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Macrophages contribute to post-transplant lung rejection. Disulfiram (DSF), an anti-alcoholic drug, has an anti-inflammatory effect and regulates macrophage chemotactic activity. Here, we investigated DSF efficacy in suppressing acute rejection post-lung transplantation. Male Lewis rats (280–300 g) received orthotopic left lung transplants from Fisher 344 rats (minor histocompatibility antigen-mismatched transplantation). DSF (0.75 mg/h) monotherapy or co-solvent only (50% hydroxypropyl-β-cyclodextrin) as control was subcutaneously administered for 7 days (n = 10/group). No post-transplant immunosuppressant was administered. Grades of acute rejection, infiltration of immune cells positive for CD68, CD3, or CD79a, and gene expression of monocyte chemoattractant protein and pro-inflammatory cytokines in the grafts were assessed 7 days post-transplantation. The DSF-treated group had significantly milder lymphocytic bronchiolitis than the control group. The infiltration levels of CD68+ or CD3+ cells to the peribronchial area were significantly lower in the DSF than in the control groups. The normalized expression of chemokine ligand 2 and interleukin-6 mRNA in allografts was lower in the DSF than in the control groups. Validation assay revealed interleukin-6 expression to be significantly lower in the DSF than in the control groups. DSF can alleviate acute rejection post-lung transplantation by reducing macrophage accumulation around peripheral bronchi and suppressing pro-inflammatory cytokine expression.

A 70-year-old man began to cough. Chest X-ray showed a tumor in the center, pleural effusion on the left side, and diffuse granular shadows on the right side. Chest computed tomography (CT) showed bronchial wall thickening and numerous granular shadows. We suspected diffuse panbronchiolitis. Thus, transbronchial lung biopsy (TBLB) and transbronchial lung cryobiopsy (TBLC) were performed. The tissue size obtained was 1 mm by TBLB and 6 mm at 5 seconds by TBLC. Histological analysis of the TBLB specimen showed lymphocyte infiltration, no fibrosis in Hematoxylin-eosin (HE) staining, and no elastic fibers in Elastica van Gieson (EVG) staining. On the other hand, TBLC specimens showed inflammatory cell infiltration and fibrosis around the bronchioles in HE staining and hypertrophy of elastic fibers in EVG staining. It was diagnosed as diffuse panbronchiolitis (DPB) from clinical and pathological findings. Cryobiopsy is useful in diagnosing DPB as well as interstitial pneumonia and lung cancer.

Abstract A 37‐year‐old man was admitted to our hospital with chest pain and fever. Computed tomography showed pleural effusion and irregularly marginated, elevated lesions inside diffuse pleural thickening. Detailed medical examination showed swelling of the left testicle. 18F‐fluorodeoxyglucose positron emission tomography showed uptakes at the thickened pleura and left testis. Pelvic magnetic resonance imaging showed a mass in the left testis with a heterogeneous and partially calcified tumour present interiorly. Thoracoscopy was performed under local anaesthesia, enabling the observation of masses at the pleura and biopsy of the mass, which was diagnosed as malignant pleural mesothelioma. The affected testicle was resected and diagnosed as tunica vaginalis testis mesothelioma. Thus, simultaneous tunica vaginalis testis and pleural mesothelioma were diagnosed. It is necessary to closely examine parts of the body other than the chest.

Bronchial thermoplasty (BT) is a type of bronchoscopic treatment specifically used for patients with severe asthma. Most severe asthmatics receive systemic steroids and are at risk of being immunocompromised. This raises the clinical question of whether or not BT can be effectively and safely performed in such patients. Herein, we report a case highlighting the effectiveness and safety of BT in a patient with severe persistent bronchial asthma and Pseudomonas aeruginosa infection. We performed BT on a 46-year-old woman undergoing treatment for severe persistent asthma with inhaled steroids and 20 mg prednisolone orally. Although she was deemed to be infection-free before the procedure, culture of endobronchial secretions obtained during the first BT procedure grew Pseudomonas aeruginosa. After the first BT, she was given clarithromycin 400 mg orally daily. The amount of sputum decreased with each BT session, and sputum culture for Pseudomonas aeruginosa turned negative by the third BT session. Respiratory function tests showed 23.7% improvement in % post-bronchodilator forced expiratory volume in 1.0 s (%FEV1.0) and the asthma quality of life questionnaire (AQLQ) score increased by 2.41 points after the third BT. Bronchial wall thickness decreased and infiltrative shadows on CT disappeared after the three BT sessions, along with decrease in the amount of purulent sputum. Improvement in her asthma symptoms, after three BT sessions allowed decrease in the prednisolone dose.We report the effectiveness of BT and infection control in a severe asthmatic with Pseudomonas aeruginosa infection.

Temsirolimus is an inhibitor of mammalian target of rapamycin and interstitial lung disease (ILD) is known to be one of the adverse events associated with temsirolimus, which usually improves rapidly after discontinuation of the drug and rarely worsens thereafter. Herein, we report a case of delayed exacerbation of ILD after discontinuation of temsirolimus for metastatic renal cell carcinoma in an 86-year-old male with chronic ILD. The patient developed gradually worsening dyspnea five weeks after an initiation of temsirolimus and was admitted to our facility. On his admission, although a pulmonary function test revealed a decreased diffusion capacity, there was no obvious progression of ILD on HRCT scan. His dyspnea once improved after discontinuation of temsirolimus, but it recurred and acute exacerbation of ILD was diagnosed 40 days after his last administration of temsirolimus. He received high-dose steroid therapy, however, he deteriorated and died. Histopathological examination of the lungs at autopsy revealed overlapping diffuse alveolar damage with chronic interstitial changes. In the present case, since there were no specific factors that could have caused acute exacerbation of ILD except for temsirolimus, it was considered to contribute to the exacerbation of underlying ILD. In conclusion, physicians should be aware of the possibility of temsirolimus-induced ILD not only while the medication is administered, but also even after it is discontinued. It is important to carefully interview the patient and to recognize the value of physiological tests, such as respiratory function tests and blood gas analysis, as well as imaging findings on HRCT.