Thompson George R, Chang Diana, Wittenberg Rebecca R, McHardy Ian, Semrad Alison
Department of Medical Microbiology and Immunology, University of California-Davis, Davis, California, USA
Department of Internal Medicine, Division of Infectious Diseases, University of California Davis Medical Center, Davis, California, USA.
Antimicrob Agents Chemother. 2017 Jul 25;61(8). doi: 10.1128/AAC.00760-17. Print 2017 Aug.
We describe a case of apparent mineralocorticoid excess (AME) secondary to posaconazole therapy and suggest the biochemical mechanism. Clinical and laboratory investigation confirmed 11β-hydroxysteroid dehydrogenase inhibition and withholding therapy led to a resolution of all clinical and laboratory abnormalities. Posaconazole was later restarted at a lower dose and prevented recurrence of this syndrome. Additional studies are necessary to determine the frequency of posaconazole-induced AME and whether other azole antifungals can be associated with this phenomenon.
我们描述了一例因泊沙康唑治疗继发的明显盐皮质激素过多（AME）病例，并提出了其生化机制。临床和实验室检查证实存在11β-羟类固醇脱氢酶抑制，停用该治疗后所有临床和实验室异常均得到缓解。随后以较低剂量重新开始使用泊沙康唑，该综合征未再复发。需要进一步研究以确定泊沙康唑诱导AME的频率，以及其他唑类抗真菌药是否也会出现这种现象。
