Obscured meshwork structure after treatment for heart failure: a case study.

An 87-year-old man with heart failure was admitted to our hospital. A transthoracic echocardiography showed diffuse mild left ventricular (LV) hypokinesis and LV noncompaction at the apex. A three-dimensional transthoracic echocardiography confirmed a trabecular meshwork. After treatment for heart failure, LV end-systolic dimension decreased and trabeculae seemed to converge and became obscure in end-systole. This is a rare case suggesting mechanism of obscured LV noncompaction after treatment for heart failure.

[Successful treatment of pleurodesis for seemingly intractable pleural effusion in pleural amyloidosis with rheumatoid arthritis].

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 case of AIDS with Pneumocystis jirovecii pneumonia which required differentiation from ANCA-related lung disease].

A 41-year-old man with fever, diarrhea and skin rash received a diagnosis of drug-induced lupus. He was given corticosteroids for 3 months and was subsequently admitted to a local hospital due to dyspnea. Pneumonia was then diagnosed and he was given a new quinolone antibacterial agent. Despite this treatment, his symptoms and signs gradually worsened and he was referred to our hospital. High resolution CT (HRCT) of the chest showed diffuse ground-glass opacities, reticular shadows, parenchymal abnormalities, traction bronchiectasis, a subpleural curvilinear shadow and septal lines. Serological examinations were positive for anti-myeloperoxidase antineutrophil cytoplasmic antibodies (MPO-ANCA) and subsequent HRCT findings were consistent with ANCA-related lung disease. However, the patient had complications such as previous syphilis infection, oral candidiasis, herpes zoster, hepatitis B virus and cytomegalovirus infection. Additionally, his serum was positive for HIV antibody and HIV-1 RNA, and therefore we diagnosed AIDS. His bronchoalveolar lavage fluid revealed Pneumocystis jirovecii. It is known that HIV infection is associated with many types of autoantibodies including MPO-ANCA. Therefore, in HIV/AIDS patients with interstitial lung diseases, it is important to differentiate opportunistic Pneumocystis pneumonia infection from collagen vascular disease-associated interstitial lung diseases.