改进阿莫西林胶囊溶出度的测定方法

目的改进阿莫西林胶囊溶出度的测定方法。方法采用HPLC测定阿莫西林胶囊溶出度,同时将改进方法的测定结果与药典方法进行比较。结果在0.2～1.0mg/mL浓度范围内峰面积与浓度呈良好的线性关系（r=0.9997）。回收率为99.8%,RSD=1.1%（n=6）。结论改进后的方法更准确、更精密、更科学,结果比药典方法测得结果更满意。     

3种含酶抑制剂的青霉素类药在木糖醇注射液中稳定性考察

目的:考察3种含β-内酰胺酶抑制剂的青霉素类药在木糖醇输液中的稳定性。方法:模拟临床用法用量,采用高效液相色谱法测定了阿莫西林钠舒巴坦钠、哌拉西林钠舒巴坦钠、哌拉西林钠他唑巴坦钠(2个厂家)在室温下与木糖醇配伍后8h之内不同时间的含量变化,并观察配伍液在8h之内的外观、pH变化。结果:哌拉西林钠舒巴坦钠、哌拉西林钠他唑巴坦钠在5%木糖醇注射液中相对较稳定,4h内含量均在94%以上,可以配伍使用,而阿莫西林钠舒巴坦不稳定,4h阿莫西林的含量已降至87%。结论:哌拉西林钠舒巴坦钠、哌拉西林钠他唑巴坦钠与木糖醇注射液可在室温下配伍4h内静脉滴注完;阿莫西林钠舒巴坦钠与木糖醇注射液配伍液在配制后2h尽量使用完。     

社区中两种三联疗法根除幽门螺旋杆菌的比较

目的比较不同药物治疗方案根除幽门螺旋杆菌(Hp)的效果。方法将经胃镜检查和14C呼气试验证实有Hp感染的115例患者,随机分为两组,A组为53例,接受克拉霉素、奥美拉唑、阿莫西林治疗1周;B组为62例,接受甲硝唑、奥美拉唑、阿莫西林治疗1周。停药4周后复查胃镜和14C呼气试验确定Hp根除率。结果A组根除率为94.34%,B组根除率为88.71%,二者比较差异无统计学意义(P>0.05),不良反应发生率A组为3.77%,B组为12.90%,两组间差异有显著意义(P<0.05)。结论克拉霉素、奥美拉唑、阿莫西林疗法与甲硝唑、奥美拉唑、阿莫西林疗法效果相当,但前者三联疗法HP根除率高,不良反应率低。     

HPLC法测定阿莫西林含量的测量不确定度评估

目的:评估高效液相色谱(HPLC)法测定阿莫西林含量的测量不确定度。方法:建立HPLC法测定含量的数学模型,分析测量不确定度的来源,量化各个测量不确定度分量,合成标准测量不确定度,给出扩展测量不确定度报告。结果:HPLC法测定阿莫西林含量的扩展测量不确定度为1.62%,测量结果表示为(87.32±1.62)%,k=2。结论:HPLC法测定阿莫西林含量的测量不确定度评估,方法简单合理,保证了测量结果准确可靠。     

2种治疗方案根除幽门螺杆菌的疗效观察

目的:比较2种根除幽门螺杆菌(Hp)方案的优劣。方法:将197例因各种上消化道症状行胃镜检查并14C-尿素呼气阳性的患者,随机分为A、B组(均符合根除Hp的条件及排除条件)。A组109例,给予雷贝拉唑10mg,阿莫西林-克拉维酸钾分散片(2:1)2片,甲硝唑0.4g;B组88例,给予雷贝拉唑10mg,阿莫西林1g,甲硝唑0.4g。2组给药方法均为每日2次,连用7d。总疗程结束后2周,再行内镜和14C-尿素呼气试验,判断Hp的根除效果。结果:A组根除率为88.07%,B组为73.90%。2组比较,差异有统计学意义(P<0.05)。结论:2种根除Hp的方案中,A组Hp根除率显著高于B组。     

阿莫西林口服制剂微生物限度检查方法学验证研究

目的:建立阿莫西林口服制剂微生物限度的检查方法。方法:供试液采用一般处理或加入不同量青霉素酶进行处理,考察阿莫西林颗粒、胶囊、分散片3种剂型中金黄色葡萄球菌、大肠埃希菌、枯草芽孢杆菌、白色念珠菌、黑曲霉5种菌的回收率,确定阿莫西林的敏感菌,同时对建立的方法进行验证。结果:3种阿莫西林制剂供试液在一般处理下白色念珠菌、黑曲霉的回收率均大于70%,但各细菌回收率为0;各制剂供试液在加入酶后各菌回收率大于70%,但分散片供试液对大肠埃希菌的回收率小于70%,在加大酶加入量后达到70%;大肠埃希菌为敏感菌,验证试验表明方法可行。结论:在阿莫西林口服制剂的微生物限度检查中,霉菌及酵母菌计数可采用平皿法,细菌计数可采用加入酶后的平皿法。     

大肠埃希菌对阿莫西林/克拉维酸耐药机制的研究

目的 探讨大肠埃希菌对阿莫西林/克拉维酸的耐药特点和机制,为临床合理用药提供依据.方法 收集四川大学华西医院2005年5月至12月临床分离的544株大肠埃希菌经微量肉汤稀释法确认对氨苄西林/舒巴坦耐药的大肠埃希菌,从中随机选取276株用药敏纸片检测,仅52株对阿莫西林/克拉维酸耐药.对符合耐酶抑制剂β-内酰胺酶耐药表型的2株大肠埃希菌进行TEM型β-内酰胺酶基因的克隆表达.采用多重PCR技术检测耐阿莫西林/克拉维酸大肠埃希菌的TEM、SHV、OXA型3种β-内酰胺酶.结果 52株大肠埃希菌含TEM型46株,SHV型1株,OXA型6株.其中同时含TEM型和SHV型1株以及含TEM型和OXA型5株.结论 TEM-1型广谱酶的高产是华西医院大肠埃希菌对阿莫西林/克拉维酸耐药主要机制,另外本次研究首次在西南地区发现OXA-1型ESBLs,也是造成耐药的重要机制.     

大肠埃希菌对阿莫西林／克拉维酸耐药机制的研究

目的探讨大肠埃希菌对阿莫西林／克拉维酸的耐药特点和机制,从而为临床合理用药及减少耐药的发生和耐药基因传播提供实验研究依据。方法将对氨苄西林／舒巴坦耐药的大肠埃希菌544株,随机选取276株进行阿莫西林／克拉维酸纸片的筛查,对筛出的耐药菌株采用琼脂对倍稀释法进行MIC值测定和PCR扩增分析。对符合耐酶抑制剂β-内酰胺酶耐药表型的大肠埃希菌进行TEM型β-内酰胺酶基因的克隆表达。采用多重PCR技术对耐阿莫西林／克拉维酸大肠埃希菌进行TEM、SHV、OXA型三种β-内酰胺酶的筛查。结果TEM型46株,SHV型1株,0xA型6株,TEM型和SHV型均阳性1株,TEM型和OXA型均阳性5株。产TEM型β-内酰胺酶中TEM-1型最常见,耐酶抑制剂TEM型β-内酰胺酶（IRT）未发现。结论TEM-1型广谱酶的高产是华西医院大肠埃希菌对阿莫西林／克拉维酸耐药主要机制,本研究首次在西南地区发现OXA-1,是造成耐药的重要原因。     

Dual therapy with high doses of rabeprazole and amoxicillin versus triple therapy with rabeprazole,amoxicillin, and metronidazole as a rescue regimen for <Emphasis Type="Italic">Helicobacter pylori</Emphasis> infection after the standard triple therapy

Backgrounds and Aims Development of safe and effective rescue regimens for eradication failure of Helicobacter pylori infection by standard regimens is an urgent task. We designed the prospective study to compare the efficacy of two rescue regimens after eradication failure by the standard triple therapy. Methods One hundred and thirty-two patients in whom eradication of H. pylori infection failed initial triple therapy with lansoprazole 30 mg b.i.d, amoxicillin 750 mg b.i.d. and clarithromycin 400 mg b.i.d. for 1 week were randomized to either the 1–week triple therapy with rabeprazole 10 mg b.i.d., amoxicillin 750 mg b.i.d., and metronidazole 250 mg b.i.d. (RAM) or the 2–week dual therapy with rabeprazole 10 mg q.i.d. and amoxicillin 500 mg q.i.d. (RA). Eradication of H. pylori was judged by ¹³C-urea breath test 1 month later. Results The intention-to-treat and per-protocol-based eradication rates were 92.4% (95% CI: 83.2–97.5) and 95.3% (95% CI: 86.9–99.0) for the RAM therapy and 90.9% (95% CI: 81.2–96.6) and 93.8% (95% CI: 84.8–98.3), respectively, for the RA therapy (P > 0.2 for both). No clinically recognizable adverse events were observed with either regimen. Conclusion RA as well as RAM therapy are safe and effective rescue regimens for H. pylori infection after eradication failure by the standard triple therapy.     

Community‐acquired pneumonia in children: what’s old? What’s new?

Community‐acquired pneumonia (CAP) still remains a significant cause for childhood morbidity worldwide. Streptococcus pneumoniae is the most important causative agent at all ages. Respiratory syncytial virus is common in young children, and Mycoplasma pneumoniae in schoolchildren. Paediatric CAP is universally treated with antibiotics; amoxicillin is the drug of choice for presumably pneumococcal and a macrolide for presumably atypical bacterial cases. Because of globally increased resistances, macrolides are not safety for pneumococcal CAP. At present, available prospective research data on the epidemiology of paediatric CAP in western countries are from 1970s to 1980s; correspondingly, data on bacterial aetiology are mainly from 1980s to 1990s. Current concepts on pneumococcal aetiology are mostly based on poorly validated antibody assays. Most data on clinical characteristics in children’s CAP, as well as on antibiotic treatment come from developing countries, thus not being directly applicable in western communities. Recent viral studies have revealed the role of rhinoviruses, metapneumovirus and bocavirus in the aetiology of paediatric CAP. This review critically summarizes the available data on epidemiology, aetiology, clinical presentation, treatment and outcome of CAP in children, with special focus on the newest microbial findings, the age and applicability of the data and the need of new studies.