OBJECTIVE:To systematically review the effect of CYP2C19 genetic polymorphism on lansoprazole pharmacoki-netics,and provide evidence-based reference for clinical individualized medication of lansoprazole. METHODS:Retrieved from PubMed,EMBase,Web of science,Cochrane Library and CJFD,retrospective studies about the effect of CYP2C19 genetic poly-morphism on lansoprazole pharmacokinetics were collected,Meta-analysis was performed by Rev Man 5.2 software after data ex-tract and quality evaluation. RESULTS:Totally 11 retrospective studies were included,involving 200 patients. The gene type in-cluded homozygote express metabolizers (EM),heterozygous express metabolizers (HEM) and slow metabolizers (PM). Results of Meta-analysis showed CYP2C19 polymorphism significantly affected cmax,AUC,t1/2,tmax and CL/F. The cmax and AUC in group PM were higher than group HEM and group EM;CL/F in group EM was higher than group HEM and group PM;t1/2 in group PM was higher than group HEM and group EM,while there was no significant difference in the t1/2 between group HEM and group EM;tmax in HEM and group PM were higher than group EM,while there was no significant difference in the tmax between group PM and group HEM. CONCLUSIONS:CYP2C19 genetic polymorphism shows obvious effect on lansoprazole pharmacokinetics, which is the key factor for causing efficacy of lansoprazole and individual differences among adverse reactions,and clinic should take into account individualized dose regimen of lansoprazole.

Mycoplasma pneumoniae pneumonia is an important component of community-acquired pneumonia, which can cause severe extrapulmonary complications of digestive, cardiovascular, blood, urinary and other systems.Accurate and effective biomarkers are significant for the diagnosis and treatment of Mycoplasma pneumoniae pneumonia.Recent studies have shown that new biomarkers such as IL-35, IL-17, neutrophil to lymphocyte ratio(NLR) and S100 protein are involved in the development of Mycoplasma pneumoniae pneumonia.In order to provide reference for the clinical diagnosis and treatment of Mycoplasma pneumoniae pneumonia, this paper reviews the progress of new biomarkers in Mycoplasma pneumoniae pneumonia.

OBJECTIVE： To provide reference for reasonable selection of tyrosine kinase inhibitors （TKI） in chronic myeloid leukemia （CML） patients with BCR-ABL35INS mutation. METHODS： Using “BCR-ABL insertional mutation” “ABL1 35ins mutation” “BCR-ABL c.1423_1424ins35” “ABL1 p.C475Tyrfs*11” as keywords， retrieved from CNKI， Wanfang database， Medline and COSMIC database， BCR-ABL35INS mutation CML patients were summarized and analyzed in respects of general information and treatment （treatment plan， patient compliance and drug withdrawal）， therapeutic effect （molecular biological mitigation and disease progress） and safety data （ADR） during 2007-2018. RESULTS： Totally 9 related literatures were included， involving 70 patients with BCR-ABL35INS mutation， all of them were foreign cases. Among them， 39 cases were male and 31 cases were female， with a median age of 49.2 years. The median time from the diagnosis of CML to the detection of BCR-ABL35INS mutation was 19 months. After detecting gene mutation， 39 cases were treated with imatinib （initial dose of 400 mg， po， once a day）， and molecular biological remission was achieved in 5 patients （12.9％）； 15 cases （38.5％） had molecular biological response but had disease progression； 8 patients （20.5％） had no response. Seventeen patients were treated with dasatinib （100 mg， po， once a day or 2 divided dose）， and 8 cases （47.1％） achieved molecular biological response. Twenty-one patients were treated with nilotinib （400 mg， po， 2 divided dose）， and 3 patients （14.3％） achieved molecular biological response； 2 patients achieved molecular biological response， but the disease progressed. Seven， three and seven of these patients stopped taking drugs due to adverse reactions， accounting for 17.9％， 17.6％ and 33.3％ respectively. All the ADRs were classified as grade 3-4 of the National Cancer Institute’s Common Terminology Criteria for Adverse Events， and most of them were hematological toxicity. CONCLUSIONS： CML patients with BCR-ABL35INS mutation are less likely to achieve molecular response on imatinib therapy but are more sensitive to dashatinib. In the course of treatment， we should strengthen the monitoring of blood system and other related indicators to ensure the safety and effectiveness of drug use.