Sub-acute Toxicosis Caused by a Multiple Doses Tegafur/Uracil (UFT) for Suicide : A Case Report

Tegafur/uracil (UFT) is an oral anticancer drug composed of tegafur which is a derivative of fluorouracil (5-FU) and uracil in a molar ratio of 1:4. UFT is effective as adjuvant chemotherapy for breast cancer2, colorectal cancer3, non-small cell lung carcinoma4, head and neck cancer5 and other tumors. We report a 41-year-old man who orally ingested a large dose of UFT (tegafur: 40000 mg/ uracil 9960mg)in an effort to commit suicide, and suffered from sub-acute toxicosis(main symptoms were bone-marrow suppression, and hair loss) of UFT. His life was saved by empiric antibiotic chemical treatment (meropenem, isapamicin, and micafungin), and granulocyte colony-stimulating factor (G -CSF). In the case of toxicosis of UFT, strong antibacterial empiric chemotherapy and G-CSF are necessary for rescue. If G-CSF is not work, biopsy of bone marrow woud be necessary, and the case of no stem cells, bone marrow transfusion should be thought

Monocyte-derived dendritic cells perform hemophagocytosis to fine-tune excessive immune responses

SummaryBecause immune responses simultaneously defend and injure the host, the immune system must be finely regulated to ensure the host’s survival. Here, we have shown that when injected with high Toll-like receptor ligand doses or infected with lymphocytic choriomeningitis virus (LCMV) clone 13, which has a high viral turnover, inflammatory monocyte-derived dendritic cells (Mo-DCs) engulfed apoptotic erythroid cells. In this process, called hemophagocytosis, phosphatidylserine (PS) served as an “eat-me” signal. Type I interferons were necessary for both PS exposure on erythroid cells and the expression of PS receptors in the Mo-DCs. Importantly, hemophagocytosis was required for interleukin-10 (IL-10) production from Mo-DCs. Blocking hemophagocytosis or Mo-DC-derived IL-10 significantly increased cytotoxic T cell lymphocyte activity, tissue damage, and mortality in virus-infected hosts, suggesting that hemophagocytosis moderates immune responses to ensure the host’s survival in vivo. This sheds light on the physiological relevance of hemophagocytosis in severe inflammatory and infectious diseases