Department of Medical Microbiology, Radboud University Nijmegen Medical Centre, and Department of Medical Microbiology and Infectious Diseases, Canisius Wilhelmina Hospital, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands.
Antimicrob Agents Chemother. 2010 Feb;54(2):860-5. doi: 10.1128/AAC.00931-09. Epub 2009 Nov 16.
The in vivo efficacy of posaconazole against 4 clinical Aspergillus fumigatus isolates with posaconazole MICs ranging from 0.03 to 16 mg/liter, as determined by CLSI method M38A, was assessed in a nonneutropenic murine model of disseminated aspergillosis. The underlying resistance mechanisms of the isolates included substitutions in the cyp51A gene at codon 220 (M220I), codon 54 (G54W), and codon 98 (L98H). The latter was combined with a 34-bp tandem repeat in the gene promoter region (TR L98H). The control isolate exhibited a wild-type phenotype without any known resistance mechanism. Oral posaconazole therapy was started 24 h after infection and was given once daily for 14 consecutive days. Mice were treated with four different doses (1 to 64 mg/kg of body weight), and survival was used as the end point. Survival was dependent both on the dose and on the MIC. The Hill equation with a variable slope fitted the relationship between the dose/MIC ratio and 14-day survival well (R2, 0.92), with a 50% effective dose (ED50) of 29.0 mg/kg (95% confidence interval [CI], 15.6 to 53.6 mg/kg). This also applied to the relationship between the area under the plasma concentration-time curve (AUC)/MIC ratio and 14-day survival (50% effective pharmacodynamic index [EI50], 321.3 [95% CI, 222.7 to 463.4]). Near-maximum survival was reached at an AUC/MIC ratio of nearly 1,000. These results indicate that treatment of infections with A. fumigatus strains for which MICs are 0.5 mg/liter requires doses exceeding the present licensed doses. Increasing the standard dosing regimen may have some effect and may be clinically useful if no alternatives are available.
我们评估了一种体内疗效,该疗效针对的是 4 株临床分离的烟曲霉,这些菌株对泊沙康唑的 MIC 值在 0.03 至 16mg/L 之间,采用 CLSI 方法 M38A 进行检测。这些菌株的潜在耐药机制包括 CYP51A 基因密码子 220(M220I)、54(G54W)和 98(L98H)的取代,以及基因启动子区域 34 个碱基对串联重复(TR L98H)。对照分离株表现出野生型表型,没有任何已知的耐药机制。在感染后 24 小时开始口服泊沙康唑治疗,连续 14 天每天给药一次。小鼠接受了 4 个不同剂量(1 至 64mg/kg 体重)的治疗,以生存作为终点。生存既依赖于剂量,也依赖于 MIC 值。Hill 方程与可变斜率很好地拟合了剂量/MIC 比值与 14 天生存之间的关系(R2,0.92),50%有效剂量(ED50)为 29.0mg/kg(95%置信区间 [CI],15.6 至 53.6mg/kg)。这同样适用于血浆浓度-时间曲线下面积(AUC)/MIC 比值与 14 天生存之间的关系(50%有效药效学指数 [EI50],321.3[95%CI,222.7 至 463.4])。在 AUC/MIC 比值接近 1000 时,接近达到最大生存。这些结果表明,对于 MIC 值为 0.5mg/L 的烟曲霉菌株感染,需要超过目前许可剂量的剂量进行治疗。增加标准给药方案可能会有一些效果,如果没有其他选择,可能具有临床意义。