环丙沙星滴眼液治疗急性细菌性结膜炎的临床疗效

本文对１０９例（１３０眼）临床诊断急性细菌性结膜炎，应用０．３％环丙沙星（ＣＰＬＸ）滴眼液（７０眼）和０．３％诺氟沙星（ＮＦＬＸ）滴眼液（６０眼），作了双盲随机治疗研究各１个星期。治愈率ＣＰＬＸ组６２．８６％、ＮＦＬＸ组４５％，显效ＣＰＬＸ组３２．８５％，ＮＦＬＸ组４６．６６％。治疗后细菌清除率ＣＰＬＸ组９４．７８％、ＮＦＬＸ组９２．９５％。两种抗菌素对革兰氏阳性和阴性菌的作用相似，治疗中无一例有任何副反应或局部不能耐受。ＣＰＬＸ对治疗外眼部细菌感染如急性细菌性结膜炎为一安全有效的药物，其临床疗效与对微生物作用在本组试验中与ＮＦＬＸ相似。     

甲氟哌酸体外抗菌活性及对耐药感染者的治疗

对天津市新近临床分离的414株细菌进行了甲氟哌酸(Pflx)和氟哌酸(Nflx)体外抗菌活性研究。结果显示Pflx对绝大多数肠杆菌和细菌、不动杆菌有良好抗菌活性,抑菌率>90％。对绿脓杆菌、MSSA及凝固酶阴性葡萄球菌有中度抗菌作用,抑菌率分别为85％、87.5％、87.5％。对MRSA和链球菌抗菌活性稍差,抑菌率在40％～68.42％之间。Nflx体外抗菌活性和Pflx相似。此外,18例药敏试验耐Pflx和Nflx细菌感染患者,经Pflx治疗,肺化脓症1例显效,余17例难治性尿路感染者1例痊愈、9例显效、5例进步、2例无效。     

905株革兰阴性杆菌对氟哌酸耐药性的观察

本文就氟哌酸广泛应用于临床后,对近三年来从各种标本中分离出的905株革兰阴性杆菌吋氟哌酸的耐药性进行了观察研究,发现其敏感率呈逐年下降趋势,敏感率依次为93.39%、85.56%、79.38%,同时耐药性逐年升高,耐药率依次为4.96%、8.45%、17.27%。     

在非溃疡性消化不良中ELISA法测抗幽门螺旋杆菌抗体的临床意义

非溃疡性消化不良(NUD, non-ulcer dyspepsia)是常见症候群,其病因尚未完全明了。NUD中幽门螺旋杆菌(HP Helicobacter Pylori)相关性胃炎占很大比例。针对该菌产生之抗体反应,应用酶联免疫法(ILISA)检测了335例NUD患者血清抗-HP抗体。其中208例为经细菌培养及(或)组织学检查证实的HP相关性胃炎,对其中164例进行前瞻性随机安慰剂对照研究,以评价胶态次枸橡酸铋加氟哌酸治疗效果.治疗组与安慰剂组HP清除率分别为69％与6％(P<0.01)。HP清除后患者胃粘膜炎症好转或消除,症状明显减轻,抗-HP抗体滴度下降。     

诺氟沙星合成工艺概述

对诺氟沙星的生产工艺作了简要述评,着重对生产上存在的技术问题及可能解决的途径提出了看法。     

诺氟沙星微囊包囊率及收率的测定

采用6种不同溶剂-非溶剂制备诺氟沙星微囊,并测定包囊率和收率.结果表明,选用二氯甲烷-正已烷制备诺氟沙星微囊其包囊率在6种溶剂-非溶剂组成中最高,达90.90%,收率也较高为87.27%.     

HPLC法测定复方乳酸诺氟沙星制剂中乳酸诺氟沙星和乳酸甲氧苄氨嘧啶的含量

采用高效液相色谱法,以水乙腈三乙胺（３２５∶１７５∶２２ ,用磷酸调ｐ Ｈ 至３ ．０） 为流动相,在λ＝ ２４０ ｎｍ 进行检测。该方法可使乳酸诺氟沙星和乳酸甲氧苄氨嘧啶达到良好分离。该方法操作简便、灵敏、重现性好。     

诺氟沙星衍生物的合成及其抗菌活性研究

目的 设计合成具有抗菌活性的诺氟沙星衍生物。方法 采用2-甲基-5-硝基咪唑、诺氟沙星等为原料，通过亲核取代反应合成目的物；测定目的物的体内抗菌活性。结果 合成的9个化合物的结构经MS、^1H-NMR和元素分析所确证。结论 合成了9个未见报道的新化合物，体内活性测试结果表明：其中的3个化合物具有较高的抗菌活性。     

高效液相色谱法测定甲诺参洗剂中甲硝唑及诺氟沙星的含量

目的:建立同时测定甲诺参洗剂中甲硝唑和诺氟沙星含量的高效液相色谱法.方法:采用Kromasil C 18 色谱柱(250 mm× 4.6 mm,5 μm),0.7%三乙胺(以磷酸调pH至 3.0 )-甲醇(200∶300)为流动相,流速为 1.0 mL·min -1 ,检测波长为290 nm.结果:甲硝唑在 20.0 ～ 150.0 mg·L -1 范围内,峰面积与其浓度线性关系良好(r= 0.999 9 ),平均回收率为 100.4% ,重复性试验RSD为 0.4% (n=5),检测限为 4.0 ×10 -3 μg;诺氟沙星在 10.0 ～ 75.0 mg·L -1 的范围内,峰面积与其浓度线性关系良好(r= 0.999 9 ),平均回收率为 98.6% ,重复性试验RSD为 0.5% (n=5),检测限为 2.0 ×10 -3 μg.结论:本法准确、简便、快速,具有专属性强,灵敏度高的特点,适用于含甲硝唑及诺氟沙星制剂的含量测定.     

Norfloxacin and cisapride combination decreases the incidence of spontaneous bacterial peritonitis in cirrhotic ascites

BACKGROUND: Spontaneous bacterial peritonitis (SBP) is a serious complication of cirrhosis with ascites, having high recurrence despite antibiotic prophylaxis. Small bowel dysmotility and bacterial overgrowth have been documented to be related to SBP. The purpose of the present paper was (i) to study whether addition of a prokinetic agent to norfloxacin ameliorates the development of SBP in high-risk patients; and (ii) to identify risk factors for SBP development. METHODS: A prospective, single blinded, randomized controlled trial was conducted in high-risk cirrhotic patients with ascites who had either recovered from an episode of SBP or who had low ascitic fluid protein. Norfloxacin 400 mg once daily (group I) or norfloxacin 400 mg once daily with cisapride 20 mg twice a day (group II) was given and occurrence of side-effects of therapy and mortality were recorded. RESULTS: Of the 94 patients, 48 (51%) were in group I, and 46 (49%) in group II. The actuarial probability of developing SBP at 12 month in group I was 56.8% and in group II, 21.7% (P = 0.026). Treatment failure was observed in five patients (10%) in group I and none in group II (P = 0.003). The actuarial probability of death at 18 months was 20.6% in group I and 6.2% in group II (P = 0.1). Low serum albumin, low ascitic fluid protein and alcoholic cirrhosis were related to development of SBP (P < 0.05). Additionally, low serum albumin (2.8 g/dL), gastrointestinal bleeding, alcoholic cirrhosis and low ascitic fluid protein were significantly associated with multiple occurrences of SBP. CONCLUSIONS: Prophylaxis with norfloxacin and cisapride significantly reduces the incidence of SBP in high-risk cirrhosis patients; low serum albumin, low ascitic fluid protein and alcoholic cirrhosis predispose to the development of SBP in high-risk cirrhosis patients; and low ascitic fluid protein should also be considered as a risk factor for the development of SBP requiring prophylaxis.