克霉唑与咪康唑对重度外阴阴道假丝酵母菌病乳杆菌属的影响

目的探讨克霉唑与咪康唑治疗重度外阴阴道假丝酵母菌病的疗效及对阴道乳杆菌属的影响。方法将90例确诊为重度外阴阴道假丝酵母菌病的患者随机分为2组,各45例,分别给予克霉唑阴道片500 mg,阴道置入,间隔3 d序贯治疗或咪康唑阴道栓400 mg,阴道置入,1次/d,共7 d;记录治疗第7天的治愈率,比较两组治疗前、停药后第14天和第28天阴道乳杆菌属的数量。结果治疗第7天,克霉唑阴道片组的治愈率为42.2%,明显高于咪康唑组的15.6%,差异有统计学意义;但第14天后克霉唑组的痊愈率为95.6%,咪康唑组为91.1%,2组的治愈率差异无统计学意义;用药后第14天,阴道乳杆菌属平均活菌数量对数值克霉唑组为6.46±1.68,咪康唑组为6.42±1.59,与用药前5.53±1.54、5.56±1.50相比,2组均有增加,但差异无统计学意义;用药后第28天,克霉唑组为7.02±1.50,咪康唑组为6.21±1.44,差异有统计学意义(P<0.05)。结论克霉唑阴道片能更快地消除症状达到治愈,而且有辅助阴道乳杆菌属生长的作用,可作为外阴阴道假丝酵母菌病,局部用药的首选药物。     

保妇康栓与克霉唑栓对念球菌性阴道炎的疗效及生活质量的影响

目的：对比分析保妇康栓与克霉唑栓对念球菌性阴道炎的疗效及生活质量的影响。方法：随机选取我院2013年1月～2015年2月收治的念球菌性阴道炎患者100例,按照治疗方式的不同分为保妇康栓组和克霉唑栓组,保妇康栓组用保妇康栓治疗,克霉唑栓组用克霉唑栓治疗,对比分析两组治疗的总有效率,临床症状的改善时间,3、6、12个月后复发率,不良反应的发生率,生活质量评分。结果：保妇康栓组治疗的总有效率为94.00%,明显高于克霉唑栓组的72.00%,差异具有统计学意义（P<0.01）;保妇康栓组阴道瘙痒、疼痛、灼热感以及白带异常等临床症状的改善时间均明显短于克霉唑栓组,差异具有统计学意义（P<0.01）;保妇康栓组治疗后3、6、12个月复发率均明显低于克霉唑栓组,差异具有统计学意义（P<0.05）;保妇康栓组不良反应的发生率明显低于克霉唑栓组,差异具有统计学意义（P<0.05）;保妇康栓组生活质量中的生理领域、心理领域、社会关系领域和环境领域等各维度的评分明显高于克霉唑栓组,差异具有统计学意义（P<0.01）。结论：保妇康栓治疗念球菌性阴道炎效果显著,能迅速改善患者的临床症状,降低复发率,提高生活质量,安全可靠,明显优于克霉唑栓。     

红核洗液联合克霉唑治疗妊娠期霉菌性阴道炎的临床观察

目的探讨红核洗液联合克霉唑治疗妊娠期霉菌性阴道炎的临床效果。方法按照抽签法将2017年1~9月本院接诊的200例妊娠期霉菌性阴道炎患者,随机分为观察组和对照组各100例,对照组患者给予克霉唑治疗,观察组患者在此基础上加用红核洗液治疗,比较两组疗程结束时治疗效果、临床症状消失时间、治疗满意度评分、不良反应以及随访6个月复发情况。结果观察组疗程结束时总有效率显著高于对照组,随访6个月复发率显著低于对照组(P0.05);观察组各临床症状消失时间均显著低于对照组,治疗满意度评分显著高于对照组(P0.05);两组治疗期间均未见明显不良反应。结论红核洗液联合克霉唑治疗妊娠期霉菌性阴道炎疗效显著,复发率低,安全性良好,值得临床推荐。     

Induction of the rat hepatic microsomal mixed-function oxidases by 3 imidazole-containing antifungal agents: selectivity for the cytochrome P-450IIB and P-450III families of cytochromes P-450

Administration of the imidazole antifungal agents ketoconazole, miconazole and clotrimazole gave rise to increases in the microsomal cytochrome P-450 levels and the NADPH-dependent reduction of cytochrome c. Clotrimazole, and to a much lesser extent miconazole and ketoconazole, stimulated the dealkylation of pentoxyresorufin. All 3 agents gave rise to small, but significant increases in the O-deethylations of ethoxycoumarin and ethoxyresorufin. The antifungal-induced O-deethylation of ethoxycoumarin was much more sensitive to inhibition by metyrapone rather than by -naphthoflavone. The binding of metyrapone to reduced microsomes was enhanced by treatment of animals with the 3 antifungal agents, clotrimazole being clearly the most potent. Immunoquantitation of cytochrome P-450 proteins using an ELISA procedure and employing anti-cytochrome P-450c (P-450IA1, P-448 low spin) and P-450b (P-450IIB1) antisera revealed that clotrimazole and miconazole, but not ketoconazole, induced the levels of phenobarbital-induced cytochromes P-450, while none of the antifungal agents increased the levels of cytochrome of P-448 proteins. Similar results were obtained using Western blots employing the above antibodies.

On SDS-polyacrylamide gel electrophoresis microsomes derived from animals pretreated with clotrimazole showed intensification of a band at 51 kDa which was identified by Western blotting as the PCN-inducible form of cytochrome P-450 (cytochrome P-450p, P-450III family). Similar, but less pronounced intensification was seen with microsomes from animals pretreated with miconazole and ketoconazole. Furthermore, microsomes from clotrimazole- and ketoconazole-treated animals interacted with erythromycin to yield type I spectra.

It is concluded that the imidazole-containing agents clotrimazole and miconazole, and to a much lesser extent ketoconazole, are potent inducers of the rat hepatic microsomal mixed-function oxidases, displaying selectivity towards the P-450IIB (phenobarbital-inducible) and P-450III (PCN-inducible) families of cytochrome P-450 proteins.     

Clotrimazole and efaroxan stimulate insulin secretion by different mechanisms in rat pancreatic islets

It is now well established that the imidazoline insulin secretagogue efaroxan mediates its effects by inducing closure of ATP-sensitive potassium channels in the pancreatic β-cell, leading to membrane depolarisation, Ca²⁺ influx and increased insulin secretion. However, a recent study has shown that efaroxan may also act as a blocker of a second class of potassium channel (the K_maxi channel) in red blood cells, raising the possibility that its effects in islets could be mediated by interactions with both types of channel. Since the antimycotic imidazole compound clotrimazole is a highly potent blocker of K_maxi channels, we have studied the effects of this drug on insulin secretion. Received: 10 July 1997 / Accepted: 2 September 1997     

替勃龙片联合双唑泰泡腾片治疗老年性阴道炎疗效观察

目的探讨替勃龙片联合双唑泰泡腾片治疗老年性阴道炎的临床疗效。方法选取2016年1月—2016年7月在信阳市第四人民医院接受诊治的老年性阴道炎患者90例,所有患者根据用药方案的不同分为对照组和治疗组,每组各45例。对照组每晚清洁外阴后于阴道深处置入双唑泰泡腾片,1片/次,1次/d。治疗组在对照组基础上口服替勃龙片,1片/次,1次/d。两组患者均连续治疗3个月。观察两组的临床疗效,比较两组的临床症状消失时间和生活质量。结果治疗后,对照组和治疗组的总有效率分别为77.78%、95.56%,两组比较差异有统计学意义(P0.05)。治疗后,治疗组外阴瘙痒、阴道黏膜充血和阴道分泌物消失时间明显短于对照组,两组比较差异具有统计学意义(P0.05)。治疗后,两组躯体功能、心理功能、社会功能和物质生活评分均明显升高,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标的升高程度明显优于对照组,两组比较差异具有统计学意义(P0.05)。结论替勃龙片联合双唑泰泡腾片治疗老年性阴道炎具有较好的临床疗效,可缩短临床症状消失时间,改善生活质量,具有一定的临床推广应用价值。     

Inhibitory effects of clotrimazole on TNF-α-induced adhesion molecule expression and angiogenesis

Cell adhesion molecules play a pivotal role in chronic inflammation and pathological angiogenesis. In the present study, we investigated the inhibitory effects of clotrimazole (CLT) on tumor necrosis factor (TNF)-α-induced changes in adhesion molecule expression. CLT dose-dependently inhibited monocyte chemoattractant protein-1 (MCP-1), intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) expressions in TNF-α-stimulated HT29 colonic epithelial cells. This inhibitory action of CLT correlated with a significant reduction in TNF-α-induced adhesion of monocytes to HT29 cells, which was comparable to the inhibitory effects of anti-ICAM-1 and VCAM-1 monoclonal antibodies on monocyte-epithelial adhesion. These inhibitory actions of CLT were, at least in part, attributable to the inhibition of redox sensitive NF-κB activation, as CLT inhibited TNF-α-induced ROS generation as well as NF-κB nuclear translocation and activation in HT29 cells. Furthermore, the inhibition of TNF-α-induced monocyte adhesion was also mimicked by the specific NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC). Inflammatory mediators including TNF-α have known to promote angiogenesis, which in turn further contributes to inflammatory pathology. Therefore, we additionally evaluated whether CLT modulates TNF-α-induced angiogenesis using in vivo chick chorioallantoic membrane (CAM) assay. The CAM assay showed that CLT dose-dependently attenuated TNF-α-induced angiogenesis, and the effect was correlated with decreased inflammation of the CAM tissue. In conclusion, our results suggest that CLT can inhibit TNF-α-triggered expression of adhesion molecules, ICAM-1 and VCAM-1, and angiogenesis during inflammation.