We report a case of papillary adenocarcinoma of the sigmoid colon with psammoma bodies and intracytoplasmic hyaline globules. The patient was a 59-year-old woman. The tumor showed central ulceration with smooth elevated ridges. Histologically, the tumor was composed of numerous large irregular tubular structures accompanying infolded papillary growth. The tumor cells showed cytoplasmic basophilia and prominent nuclear atypia. Psammomatous-type calcification was scattered in the tumor stroma as well as in the glandular lumina. In addition, intracytoplasmic hyaline globules of various sizes were seen in the neoplastic cells. We propose the name papillary adenocarcinoma associated with psammoma bodies and hyaline globules for this tumor. Accumulation of further cases is needed to clarify the clinical significance of this type of tumor.

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A 78-year-old male with lumbar pain and dim consciousness presented the clinical pictures of plasma cell leukemia (PCL) producing a large amount of monoclonal immunoglobulin E (IgE)/kappa protein. Laboratory investigation demonstrated an elevated serum calcium level and renal dysfunction. Systemic bone X-ray survey disclosed only a solitary osteolytic lesion. Circulating plasma cells demonstrated CD19(-)/CD56(-) and MPC-1(-)/CD49e(-)/CD45(+/-), the latter indicating the immature phenotype of the tumor cells. Bone marrow was occupied with immature, atypical plasma cells, of which cytoplasms were positive for IgE by direct immunofluorescence analysis. Chromosomes revealed a translocation of (11;14)(q13;q32), which is concordant with cyclinD1-protein overexpression by immunohistochemistry. He was treated with dexamethasone and vincristine, which somewhat improved the laboratory findings. He died of tumor progression after 4-month admission. The clinical and biological characteristics of IgE-producing PCL, a very rare type of plasma cell dyscrasia, are discussed, reviewing the past literature.

Background Increasing the blood flow rate (BFR) is a useful method for increasing Kt/V and the clearance for low molecular solutes. Hemodialysis patients are often anemic due to hypoerythropoiesis and their chronic inflammatory state. Hepcidin, a hormone that regulates iron homeostasis, is considered as an indicator of iron deficiency in patients with end-stage renal disease. This study aimed to investigate the effects of an increased BFR during hemodialysis on serum hepcidin levels and anemia. Methods Between April 2014 and March 2016, 22 chronic dialysis patients (11 men [50.0 %]; mean [± standard deviation] age, 72 ± 12 years) undergoing maintenance hemodialysis treatment, thrice weekly, were enrolled and followed prospectively for 24 months. In April 2014, the BFR was 200 mL/min; in April 2015 this was increased to 400 mL/min, which was within acceptable limits. The dialysate flow rate remained stable at; 500mlL/min. Blood samples were collected in March 2015 and 2016. The primary endpoint was the comparison of the amounts of erythropoiesis-stimulating agent (ESA) required. Results The increased BFR increased the Kt/V and contributed to significantly decreased urea nitrogen (UN) (p = 0.015) and creatinine (Cr) (p = 0.005) levels. The dialysis efficiency was improved by increasing the BFR. Ferritin (p = 0.038), hepcidin (p = 0.041) and high-sensitivity interleukin-6 (p = 0.038) levels were also significantly reduced. The ESA administered was significantly reduced (p = 0.004) and the Erythropoietin Resistant Index (ERI) significantly improved (p = 0.031). The reduction rates in UN (p < 0.001), Cr (p < 0.001), and beta-2 microglobulin (p = 0.017) levels were significantly greater post the BFR increase compared to those prior to the BFR increase. However, hepcidin was not affected by the BFR change. Conclusions Increasing BFR was associated with hemodialysis efficiency, and led to reduce inflammatory cytokine interleukin-6, but did not contribute to reduce C-reactive protein. This reduced hepcidin levels, ESA dosage and ERI. Hepcidin levels were significantly correlated with ferritin levels, and it remains to be seen whether reducing hepcidin leads to improve ESA and iron availability during anemia management.