OBJECTIVE:To investigate the role of clinical pharmacists on drug therapy for a chemotherapy patient with drug-induced liver injury (DILI).METHODS:Clinical pharmacists participated in the therapy for a patient with colorectal cancer and suggested that ondansetron+metoclopramide+promethazine were given before chemotherapy for stopping vomiting because chemotherapy drugs might lead to gastrointestinal reaction.The patient suffered from DILI before second chemotherapy.According to the history of drug use and the characteristics of drug effects,clinical pharmacists estimated that DILI may be related to Chinese patent medicine (Guben yichang tablets) and TCM formula granules taken during the two chemotherapy periods.Clinical pharmacists recommended Polyene phosphatidylcholine injection 465 mg,ivgtt,qd+Reduced glutathione for injection 1 g,ivgtt,qd for protecting liver tissue,and additionally recommended Compound glycyrrhizin injection 60 mL,ivgtt,qd for inhibiting inflammation and regulating immune function.After liver function of the patient had been recovered,it was suggested to stop polyene phosphatidylcholine,reduced glutathione and compound glycyrrhizin,etc.Pharmaceutical care was also provided,including efficacy evaluation,ADR monitoring,medication education,telephone follow-up,etc.RESULTS:The physicians adopted the suggestions of clinical pharmacists.The liver function indexes of the patient recovered to normal,and then completed chemotherapy smoothly for 3 times.CONCLUSIONS:When tumor patients suffer from DILI during chemotherapy,clinical pharmacists should help physicians fmd and judge the drug factors leading to DILI based on the history of drug use and the characteristics of drug effects,and assist physicians to formulate and adjust medication plan so as to relieve the degree of DILI and guarantee the smooth development of chemotherapy.

Long-chain acyl-coenzyme A (CoA) synthase 4 (ACSL4) is an enzyme that esterifies CoA into specific polyunsaturated fatty acids, such as arachidonic acid and adrenic acid. Based on accumulated evidence, the ACSL4-catalyzed biosynthesis of arachidonoyl-CoA contributes to the execution of ferroptosis by triggering phospholipid peroxidation. Ferroptosis is a type of programmed cell death caused by iron-dependent peroxidation of lipids; ACSL4 and glutathione peroxidase 4 positively and negatively regulate ferroptosis, respectively. In addition, ACSL4 is an essential regulator of fatty acid (FA) metabolism. ACSL4 remodels the phospholipid composition of cell membranes, regulates steroidogenesis, and balances eicosanoid biosynthesis. In addition, ACSL4-mediated metabolic reprogramming and antitumor immunity have attracted much attention in cancer biology. Because it facilitates the cross-talk between ferroptosis and FA metabolism, ACSL4 is also a research hotspot in metabolic diseases and ischemia/reperfusion injuries. In this review, we focus on the structure, biological function, and unique role of ASCL4 in various human diseases. Finally, we propose that ACSL4 might be a potential therapeutic target.
Humans ; Ferroptosis ; Apoptosis ; Phospholipids/metabolism* ; Nitric Oxide Synthase