In patients with epidermal growth factor receptor (EGFR) mutation-positive lung cancer (LC) who have acquired resistance to first and/or second-generation EGFR-tyrosine kinase inhibitors (EGFR-TKIs), detection of EGFR T790M (T790M) mutation is essential before administration of osimertinib. Tissue sample is the main specimen used to detect the T790M mutation, and so cell block preparation using pleural or pericardial fluid should be considered. The utility of body cavity effusion cell block methods in T790M mutation detection have not yet been fully evaluated. This study aimed to evaluate the clinical background and treatment course of LC patients harboring the T790M mutation by using body cavity effusion cell block methods at our hospital. All patients were treated with first and/or second-generation EGFR-TKIs and had developed malignant pleural or pericardial fluid as a result of progressive disease. T790M mutation status was evaluated using body cavity effusion cell block method in 9 patients, from April 2016 to August 2017. We retrospectively evaluated the clinical characteristics and treatment course of these 9 patients (3 males and 6 females; median age 76 years). At the first diagnosis of LC, 7 patients had stage IV cancer; 4 patients were diagnosed by bronchial fibroscopy and 3 were diagnosed from pleural fluid examination. Regarding EGFR mutation, 3 and 6 patients carried the exon 19 deletion and L858R mutation, respectively. Median time interval between the first diagnosis of LC and T790M mutation evaluation was 30.8 months; 7 patients were diagnosed with positive T790M mutation by using body cavity effusion cell block methods. The T790M mutation was highly detected by examination of body cavity effusion cell blocks. Further evaluation is necessary with respect to variations in T790M detection rate based on the specimen collection site and/or progressive disease pattern in different patients.

A 68-year-old man was admitted to our hospital with complaints of fatigue, polyuria, and loss of appetite, and was diagnosed with diabetic ketosis. Chest and abdominal computed tomography (CT) showed a pulmonary tumor on the right S3 and multiple liver tumors. Blood chemistry revealed elevated levels of amylase and hepatobiliary enzymes. Pathological examination of a biopsy specimen from the liver tumor showed a small cell carcinoma. Based on the imaging and pathological findings, we made a diagnosis of extensive disease small-cell lung cancer (ED-SCLC), cT1aN3M1b (HEP, ADR). Treatment with carboplatin and etoposide evoked partial response and the serum level of amylase decreased. Immunohistochemical staining of liver biopsy specimen was positive for amylase, leading to a diagnosis of SCLC with amylase production. About 22 months after the diagnosis of SCLC, he was admitted to our hospital with fatigue, muscular weakness, edema, and hyperpigmentation. Laboratory findings showed elevated serum levels of hepatobiliary enzymes, adrenocorticotropic hormone (ACTH), and cortisol, and a decreased serum potassium level. Urinary potassium level was elevated. Pituitary magnetic resonance imaging showed a normal morphology. We made a diagnosis of SCLC complicated by Cushing’s syndrome. We report this rare case of SCLC with amylase and ACTH production, which was detected in the course of treatment of SCLC.

Objective: The utility of topotecan monotherapy for relapsed small-cell lung cancer (SCLC) after failure of amrubicin monotherapy has not been evaluated. We aimed to investigate the efficacy and safety of topotecan monotherapy in patients with relapsed SCLC after amrubicin monotherapy.Patients and Methods: We retrospectively analyzed data from 16 patients with relapsed SCLC who were treated with topotecan monotherapy after amrubicin monotherapy at our hospital.Results: The response rate, progression-free survival, and overall survival were 0%, 32.5 days (95% confidence interval [CI] = 18–51), and 112 days (95% CI = 55–267), respectively. The most common adverse events (grade ≥3) were leukopenia (31.3%) and thrombocytopenia (31.3%), followed by anemia, anorexia, edema, and lung infections.Conclusion: The efficacy of topotecan monotherapy for relapsed SCLC after amrubicin monotherapy is inconclusive. Therefore, further studies are warranted.

A 38-year-old man was admitted to our hospital with fever and skin rash, and he was diagnosed as having dermatomyositis. He was treated with anti-inflammatory steroid and immunosuppressive agents. On hospital day 48, chest computed tomography (CT) revealed a nodule measuring approximately 2 cm in size in the lower lobe of the right lung (S9). Bacterial and/or fungal infection was suspected, but there was no response to antibiotic or antifungal treatment. A week later, repeat chest CT revealed the tumor now measuring approximately 6 cm in size in the lower lobe of the right lung. We performed bronchoscopy, and bacteriological examination of the transbronchial biopsy specimen revealed pulmonary tuberculosis. Interferongamma release assay (IGRA) before the initiation of immunosuppressive treatment was negative, so we did not administer treatment for latent tuberculosis infection. He was, however, treated with isoniazid, rifampicin, ethambutol, and pyrazinamide for 9 months, following which radiological features improved gradually. Here we describe in detail this rare case of a negative IGRA result before immunosuppressive therapy in a relatively young Japanese man who went on to develop active tuberculosis with a rapidly-growing pulmonary lesion during hospitalization.

Endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) is useful for diagnosing mediastinal lymph node lesions. Cell blocks prepared from the needle washing fluid and flow cytometry of tissue samples are helpful in making the diagnosis, but the combination of both examinations is not routinely performed. A 77-year-old woman with fever, dyspnea, and anorexia was admitted to our hospital. Computed tomography showed enlarged mediastinal lymph nodes with calcification and left ureteral calculus; however, no focus of infection was identified. We suspected lymph node tuberculosis or malignant lymphoma, and EBUS-TBNA was performed to evaluate the mediastinal lymph node lesions. Because a cell block prepared from the needle rinse fluid was suspicious for malignant lymphoma, we changed the puncture needle from 22 G to 19 G and performed a second EBUS-TBNA. Diffuse large B-cell lymphoma (DLBCL) was diagnosed based on the results of flow cytometry of the EBUS-TBNA samples. Here we report this case of DLBCL in which mediastinal lymph node tuberculosis was suspected and cell block preparation and flow cytometry using EBUS-TBNA specimens were useful for the diagnosis.