ABSTRACT
Helicobacter pylori (HP) infection is one of the most prevalent chronic bacterial infections in the world, which is closely related to the development of gastrointestinal diseases, such as chronic gastritis, gastroduodenal ulcer and gastric cancer. Empirical treatment of HP infection may lead to antibiotic resistance, adverse reactions and poor compliance. The decreased HP eradication rate is related to antibiotic resistance, HP converting to coccoid form and admission of proton pump inhibitors (PPI). The implementation of precise therapy can effectively enhance the HP eradication rate, through antibiotics selecting based on detection of drug sensitivity phenotype and drug resistance genes, reducing adverse drug reactions, increasing patient compliance, and rationally administrating PPI, etc. This article reviews the research progress of precision therapy for HP infection to provide reference for clinicians.
ABSTRACT
The neurotrophin receptor kinase (NTRK) gene encodes neurotrophic factor receptor tyrosine kinase (NTRK), which plays an important role in the development and function of the nervous system. NTRK gene fusion mutation results in the production of chimeric NTRK proteins, which have carcinogenic potential through constitutive activation or overexpression. NTRK gene fusion mutation can lead to a special type of wild type gastrointestinal stromal tumor (GIST), whose clinical manifestations and treatment are completely different from other types of GIST. This fusion mutation can be detected clinically by a variety of methods, including tumor DNA and RNA sequencing and immunohistochemical staining. In patients with NTRK fusion positive tumors, NTRK inhibitors such as larotrectinib and entrectinib have shown good antitumor efficacy, with clinical response rates as high as 75%. Therefore, there is a need to improve the recognition and detection of fuch patients and to improve their prognosis by individualized and precise treatment with TRK inhibitors.
Subject(s)
Humans , Gastrointestinal Stromal Tumors/genetics , Gene Fusion , Neoplasms , Nerve Growth Factors , Protein Kinase Inhibitors , Receptor, trkA/genetics , Receptors, Nerve Growth Factor/geneticsABSTRACT
Objective To investigate the efficacy and safety of CT portograph combined with endoscopic ultrasonography for the pricision treatment of esophagogastric varices in patients with cirrhosis. Methods A total of 130 inpatients with cirrhosis complicated with esophagogastric variceal bleeding who received endoscopic treatment from January 2013 to January 2015 were selected. Using prospective randomized controlled design, the patients were divided into two groups, the experimental group and the control group, with 65 cases in each group. The number and degree of esophagogastric varices were assessed by CT portography in the experimental group. Then endoscopic ultrasonography was used to assess the paraesophageal vein and perforator vein before endoscopic treatment. The range and degree of esophagogastric varices were observed and the lesions were treated by endoscopy in the control group. Results A total of 62 patients completed the study in the experimental group, and 63 in the control group. The number of treatment was significantly lower in the experimental group than that in the control group(3. 00±0. 76 VS 5. 63±0. 92, P=0. 000) . The disappearance time of varices was significantly shorter in the experimental group than that in the control group(7. 25±1. 16 months VS 8. 88±1. 64 months, P=0. 039). The variceal recurrence rate of the experimental group was significantly lower than that of the control group [ 1. 6％ ( 1/62 ) VS 12. 7％( 8/63) , P=0. 040] . The incidence of pleural effusion was significantly lower in the experimental group than that in the control group [ 0 ( 0/62 ) VS 9. 5％ ( 6/63 ) , P= 0. 040 ] . The total complication rate was significantly lower in the experimental group than that in the control group [ 27. 4％ ( 17/62 ) VS 58. 7％(37/63), P=0. 003]. Conclusion CT portography combined with endoscopic ultrasonography is safe and effective for esophageal gastric varices in patients with cirrhosis.
ABSTRACT
Precise medicine is an emerging clinical therapeutic concept based on genomic and genetic information of patients. Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) is an important component of precise therapy for lung cancer patients. EGFR mutations occur mainly in exon 18 to 21, in which exon 19 deletion and exon 21 L858R point mutation that are known as sensitive mutations account for nearly 45% and 40%, respectively. Except for the above two mutations and T790M point mutation, the rest are rare mutations, including Ins19, Ins20, E709, G719, S768, L861 and some compound mutations. Some previous retrospective studies of small sample size and case reports showed that most of EGFR exon19 (Ins), exon 21 (L861), exon 18 (G719X) and exon20 (S768I) mutations were sensitive to TKIs. And although the exon 20 insertion mutation is usually predicted to the first and second generations of EGFR-TKIs resistance, some specific types are sensitive to the third generation of EGFR-TKIs. Currently, targeted drugs for Ins20 -Ap32788 mutation has entered into clinical trials. Patients with complex mutations have similar efficacy on EGFR-TKIs in comparison with those with single sensitivity mutations. In conclusion, when patients with rare sensitive mutations received EGFR-TKIs therapy, the efficacy and progression-free survival time is similar to or slightly lower than those with classical sensitive mutations, whereas it is higher than those with wild-type EGFR. Compared with the first generation of EGFR-TKIs, second generation EGFR-TKIs may be more suitable for the treatment of lung cancer patients harboring rare sensitive EGFR mutations.