Primary bone adult T cell lymphoma with multiple skeletal lesions and debilitating painful osteolysis: a case report.

There have been only a limited number of reports on primary adult T cell lymphoma/leukemia (ATL) in the bone. This is a case report of a 75-year-old patient initially reporting multiple bone pains that were attributed to osteolytic ATL. The patient developed spontaneous chest/back pain and visited a local hospital. Laboratory tests showed high levels of alkaline phosphatase (ALP), and computed tomography (CT) revealed skeletal lesions with osteolysis. Although multiple myeloma was initially suspected, the results of bone marrow aspiration and bone biopsy were inconsistent. After he was referred to our hospital, mild hypercalcemia (10.4 mg/dL) with low-normal intact parathyroid hormone (PTH) (27 pg/mL), low parathyroid hormone-related protein (PTHrP), and elevated 1,25-dihydroxy vitamin D (1,25OH2D) levels (136 pg/mL) narrowed the differential diagnosis down to lymphomatous and granulomatous diseases, and then, the high serum soluble IL-2 receptor (3,450 U/mL) and the flower cells recognized in the peripheral blood sample suggested the involvement of ATL. Finally, the reevaluation of the iliac bone biopsy sample led us to the histological diagnosis of ATL infiltration in the bone. The subsequent two courses of chemotherapy in addition to denosumab resulted in an objective partial metabolic response indicated in 18-fluorine-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT). Although very rare, the bone involvement of ATL could be used for the differential diagnosis for local osteolytic bone pain in addition to multiple myeloma and metastatic bone diseases.

Combining cisplatin with cationized catalase decreases nephrotoxicity while improving antitumor activity.

Cisplatin is frequently used to treat solid tumors; however, nephrotoxicity due to its reactive oxygen species-mediated effect limits its use. We tested the ability of cationized catalase, a catalase derivative, to inhibit nephrotoxicity in cisplatin-treated mice. Immunohistochemical analysis showed that the catalase derivative concentrated in the kidney more efficiently than native catalase. Repeated intravenous doses of cationized catalase significantly decreased cisplatin-induced changes in serum creatinine, blood urea nitrogen, nitrite/nitrate levels, lactic dehydrogenase activity, and renal total glutathione and malondialdehyde contents. In addition, cationized catalase effectively blunted cisplatin-induced proximal tubule necrosis but had no significant effect on the cisplatin-induced inhibition of subcutaneous tumor growth. Repeated doses of catalase, especially cationized catalase, significantly increased the survival of cisplatin-treated tumor-bearing mice preventing cisplatin-induced acute death. Our studies suggest that catalase and its derivatives inhibit cisplatin-induced nephrotoxicity, thus improving the efficiency of cisplatin to treat solid tumors.

[Pseudoaneurysm of the left ventricle serially demonstrated from on-set using two-dimensional echocardiography: a case report].

A case of so-called pseudoaneurysm of the left ventricle without pericardial adhesion, serially demonstrated by two-dimensional echocardiography, was reported. A 76-year-old man developed congestive heart failure 10 hours after gastrectomy, and was diagnosed as having acute myocardial infarction. Two-dimensional echocardiography on the 21st day after onset revealed moderate pericardial effusion and an echo-free space in the posterolateral myocardium of the left ventricle. The echo-free space gradually expanded exteriorly and formed an aneurysm, which remained unchanged after the resolution of the pericardial effusion. Clinical diagnosis of pseudoaneurysm of the left ventricle was made by left ventriculography and coronary angiography. At autopsy, there was an aneurysm measuring 2.3 X 3.0 X 5.0 cm which communicated with the left ventricle via two small ostia, 5 mm each in diameter. There was a loose fibrous adhesion between the pericardium and the epicardium. The wall of the aneurysm consisted of organized fibrous tissue without any elements of the myocardium. Both myocardium and fibrous tissue were located at the junction of the left ventricular wall and the aneurysm. It is surmised that dissection of the infarcted myocardium expanded so greatly as to form an aneurysmal cavity, resulting in the formation of a so-called pseudoaneurysm of the left ventricle after fibrous changes of the outer wall in the infarcted myocardium. Therefore, this aneurysm might be termed a "dissecting" aneurysm of the left ventricle. The hypothesis that a pseudoaneurysm is derived from a localized hemopericardium should be reconsidered.