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5 results on '"CHENG Shuquan"'

1. Research advances in chronic hepatitis B complicated by pulmonary tuberculosis

Author

LIU Pingxiang and CHENG Shuquan

Subjects
lcsh:Diseases of the digestive system. Gastroenterology, lcsh:RC799-869
Abstract

In recent years, increasing attention has been paid to co-infection with hepatitis B virus and mycobacterium tuberculosis, which is characterized by a high incidence, as well as the changes in the progression, prognosis, and treatment outcome of original diseases, toxic or side effects, and even the drug resistance of pathogens. This article reviews the incidence, pathogenesis, and therapeutic progress in patients with chronic hepatitis B complicated by pulmonary tuberculosis, so as to provide new ideas for further research.

Published
2016

4. Analysis of hepatic CD4+, CD8+, CD20+, and CD57 + T lymphocytes in chronic hepatitis B patients with different HBeAg status.

Author

XIAN Yongchao, CHENG Shuquan, and NI Hui

Subjects
*CD4 antigen, *T cells, *CHRONIC hepatitis B, *LIVER biopsy, *IMMUNOHISTOCHEMISTRY, *STATISTICAL correlation, *HEPATITIS associated antigen, *PATIENTS
Abstract

Objective To investigate the relationship of hepatic immune cells (CD4+, CD8+, CD20+, and CD57+ T lymphocytes) with liver pathology and clinical relevance in chronic hepatitis B (CHB) patients with different HBeAg status. Methods A total of 70 CHB patients admitted to our hospital from January 2008 to December 2013 underwent liver biopsy, among whom 38 were HBeAg positive and 32 were HBeAg negative. Immunohistochemistry was used to examine the expression of CD4+, CD8+, CD20+, and CD57+ T lymphocytes in hepatic tissues, and the correlation between their expression and clinical relevance was analyzed in patients with different HBeAg status. Ranked data were analyzed by Kruskal - Walls H test. Comparison between groups was made by Nemenyi test. Correlation analysis was made by linear regression method. Results When inflammation reached to the level of G3 - G4 in patients with either positive or negative HBeAg, the expression of hepatic CD8+ and CD20+ cells in them was significantly higher than that in patients with inflammation level of G1 (all P < 0.05). When the levels of inflammation reached G4 in patients with positive HBeAg and G3 in those with negative HBeAg, the expression of hepatic CD4+ cells was significantly higher than that in patients with G1 inflammation (all P < 0.05). In patients with negative HBeAg, the CD4+, CD8+, CD20+, and CD57+ lymphocytes all showed a positive correlation with alanine aminotransferase (ALT) level (r = 0.353, 0.628, 0.693, and 0.540, respectively; all P < 0.05). In addition, CD20+ lymphocytes also showed a positive correlation with hepatitis B virus (HBV) DNA (r = 0.378, P < 0.05). However, in patients with positive HBeAg, only CD8+ and CD20+ lymphocytes showed a positive correlation with ALT level, and no correlation was found between all lymphocyte populations and HBV DNA. Conclusion The expression of CD4+, CD8+, and CD20+ lymphocytes was significantly correlated with the grade of inflammation in hepatic tissues in patients with different HBeAg status, whereas the correlations between hepatic immune cells and levels of ALT and HBV DNA vary. [ABSTRACT FROM AUTHOR]

Published
2015
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5. Increased Occurrence of Mutant rtI233V of HBV in Patients Receiving Adefovir Therapy

Author

Liu, Yan, Xin, Shaojie, Ye, Xiaoling, Chen, Rongjuan, Xu, Zhihui, Li, Xiaodong, Ye, Haiyan, Cheng, Shuquan, and Xu, Dongping

Abstract

Background The study aimed to clarify whether the rtI233V substitution affects adefovir (ADV) resistance.Methods A total of 18,419 patients from Beijing 302 Hospital were investigated. HBV complete reverse transcriptase region of the polymerase was screened by direct sequencing and verified by clonal sequencing if necessary. Replication-competent wild-type and mutant HBV genomic amplicons were transfected into HepG2 cells for phenotypic analysis of viral replication capacity and drug susceptibility.Results The rtI233V substitution was detected in 38/5,344 (0.71%) ADV-treated patients and in 8/13,075 patients without receiving ADV (P<0.001). Eight patients with rtI233V ± rtA181V/rtN236T had virological breakthrough in the clinical course of ADV treatment. Phenotypic analysis showed that rtI233V mutants from patient 1 and patient 2 exhibited 1.57-fold and 1.51-fold decreased susceptibility to ADV, respectively, compared to wild-type virus; by contrast, rtN236T and rtI233V+N236T mutants from patient 1 had 6.82-fold and 5.28-fold decreased susceptibility to ADV. rtI233V, rtN236T and rtI233V+N236T mutants had 97.5%, 30.2% and 69.7% of replication capacity compared to wild-type virus in the absence of antivirals and all remained susceptible to lamivudine, entecavir and tenofovir. Viral replication capacity correspondingly decreased after eliminating rtI233V from rtI233V+N236T mutant and was restored after introducing rtI233V into rtN236T mutant. In clinical practice, switching to entecavir rescue therapy suppressed HBV DNA to an undetectable level for both patients.Conclusions rtI233V usually emerged in ADV-treated patients with little impact on ADV susceptibility but it effectively restored replication capacity of the rtN236T mutant, suggesting that rtI233V may partly serve as a compensatory mutation associated with ADV resistance.

Published
2016
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