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“Everolimus, an inhibitor of the mammalian target of rapamycin (mTOR), is an effective antitumor drug for renal cell carcinomas (RCCs), with its use increasing for management of other neoplasms such as breast cancer [1], neuroendocrine tumors [2], and angiomyolipoma [3]. Because of the high incidence of pulmonary adverse effects

caused by the drug, this increased use of everolimus is expected to result in find more an increased number of patients with drug-induced interstitial lung disease (ILD). In fact, drug-induced ILD was reported to occur in 13.5% patients receiving everolimus in a phase III clinical trial for RCC [4]. In addition to its antitumor effects, everolimus has been used as an immunosuppressant to prevent the rejection of heart and kidney transplants [5]. Therefore,

scrupulous care must be taken against opportunistic infections whenever everolimus is used; however, to our knowledge, there is only limited information regarding pulmonary infectious complications associated with everolimus therapy. In this paper we describe a case of pneumocystis pneumonia (PCP), which was clinically similar to everolimus-induced ILD and was initially managed with a corticosteroid. The patient was successfully treated with trimethoprim-sulfamethoxazole immediately after being diagnosed with PCP on the basis of a PCR assay for Pneumocystis jirovecii and elevated β-D-glucan levels. A 66-year-old Japanese Trametinib male with advanced renal cell carcinoma (RCC) visited our respiratory outpatient clinic complaining of progressive exertional dyspnea for 1 month after administration of everolimus. He had suffered from unresectable RCC with multiple bone metastases for 2 years (clear cell carcinoma. cT3cN0M1. stage IV). Previous therapy included sunitinib

for 1 year, followed by axitinib for 2 months. This regimen failed to prevent disease progression. Thereafter, third-line therapy with everolimus was initiated. Rebamipide The patient was an exsmoker and had stopped smoking 35 years back. Annual check-ups had revealed that he was asymptomatic for any breathing problems, with no abnormalities in the pulmonary function tests or chest computed tomography (CT) scans. On his first visit to our clinic, he was afebrile but presented with general malaise and tachypnea accompanied by hypoxemia (SpO2, 96% after inhaling oxygen by mask at 4 L/min). He had slight systemic edema, probably caused by renal insufficiency and/or hypoalbuminemia. Cardiac pulmonary edema was excluded by echocardiography. On chest auscultation, no wheeze or crackle was audible. Chest radiograph revealed bilateral infiltration on both lungs, while chest CT revealed diffuse ground glass opacities in both lung fields (Fig. 1A and B). The laboratory findings on admission are presented in Table 1. In brief, we observed mild lymphocytosis, mild anemia, thrombocytopenia, slight liver dysfunction, and renal insufficiency.