(Hepatology 2014;60:158–168)

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“Gastroesophageal variceal hemorrhage is an important complication of cirrhosis. We investigated the in-hospital mortality and its risk factors after variceal hemorrhage in a large sample population, using a nationwide Japanese database. Data on the patients with variceal hemorrhage were collected for a total of 39 months from a nationwide administrative database covering approximately 1000 hospitals in Japan. The risk factors for fatal outcome after variceal hemorrhage were analyzed with receiver–operator curves (ROC) and univariate and multivariate logistic regression. Comorbidities were assessed with the Charlson Comorbidity Index. selleck inhibitor We identified 9987 patients with variceal hemorrhage from a total of 20.3 million inpatients in the database. The median age was 63 years and 68.8% were male. The overall in-hospital mortality was 16.8% (1676 cases). In univariate analysis, Child–Pugh class was the strongest predictor; the area under the ROC of Child–Pugh score for predicting in-hospital mortality was 0.802. In multivariate analysis, increased in-hospital mortality was significantly associated with male sex (vs female: odds ratio [OR] = 1.19, P = 0.01), older age, Child–Pugh class B or C (B vs A: OR = 2.80, P < 0.001; C vs A: OR = 20.1, P < 0.001) and higher Charlson Comorbidity Decitabine supplier Index (≥6 vs ≤5; OR = 1.29, P < 0.001). In spite

of recent advances in the treatment of variceal hemorrhage, the in-hospital mortality remained as high as 16%. Poor liver function was the most important predictor, suggesting that liver failure after variceal hemorrhage might have been the cause of death. “
“Although cancer patients exhibit a generalized immunosuppressive

status, substantial evidence indicates that the inflammatory reaction at a tumor site can promote tumor growth and progression. Hepatocellular carcinoma (HCC) is usually derived from inflamed cirrhotic liver with extensive leukocyte infiltration. We recently found that proinflammatory T helper (Th)17 cells are accumulated in HCC tissue, where they promote disease progression by fostering angiogenesis. Here we show that interleukin (IL)-17-producing cells were enriched predominantly in peritumoral stroma of HCC tissues, and their levels were well correlated with monocyte/macrophage density in the same area. Most peritumoral CD68+ cells C59 exhibited an activated phenotype. Accordingly, tumor-activated monocytes were significantly superior to the suppressive tumor macrophages in inducing expansion of Th17 cells from circulating memory T cells in vitro with phenotypic features similar to those isolated from HCCs. Moreover, we found that tumor-activated monocytes secreted a set of key proinflammatory cytokines that triggered proliferation of functional Th17 cells. Inhibition of monocytes/macrophages inflammation in liver markedly reduced the level of tumor-infiltrating Th17 cells and tumor growth in vivo.