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INTRODUCTION AND OBJECTIVE:Locally advanced or metastatic upper tract urothelial carcinoma (UTUC) is a lethal disease with limited treatment options for patients who do not positively respond to pl...

Asymptomatic prostatic inflammation may cause increased prostate specific antigen in some men, leading to unnecessary repeat prostate biopsy. We determined whether histological findings of inflammation in initial biopsy specimens and/or clinical indicators of inflammation could predict the outcome of subsequent biopsy in men with a negative initial biopsy.A total of 105 Japanese men with increased prostate specific antigen underwent repeat prostate biopsy after initial biopsy revealed no evidence of carcinoma. Of the cases 45 (42.8%) were positive for prostate cancer at repeat biopsy. We evaluated initial biopsy specimens for evidence of inflammation by mononuclear and polymorphonuclear leukocytes, serum and urinary white blood count, and C-reactive protein.Polymorphonuclear leukocyte infiltrates, urinary white blood count, patient age, prostate specific antigen at repeat biopsy, prostate volume, prostate specific antigen velocity and prostate specific antigen density were associated with the repeat biopsy outcome (p0.05). Multivariate analysis revealed that age, prostate specific antigen density and urinary white blood count were independent predictors of outcome. On subgroup analysis of 63 men with serum prostate specific antigen less than 10 ng/ml before initial biopsy polymorphonuclear and mononuclear leukocyte inflammation, age, prostate specific antigen at repeat biopsy, prostate volume, prostate specific antigen velocity and prostate specific antigen density were associated with the outcome of repeat biopsy (p0.05). Multivariate analysis showed that polymorphonuclear leukocyte infiltrate, prostate specific antigen density and age were independent predictors.Age, prostate specific antigen density, polymorphonuclear leukocyte inflammation in initial biopsy specimens and urinary pyuria are indicators of benign repeat biopsy. They help avoid unnecessary repeat biopsy in men with increased prostate specific antigen.

A girl, aged 19 months, presented with a sacrococcygeal tumor that developed at 5 months after birth and gradually enlarged. Serum tumor marker levels were negative. Ultrasound imaging showed abundant blood flow in the tumor. However, neither computed tomography (CT) nor magnetic resonance imaging (MRI) showed contrast agent incorporation. The surgically resected tumor consisted of immature cells with myxoid stroma and proliferating small blood vessels. Immunostaining showed extensive vimentin expression. However, smooth muscle actin, muscle-specific actin, and S-100 protein expression was negative. Neither the ETV6-NTRK3 fusion gene nor the FUS gene rearrangement was detected. Thus, the patient was diagnosed with a primitive myxoid mesenchymal tumor of infancy. This tumor primarily consisted of a mucosal stroma with a low absorption on CT, a low signal on T1-weighted MRI, and a high signal on T2-weighted MRI. A diagnosis of primitive myxoid mesenchymal tumor of infancy should be considered in cases of soft tissue tumors in infants that show prominent vascularity but little contrast enhancement on MRI or CT.

Abstract —The biological actions of tumor necrosis factor-α (TNF-α) are mediated by 2 distinct receptors, TNF-RI (p55) and TNF-RII (p75). The extracellular domains of both receptors are shed in soluble form (sTNF-RI and sTNF-RII). The soluble receptors are involved in regulating TNF-α activities and may have therapeutic potential as TNF-neutralizing agents. However, it remains unclear as to what kind of physiological molecule can regulate TNF receptors. Nitric oxide (NO) mediates a variety of biological and pathophysiological functions. We hypothesized that NO may modulate the expression and shedding of TNF-RI. An NO donor, diethylamine/NO complex (NOC 5), increased sTNF-RI in the supernatants of ECV304, a human umbilical vein cell line, in a dose-dependent manner. TNF-RI mRNA in these cells was upregulated by NOC 5. 8-Br-cGMP and peroxynitrate had no effect on sTNF-RI release. Genistein and herbimycin A, inhibitors of tyrosine kinase, inhibited sTNF-RI release. Herbimycin A inhibited the levels of TNF-RI mRNA enhanced by NOC 5, which downregulated the surface expression of TNF-RI, indicating that NO is also involved in the shedding process of TNF-RI. The shedding of TNF-RI was abolished by a synthetic inhibitor of matrix metalloproteinase, KB-R8301. In conclusion, NO enhanced the release of sTNF-RI from endothelial cells by a cGMP-independent mechanism. Dual pathways suggested for NO-induced sTNF-RI release include (1) enhanced expression of TNF-RI, at least partially, by a tyrosine kinase–dependent mechanism and (2) increased shedding of TNF-RI by a type of metalloproteinase.

Linezolid (LZD)-induced myelosuppression has been reported in adults; however, LZD-induced pure red cell precursor toxicity rarely occurs. A 2-year-old boy diagnosed with infective endocarditis by Streptococcus mitis received LZD after developing resistance to multiple antibiotics. Although his infective symptoms were improved by LZD, progressive anemia was noticed 2 weeks after LZD therapy. Four weeks after LZD administration, his hemoglobin level was 6.5 g/dL and reticulocytes less than 0.1%. Bone marrow examination revealed markedly decreased erythropoiesis with cytoplasmic vacuolation of erythroblasts. Anemia recovered 19 days after cessation of LZD. Elevated protoporphyrin and a high LZD level in the blood suggested that mitochondrial disturbance by high-dose and long-term treatment with LZD may have been responsible for LZD-induced pure red cell precursor toxicity.