四联疗法作为二线方案根除幽门螺杆菌感染的疗效

目的 :观察 2种四联疗法作为二线方案根除幽门螺杆菌 (Hp)感染的疗效。方法 :10 8例经以质子泵抑制药为基础的三联疗法根除Hp失败或根除后复发的病人 ,分为A组 5 4例和B组 5 4例。 2组均予奥美拉唑 2 0mg、胶体次枸椽酸铋 2 4 0mg及甲硝唑 4 0 0mg ,po ,bid ,A组加四环素 5 0 0mg ,po ,qid ;B组加阿莫西林 10 0 0mg ,po ,bid ;疗程均为 7d。疗程结束 1mo后复查Hp。结果 :A ,B 2组Hp根除率按方案分析分别为 82 % (42 / 5 1)和 81%(42 / 5 2 ) ,按意图治疗分析均为 78% (42 / 5 4)。 2组不良反应发生率分别为 2 3% (15 / 5 3)和 11% (6 /5 3)。 2组间疗效比较差异无显著意义 (P >0 .0 5 )。结论 :2种四联疗法作为二线方案根除幽门螺杆菌均有良好的疗效 ,且疗效相近 ,无严重不良反应     

抑酸与不同抗菌药治疗幽门螺杆菌相关性消化性溃疡的对照研究

目的:评价洛赛克、羟氨苄青霉素二联疗法对幽门螺杆菌(HP)相关性消化性溃疡的疗效。方法:将83例HP阳性的胃和十二脂肠溃疡患者按就诊顺序分为A、B两组。A组43例,每次口服洛赛克20mg,1天1次,21天,羟氨苄青霉素500mg,1天3次,14天。B组40例,在A组服药的基础上再给甲硝唑400mg,1天3次,14天。结果:两组溃疡愈合率分别为93.0%、95.0%,HP消除率分别为81.4%、85.0%。结论:两组溃疡治愈率和HP消除率差异无显著性(P>0.05),B组副作用明显高于A组(P<0.05)。     

奥曲肽联合奥美拉唑治疗非曲张静脉上消化道出血的疗效观察

目的观察奥曲肽联合奥美拉唑治疗非曲张静脉上消化道出血的疗效。方法将143例非曲张静脉上消化道出血患者，包括消化性溃疡、急性胃黏膜病变、胃癌、肝硬化门脉高压性胃出血等，随机分为A组（83例）和B组（60例），A组为奥曲肽联合奥美拉唑组，B组为单用奥美拉唑组，观察两组的止血效果。结果A组24h止血显效率为81．93％，明显高于B组（61．67％），P〈0．01；止血时间为（20．53±5．46）h，短于B组[（28．96±5．95）h]，输血量为（1．02±0．56）u，少于B组[（2．52±0．53）u]，48h再出血率为1．20％，低于B组（8．33％），均P〈0．05。结论奥曲肽联合奥美拉唑治疗非曲张静脉上消化道出血有显著疗效，较单用奥美拉唑有止血速度快、输血量减少、早期再出血发生率低的特点。     

洛赛克联合凝血酶治疗危重患儿应激性溃疡出血的观察及护理

目的 :探讨洛赛克联合凝血酶治疗危重病儿应激性溃疡出血的临床疗效及护理对策。方法 :将 6 5例应激性溃疡出血的危重病儿随机分为洛赛克、凝血酶联合治疗组和对照治疗组。观察应激性溃疡出血临床好转情况 ,同时加强护理并观察不良反应的发生情况。结果 :治疗组总有效 91 4 % ,对照组总有效73 3% ,两组相比差异有显著性意义 (P <0 0 1)。结论 :洛赛克联合凝血酶治疗危重病儿应激性溃疡出血疗效显著 ,且不良反应少     

Effect of intravenous omeprazole on intragastric pH during intravenous infusion of amino acids

Intravenous amino acids stimulate gastric acid secretion by an unknown mechanism. In patients on parenteral nutrition, this amino acid-induced gastric acid secretion might contribute to the failure of H₂-receptor antagonists to raise intragastric pH above 4.0, a level thought to be needed to prevent stress ulceration. Therefore we studied the effect of single and repeated doses of the H⁺/K⁺-ATPase blocker omeprazole on the intragastric pH during a 3-hr infusion of amino acids in 10 healthy volunteers; 5% glucose was used as a control infusion. Amino acids significantly decreased intragastric pH when compared to glucose infusion (P <0.05). After intravenous administration of 40 mg, 80 mg and 2 × 40 mg omeprazole, this amino acid-induced fall in pH was significantly inhibited (P < 0.01). No advantage of the 80-mg dose over the 40-mg dose could be demonstrated. The repeated dose of 40 mg showed a tendency to higher pH values compared to the single-dose experiments, which reached significance in the amino acid experiments only (P <0.05). Neither during the infusion of amino acids nor the glucose infusion omeprazole was able to continuously raise intragastric pH above 4.0. In conclusion, this study shows that intravenous omeprazole prevents gastric acid stimulation by intravenous amino acids but fails to continuously raise intragastric pH above 4.     

Treatment with proton pump inhibitors in acute non-variceal upper gastrointestinal bleeding: a meta-analysis

Medical therapy is an attractive adjuvant to endoscopic treatment in upper gastrointestinal (UGI) bleeding. This review aims to assess the treatment effects of proton pump inhibitor (PPI) therapy in acute non-variceal UGI bleeding. Outcome measures evaluated were further bleeding, surgery, all-cause deaths, ulcer deaths and non-ulcer deaths. We searched MEDLINE (1966-2002) and EMBASE (1974-2002) using the terms 'gastrointestinal hemorrhage', 'peptic ulcer hemorrhage', 'proton pump inhibitor', 'omeprazole', 'pantoprazole', 'lansoprazole', 'rabeprazole' and 'esomeprazole'. The search was extended to the Cochrane controlled trials registry database, published abstracts from five international gastroenterology conferences, manufacturers of PPI, known contacts and bibliographies from each full-length published report. We included trials published in English and non-English languages. Eligible studies were randomized controlled trials that compared the treatment effects of PPI therapy with placebo or H2 receptor antagonists in patients with acute non-variceal UGI bleeding. Of the 175 articles screened, 26 controlled trials including 4670 subjects (2317 in treatment arm and 2353 in control arm) were analyzed. The methodology, population, intervention, and outcomes of each selected trial were evaluated using duplicate independent review. Disagreements were resolved by consensus. PPI therapy significantly reduced rates of further bleeding (odds ratio [OR], 0.48; 95% confidence interval [CI], 0.40-0.57) and surgery (OR, 0.61; 95% CI, 0.48-0.76). All-cause deaths were unaffected (OR, 1.02; 95% CI, 0.76-1.37). Ulcer deaths showed a significant reduction (OR, 0.58; 95% CI, 0.35-0.96), while non-ulcer deaths showed a significant increase (OR, 1.60; 95% CI, 1.06-2.41) in the PPI therapy group. Sensitivity analysis of 22 trials published in peer-reviewed journals, 10 trials with double-blind design and 19 trials with high quality score and 22 trials using omeprazole in the treatment group showed results similar to those seen in the analysis of all 26 trials, confirming the stability of the conclusions. Subgroup analysis revealed that summary outcome measures were not influenced by control group therapy (placebo vs H2 receptor antagonists) or the use of prior endoscopic treatment to achieve hemostasis (given vs not given). However, the summary treatment effects for further bleeding and need for surgery were significant in only those trials enrolling patients with peptic ulcers having high risk for rebleeding and not in those trials enrolling patients with all causes of UGI bleeding. The summary treatment effects for further bleeding and need for surgery were significant in trials using intravenous as well as oral PPI. However, summary OR for all-cause deaths and non-ulcer deaths in trials using intravenous PPI were higher in the treatment group and not in trials using oral PPI. This raised the possibility of intravenous PPI-therapy-associated non-ulcer deaths in high-risk patients. PPI therapy in acute non-variceal UGI bleeding reduced rates of further bleeding, surgery and deaths caused by ulcer complications. However, non-ulcer deaths were increased. The overall mortality was unaffected. PPI therapy is useful only in a selected group of patients with acute non-variceal UGI bleeding, namely those with peptic ulcers having endoscopic high-risk stigmata for rebleeding.     

国内奥美拉唑(盐)口服制剂人体生物等效性试验的问题和对策

奥美拉唑是质子泵抑制剂类代表药物,临床上应用广泛.文中通过对国内26篇奥美拉唑(盐)12服制剂人体生物等效性试验文献进行分析,探讨了试验内容、参比制剂、受试者、生物样品采集及分析、药动学参数、上市后生物等效性再评价或监测等方面的问题和对策,以期为奥美拉唑(盐)口服制剂人体生物等效性研究和临床应用提供参考信息,并基于现有...     

高效液相色谱法测定复方奥美拉唑干混悬剂中的有关物质及奥美拉唑磺酰化物的含量

目的建立复方奥美拉唑干混悬剂中有关物质及奥美拉唑磺酰化物的测定方法。方法色谱柱:Agilent-C8(4.6 mm×200 mm,5μm);流动相:0.01 mol.L-1磷酸氢二钠(用磷酸调节pH值至7.6)-乙腈(75∶25);检测波长:280 nm;流速:1.0 mL.min-1;柱温:40℃;进样量:20μL。结果奥美拉唑磺酰化物在0.2~1.0μg.mL-1与峰面积呈良好的线性关系(r=1.0,n=5)。平均回收率99.6%,RSD=0.2%(n=6)。结论本方法简便、迅速、准确。     

RP-HPLC法考察硫酸头孢噻利与奥美拉唑钠的配伍稳定性

目的观察硫酸头孢噻利(第4代头孢菌素类抗生素)与奥美拉唑钠(抗溃疡药)的配伍稳定性。方法用反相高效液相色谱法测定硫酸头孢噻利与奥美拉唑钠配伍后在不同温度下8 h内的相对百分含量,并考察其外观与pH值。结果硫酸头孢噻利与奥美拉唑钠配伍后,在4℃放置8 h、25℃放置3 h、37℃放置1 h,配伍溶液的外观、pH值及两者相对百分含量基本无变化。37℃放置2 h后,奥美拉唑钠相对百分含量变化约5%,配伍液不能使用。结论硫酸头孢噻利与奥美拉唑钠的配伍液在高温环境中1 h内稳定,2 h后稳定性差。     

Steady-state pharmacokinetics of once-daily fosamprenavir/ritonavir and atazanavir/ritonavir alone and in combination with 20 mg omeprazole in healthy volunteers

OBJECTIVES: Use of proton pump inhibitors in HIV-infected patients is common. The purpose of this study was to determine the steady-state pharmacokinetics of once-daily (qd) fosamprenavir/ritonavir (FPV/r) and atazanavir/ritonavir (ATV/r) alone and in combination with 20 mg qd omeprazole (OMP) in healthy volunteers. DESIGN AND METHODS: A prospective, open-label, single-site, two-period, crossover pharmacokinetic study was carried out in healthy volunteers. Subjects received either qd FPV/r 1400 mg/200 mg or ATV/r 300 mg/100 mg in the morning for 14 days and then 20 mg OMP in the evening for an additional 7 days. The pharmacokinetics were assessed over 24 h on days 14 and 21. Following a 2-week washout, subjects repeated the process with the other regimen. Trough protease inhibitor (PI) concentrations were taken on day 16 of each period to assess the impact of a single dose of OMP on ATV and amprenavir (APV) concentrations. Plasma ATV and APV pharmacokinetic parameters were assessed by noncompartmental analysis; geometric mean ratios (GMRs; PI+OMP/PI; 90% confidence interval) were calculated between days 14 and 21. RESULTS: Nineteen healthy, non-HIV-infected volunteers were evaluated. OMP reduced ATV exposure [area under the concentration curve at 0-24 h (AUC0-24 h)] and the minimum drug concentration (Cmin) by 27% each. In contrast, APV exposure and Cmin were decreased by 4 and 2%, respectively. Four subjects (21%) experienced greater than 50% declines in both ATV AUC0-24 h and Cmin after the addition of OMP; this was not observed in any subject following receipt of FPV/r. No alterations in APV or ATV trough concentrations were observed following a single dose of OMP. CONCLUSIONS: The addition of 20 mg OMP administered in the evening has minimal effect on APV pharmacokinetics. In contrast, ATV pharmacokinetics were altered; a number of ATV-treated subjects experienced pronounced declines in exposures upon the addition of 20 mg OMP administered in the evening, whereas others experienced little to no change.