A rare case of bladder cancer producing granulocyte colony-stimulating factor (G-CSF) is reported. A 63-year-old man with a progressive, grade 3 transitional cell bladder carcinoma, showed marked leukocytosis (maximum 181,800/mm3) and an elevated serum G-CSF to 131.7 pg/mL. After radical cystectomy and neoadjuvant chemotherapy, the tumor recurred locally. Immunohistochemical examination with monoclonal antibody specific for G-CSF revealed positive staining in the local recurrent tumor. To our knowledge, there have been only seven cases reported of bladder cancer producing G-CSF.

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The time point of the most precise predictor of hepatocellular carcinoma (HCC) development after viral eradication with direct-acting antiviral (DAA) therapy is unclear. In this study we developed a scoring system that can accurately predict the occurrence of HCC using data from the optimal time point. A total of 1683 chronic hepatitis C patients without HCC who achieved sustained virological response (SVR) with DAA therapy were split into a training set (999 patients) and a validation set (684 patients). The most accurate predictive scoring system to estimate HCC incidence was developed using each of the factors at baseline, end of treatment, and SVR at 12 weeks (SVR12). Multivariate analysis identified diabetes, the fibrosis-4 (FIB-4) index, and the α-fetoprotein level as independent factors at SVR12 that contributed to HCC development. A prediction model was constructed with these factors that ranged from 0 to 6 points. No HCC was observed in the low-risk group. Five-year cumulative incidence rates of HCC were 1.9% in the intermediate-risk group and 15.3% in the high-risk group. The prediction model at SVR12 most accurately predicted HCC development compared with other time points. This simple scoring system combining factors at SVR12 can accurately evaluate HCC risk after DAA treatment.

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Keywords： amantadine, hypoalbuminemia, blood purification, acute kidney injury, malignant syndrome 〈Abstract〉 Amantadine is widely used to treat Parkinson's disease. However, it should not be used in patients with impaired renal function since it is almost exclusively metabolized through renal excretion. We experienced a rare case of amantadine intoxication in a patient with Parkinson's disease and nephrotic syndrome. A 71-year-old patient initially had normal renal function(eGFR： 62 mL/min/1.73 m 2)and received the optimal dose of amantadine(150 mg/day). The patient then developed new-onset nephrotic syndrome with severe hypoalbuminemia(1.6 g/dL) , which was complicated by an acute kidney injury. This resulted in amantadine intoxication. Treatment with both direct hemoperfusion(DHP)and hemodiafiltration(HDF)effectively reduced the patient's serum amantadine concentration； however, this caused neuroleptic malignant syndrome, which manifested as disturbed con