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We report a case of secondary amyloidosis with pleural involvement in a patient with rheumatoid arthritis. A 77-year-old man had received a diagnosis of rheumatoid arthritis 10 years previously. Bilateral pleural effusion of unknown etiology was noted 2 years prior to admission. A biopsy of the left pleura by video-assisted thoracic surgery did not reveal any evidence of the cause of his pleural effusion. The histological findings revealed chronic inflammation of the pleura on a hematoxylin-eosin (HE) stain, but treatment with an increased dose of corticosteroid did not improve his effusion. Right pneumothorax then developed. Based on the histological findings of a Congo red stain, the diagnosis was changed to pleural amyloidosis. An initial attempt at pleurodesis with OK-432 and a pleural patch with the patient's own blood was attempted but was not successful. Subsequently, pleurodesis with OK-432 and the patient's own blood improved his pleural effusion and pneumothorax. Pleural involvement in amyloidosis is extremely rare and is difficult to treat.

A 38-year-old woman with a 10-year history of migraine without aura was treated with topiramate (TPM) for increasing frequency of headache. Initially, TPM was prescribed at a dose of 25 mg per day for 7 days, and then the dose was increased to 50 mg per day. Three days later, the patient complained of blurry vision, redness, and pain in both eyes. On ophthalmological examination, the pupils were found to be mid-dilated, and her visual acuity with correction was 1.2 in both eyes. Slitlamp examination revealed conjunctival hyperemia, chemosis, and shallow anterior chambers. Intraocular pressure in the right eye was 35 mmHg, while that in the left eye was 36 mmHg. Gonioscopy showed angle closure in both eyes, and therefore, a diagnosis of bilateral angle-closure glaucoma was made. TPM was discontinued immediately, and antiglaucoma medications were started. Four days after the initiation of antiglaucoma treatment, conjunctival hyperemia and chemosis disappeared and intraocular pressure in the right and left eyes decreased to 8 mmHg and 7 mmHg, respectively. The treatment was discontinued on the 11th day. To the best of our knowledge, this is the first case of TPM-induced angle-closure glaucoma in Japan.

A 49-year-old man was admitted to our hospital for an expanding tumor in the pulmonary artery. He had visited a previous hospital complaining of dyspnea on effort and had syncope 4 months before admission, and pulmonary embolism was diagnosed because enhanced chest CT showed filling defects, with calcification in the pulmonary trunk and left pulmonary artery. Despite thrombolytic and anticoagulant therapy, the filling defects grew and expanded into the extravascular portion. Additionally, CT showed multiple pulmonary nodules and a small calcified nodule in a right-sided back muscle also appeared. At our hospital, FDG-PET showed abnormal uptake in each lesion shown on CT. We then performed a CT-guided needle biopsy of the nodule of the back muscle, which was pathologically diagnosed as osteosarcoma. He was finally given a diagnosis of osteosarcoma of the pulmonary artery. We administered cisplatin and doxorubicin with partial inhibitory effect on tumor growth. Osteosarcoma of the pulmonary artery is extremely rare, and its diagnosis is difficult before surgery or autopsy. To the best of our knowledge there have been no reports of chemotherapy for osteosarcoma of the pulmonary artery.

We report a 75-year-old man with pneumoconiosis, interstitial pneumonia and diabetes mellitus, who had carcinoma of the buccal mucosa. After resection of the carcinoma, he was given corticosteroids for the deterioration of interstitial pneumonia, but 38 days after initiating steroid therapy, he was admitted to our hospital with severe hypoxemia and multiple cavitary lesions superimposed on ground-glass attenuation in both lung fields. The Aspergillus antigen was positive in his serum and examination of his bronchoalveolar lavage (BAL) fluid revealed mixed infections with filamentous fungus and Pneumocystis jirovecii. Pulmonary aspergillosis and pneumocystis pneumonia with an immunocompromised state was diagnosed, and voriconazole, sulfamethoxazole-trimethoprim and high-dose corticosteroids were given. At 20 days after these treatments he developed bloody sputum, and Cunninghamella bertholletiae was isolated from the BAL fluid obtained at admission. A diagnosis of pulmonary zygomycosis was finally established. Amphotericin B therapy was started, and the dose was increased thereafter. Despite intensive treatment he died 18 days later. Histological examination of lung tissue obtained at autopsy showed invasive growth of zygomycetes in the necrotic tissue and the cavity wall. To the best of our knowledge, this is the first report of concurrent Cunninghamella bertholletiae and Pneumocystis jirovecii infection during steroid therapy for interstitial pneumonia.