Analysis of a case of pancytopenia complicated with delayed drug fever induced by vancomycin infusion in a child / 中国药房

OBJECTIVE To accurately identify the rare adverse drug reactions （ADR） of vancomycin-pancytopenia in order to promote its safe use. METHODS Through a case report of a child with suppurative hip arthritis who developed pancytopenia combined with delayed drug fever caused by intravenous infusion of vancomycin，Naranjo score method and related literature were used to summarize the association between the ADR and vancomycin and its possible mechanism， and suggestions for rational use of vancomycin in pediatric patients were put forward. RESULTS & CONCLUSIONS The association of pancytopenia combined with delayed drug fever and vancomycin in this child is “very likely”. In clinical practice， it is difficult to distinguish between pancytopenia combined with delayed drug fever from fever and hematopenia caused by aggravation of infection. Medical staff should increase their awareness of vancomycin rare ADR such as pancytopenia， and pharmacists should assist medical staff in timely screening for ADR. The initial dose of vancomycin infusion for children should start from 60 mg/（kg·d），and the blood concentration should be monitored 48 h after the first infusion and the dose should be adjusted in time to maintain the valley concentration of vancomycin at 5-15 mg/L to prevent the occurrence of ADR caused by excessive blood concentration. For children who have been using vancomycin for more than one week，the blood routine should be rechecked regularly. Once pancytopenia occurs，the drug should be stopped immediately，and symptomatic treatment should be given according to the situation.

Study on the Protective Effects of Schisandrin A on Hepatic Fibrosis Induced by Carbon Tetrachloride in Mice and Its Mechanism / 中国药房

OBJECTIVE：To study the pr otective effect of schisandrin A （SA）on CCl 4-induced liver fibrosis model mice and its mechanism. METHODS ：Mice were randomly divided into blank control group ，model group ，silymarin group （positive control，100 mg/kg），SA low-dose and high-dose groups （20，40 mg/kg），with 10 mice in each group. Except for blank control group，other groups were given CCl 4 subcutaneously to induce liver fibrosis model. After successful modeling ，administration groups were given relevant medicine intragastrically ，once a day ，for consecutive 6 weeks；blank control group and model group were given constant volume of 0.5％sodium carboxymethyl cellulose solution intragastrically by the same way. HE staining was used to observe the pathological changes of liver tissue in mice. UV spectrophotometry and ELISA assay were adopted to detect the serum levels of liver injury indexes （ALT and AST ）and the contents of inflammatory factors （TNF-α，IL-1β，IL-6）. Western blotting assay was used to detect the expression of NOD like receptor protein 3（NLRP3）/NF-κB and TGF-β/Smad signaling pathway protein. RESULTS ：Compared with blank control group ，obvious pathological changes of liver fibrosis were observed in model group. The serum levels of liver injury indexes and contents of inflammatory factors were significantly increased （P＜0.01）. The expression of NLRP 3，apoptosis associated spot-like protein ，Caspase-1 and IL- 1β，TGF-β1 and ratios ofp-NF-κB p65/NF-κB p65，p-IκBα/IκBα，p-Samd3/Smad3 were increased significantly （P＜0.01）. Compared with model group ，SA could significantly relieve hepatic fibrosis in mice ，reduce serum levels of liver injury indexes and contents of inflammatory factors ，as well as the expression of NLRP 3/NF-κB and TGF-β/Smad signaling pathway protein and phosphorylation level（P＜0.01）. CONCLUSIONS ： SA can effectively relieve liver injury and inflammation of CCl 4-induced hepatic fibrosis model mice ，which may be through the regulation of NLRP 3/NF-κB and TGF-β/Smad3 signaling pathways ，thus inhibiting the process of liver fibrosis.