检测ITF、TGFα及COX 2基因表达变化 ,免疫组化染色进一步证实ITF ,TGFα表达。结果　单次应激造成胃黏膜广泛损伤 ,重复应激后胃黏膜产生适应性 ,胃黏膜血流量上升 ,损伤逐渐减轻 ,4次应激后 ,损伤指数降低为单次应激的 2 1.99% ,且胃腺区细胞增殖 ,ITF、TGFα基因表达增强 (分别为 0 .0 40± 0 .0 0 1比 0 .372± 0 .0 10 ,P <0 .0 1;0 .86± 0 .0 1比 0 .93± 0 .0 1,P <0 .0 1) ,免疫组化染色证实了二者的变化趋势 ,而COX 2表达逐渐减弱 (0 .45± 0 .0 2比 0 .2 2± 0 .0 1,P <0 .0 1)。结论　胃黏膜适应性细胞保护伴有细胞增殖 ,ITF、TGFα表达水平增强及COX 2表达水平逐渐减弱 ,表明三者在这一现象中有重要的调节作用。     

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.     

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。     

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。     

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.     

治疗高血压药物的经济学评价

重视高血压治疗中的经济学评价,对利用我国有限的卫生资源来遏制高血压对人民群众的危害有着重要的现实意义。药物经济学对于药物治疗的成本和治疗的结果给予同样的关注。因为治疗高血压的费用,不仅涉及药物价格,还包括患者的危险水平,降压疗效和对临床终点事件的影响,以及治疗的依从性和安全性。因此药物经济学更强调整体成本和价-效比。低危病人,若非药价低廉,治疗的价-效比不够理想。而在高危的患者,价-效比越小越经济而不是药费越便宜越好。