卡斯波芬金
甲氧苄啶
养生
磺胺甲恶唑
肺孢子虫肺炎
棘白菌素
肺炎
医学
挽救疗法
内科学
药理学
抗生素
化疗
生物
微生物学
氟康唑
耶氏肺孢子虫
抗真菌
皮肤病科
作者
Riccardo Utili,Emanuele Durante‐Mangoni,Cristina Basilico,A. Mattei,Enrico Ragone,Paolo Grossi
出处
期刊:Transplantation
[Wolters Kluwer]
日期:2007-09-27
卷期号:84 (6): 685-688
被引量:69
标识
DOI:10.1097/01.tp.0000280546.91617.6c
摘要
Background. Pneumocystis jiroveci pneumonia may be a life-threatening opportunistic infection in immunosuppressed solid organ transplant recipients. Despite effective treatment with high-dose trimethoprim-sulfamethoxazole and steroids, morbidity is often severe and lethality remains high. New therapeutic approaches are therefore warranted. Caspofungin, a beta-1,3-glucan synthesis inhibitor, has shown activity against the cyst forms of P. jiroveci in experimental animal models. We here report our preliminary clinical experience with caspofungin as an additional drug to the standard trimethoprim-sulfamethoxazole regimen. Methods. Four solid organ transplant patients with severe hypoxemic P. jiroveci pneumonia were treated with the combination of trimethoprim-sulfametoxazole and caspofungin. In two cases, caspofungin was added as salvage treatment due to failure of trimethoprim-sulfametoxazole monotherapy. Results. In these four patients, the use of caspofungin as an additional drug to the standard trimethoprim-sulfamethoxazole regimen led to a rapid improvement and a complete cure of pneumonia. No side effects or drug interactions were observed. Discussion. This preliminary clinical experience suggests that the addition of caspofungin to trimethoprim-sulfamethoxazole, which is active against trophic forms, may provide a synergistic activity against P. jiroveci by fully inhibiting the organism life cycle.
科研通智能强力驱动
Strongly Powered by AbleSci AI