[A case of acute mediastinitis after endobronchial needle aspiration].

BACKGROUND: Endobronchial ultrasound-guided transbronchial needle aspiration (EBUS-TBNA) has become widespread, but reports of complications are rare. CASE: An enlarged mediastinal lymph node (4R) was detected in a 67-year-old man 33 months after surgery for rectal cancer, and we performed EBUS-TBNA to confirm the diagnosis. He was then admitted to hospital 13 days after the procedure, with cough, a swollen mediastinal fatty area around the 4R lymph node, and elevated WBC and CRP levels. After a diagnosis of acute mediastinitis was confirmed we gave him antibiotics, which improved his symptoms, the mediastinal fatty area and his WBC and CRP levels. CONCLUSION: We have to be aware of the possibility of acute mediastinitis after EBUS-TBNA of necrotic lymph nodes.

Transcription factor POU6F1 is important for proliferation of clear cell adenocarcinoma of the ovary and is a potential new molecular target.

OBJECTIVE: Clear cell adenocarcinoma of the ovary often shows resistance to anticancer agents. It accounts for 20% of epithelial ovarian cancer in Japan versus around 5% in other countries. We investigated new molecules to use when developing molecular-targeting therapy for clear cell adenocarcinoma. METHODS: Reverse transcriptase polymerase chain reaction and Western blot analysis were performed to confirm the expression of POU6F1 in several kinds of cell lines derived from epithelial ovarian carcinoma. Microarray analyses were performed using 2 ovarian cancer microarray data sets available on the Internet. Immunohistochemical staining was also done to confirm both the expression and the localization of POU6F1 using human ovarian epithelial ovarian carcinoma tissue specimens. In addition, the gene cluster located downstream of transcription factor POU6F1 was investigated to analyze its role in the proliferation of clear cell adenocarcinoma of the ovary via the lysophosphatidic acid receptor, a G protein-coupled receptor. Furthermore, RNA interference studies with small interfering RNA (siRNA) were performed to assess the effect of POU6F1 on proliferation of xenograft tumors after injection of clear cell adenocarcinoma cells into nude mice. RESULTS: Expression of POU6F1 at messenger RNA and protein was confirmed in cell lines derived from epithelial ovarian carcinoma. The microarray analyses performed using the 2 ovarian cancer microarray data sets available on the Internet indicated that POU6F1 expression was significantly greater in clear cell adenocarcinoma. Immunostaining confirmed the nuclear localization of POU6F1 in clear cell adenocarcinoma (100%). Exposure to the siRNA for POU6F1 reduced the expression of lysophosphatidic acid receptors, which are G protein-coupled receptors involved in tumor cell proliferation. POU6F1 siRNA dose-dependently suppressed the proliferation of clear cell adenocarcinoma cell lines, and a similar effect was confirmed for tumors transplanted into nude mice. CONCLUSIONS: Clear cell adenocarcinoma shows little response to standard therapy. The results of this study suggested that the transcription factor POU6F1 could be a new molecular target for treatment of this cancer.

Urinary fatty acids and liver-type fatty acid binding protein in diabetic nephropathy.

BACKGROUND: The aims of this clinical study were to investigate the associations of urinary free fatty acid (FFA) levels with tubulointerstitial damage, and to determine the clinical significance of urinary liver-type fatty acid binding protein (L-FABP) in diabetic nephropathy. METHODS: Fifteen patients with nephrotic syndrome due to diabetic nephropathy and 12 patients with minimal-change nephrotic syndrome (MCNS) were studied. Urinary and serum FFA concentrations (palmitic, oleic, linoleic, and arachidonic acids) were measured by gas chromatography, and urinary L-FABP levels were quantified using an ELISA technique. Tubulointerstitial damage was assessed using renal biopsy specimens. RESULTS: The levels of urinary linoleic and arachidonic acids were significantly elevated in diabetic nephropathy compared to MCNS patients, though serum FFA levels were lower in diabetic nephropathy than MCNS patients. The degree of tubulointerstitial damage was significantly severer in the patients with diabetic nephropathy than MCNS. Urinary L-FABP and 8-OHdG (8-hydroxydeoxyguanosine) concentrations were significantly higher in the diabetic nephropathy subjects. CONCLUSION: Elevated urinary excretion of FFA may be a reflection of FFA overload in the proximal tubules, and FFA may be an important promoter of tubulointerstitial damage in diabetic nephropathy patients. Urinary L-FABP levels may reflect the stress induced by FFA to the proximal tubules, leading to severe tubulointerstitial damage.

A case of biopsy-proven oxaliplatin-induced acute tubulointerstitial nephritis with thrombocytopenia and anemia.

Oxaliplatin, a third-generation platinum agent, has been used for the treatment of colon, pancreatic, and stomach cancers in recent years. It carries a reduced risk of acute kidney injury (AKI) compared to the previous platinum agents, including cisplatin and carboplatin. Several cases of oxaliplatin-induced acute tubular necrosis (ATN) have been reported; however, only one case has been reported as acute tubulointerstitial nephritis (ATIN) histopathologically. Here, we present a case of biopsy-proven and dialysis-dependent ATIN, which dramatically resolved with steroid therapy. The patient was a 67-year-old male who had undergone chemotherapy for colon adenocarcinoma. He suddenly developed shaking chills, fever, and hot flashes at the end of the 18th 5-fluorouracil (5-FU)/L-leucovorin/oxaliplatin administration, and was admitted to our hospital. On the 4th day of hospitalization, severe renal dysfunction (creatinine 6.5 mg/dL) was observed. As oliguria continued, we initiated hemodialysis therapy on the 6th day of hospitalization. Drug-induced ATIN was strongly suspected due to the history of multiple exposures to oxaliplatin with allergic reaction and sterile pyuria. We began steroid therapy on the 8th day of hospitalization. Subsequently, renal biopsy was performed and the diagnosis of ATIN was made. The patient's renal function gradually improved, and 6 months later, it had returned to baseline. Our case demonstrates that we should consider not only ATN, but also ATIN, as potential presentations of oxaliplatin-induced AKI.

Efficacy of steroid therapy for pacing failure in a patient with chronic myocarditis.

A 66-year-old man had a progressive increase in the pacing threshold over a one-year period, resulting from chronic myocarditis. Following steroid therapy, the pacing threshold decreased and became stabilized, and was accompanied by a decrease in the serum creatine kinase, cardiac myosin light chains and pro-collagen III peptide values, but cardiac function did not improve. Endocardial biopsy showed that there was no progression in the fibrosis. The pacing failure improved, but the cardiac function did not. It was believed that the steroid therapy suppressed the progression of the inflammation and fibrosis caused by the chronic myocarditis.

[A case of primary Sjögren's syndrome complicated by chronic progressive myositis].

The patient was a 64-year-old woman with a nearly 20-year history of sicca symptoms, having been given a diagnosis of primary Sjögren's syndrome. Three years previously, she experienced difficulty in walking up a slope and had leg malaise, which insidiously progressed to an inability to go up and down stairs. This disability brought her to our hospital, where her muscle strength was examined by manual muscle testing, and she was found to have reduced muscle strength in proximal muscles like the thigh muscles and the neck flexor muscles. Blood studies revealed elevated ESR, increased serum IgG, mildly increased myogenic enzymes, and positive results for anti-SS-A and -SS-B antibodies. MRI scans disclosed extensive muscle atrophy as well as fatty degeneration in the thigh. A biopsy of the quadriceps femoris muscle provided a diagnosis of myositis based on the finding of muscle fibers of unequal size, nuclear centralization, and inflammatory cell infiltration into muscle fibers. CD4-positive lymphocytes were the predominant inflammatory cells. We diagnosed the case as myositis in primary Sjögren's syndrome based on the clinical course and laboratory findings. She recovered well with steroid medication. It is noteworthy that myositis associated with primary Sjögren's syndrome presents with mild symptoms and unremarkable laboratory data but may run a chronic progressive course.