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ABSTRACT: To investigate the efficacy of 104 weeks of lamivudine (LAM) and adefovir (ADV) de novo combination therapy, as compared to optimized combination therapy administered after 48 weeks of treatment with lamivudine or adefovir mono-therapy, in chronic hepatitis B (CHB) patients. A total of 174 patients with CHB were equally divided among three treatment groups: LAM mono-therapy; ADV mono-therapy; and LAM + ADV combination therapy. The patients in the LAM + ADV group were treated with LAM plus ADV for 104 consecutive weeks. The patients in the LAM or the ADV groups were first treated for 48 weeks with LAM or ADV, respectively, after which the patient's virological response was assessed. Accoring to the results, the patient was continued on mono-therapy or switched to combination therapy for the subsequent 56 weeks. Virological and biochemical examinations were carried out at weeks 48 and 104. The rates of undetectable HBV DNA in the LAM mono-therapy, ADV mono-therapy, and LAM-ADV combination therapy groups at week 48 were 68%, 50%, and 84%, and at week 104 were 80%, 72%, and 95%, respectively. For the same groups, the virus breakthrough rates at week 48 were 15%, 0%, and 0%, and at week 104 were 18%, 2%, and 0%, respectively. Statistical analysis showed significant differences for the rate of undetectable HBV DNA between LAM + ADV group and LAM group at week 48 (x2 = 4.473, P= 0.034) and at week 104 (x2 = 5.795, P = 0.016), LAM + ADV group and ADM group at week 48 (x2 = 14.802, P less than 0.001) and week 104 (x2 = 5.547, P = 0.001). The hepatitis B e antigen (HBeAg) seroconversion rates at week 48 were 15% (x2 = 4.543, P = 0.033), 13% (x2 = 4.035, P = 0.045) and 38%, and at week 104 were 21% (x2 = 4.438, P = 0.035), 17% (x2 = 4.223, P = 0.04) and 44%, respectively, among patients positive for HBeAg. Statistical analysis showed that the differences among the three groups for each of these parameters were statistically significant (all, P less than 0.05). When compared with LAM or ADV mono-therapy followed by LAM+ADV at week 48, the LAM plus ADV de novo combination therapy for 104 weeks provided CHB patients with better virological and serological responses and a lower drug resistance rate.
Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 02/2012; 20(2):98-102.
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ABSTRACT: To investigate the efficacy of Telbivudine and Entecavir for therapy of HBeAg positive chronic hepatitis B for 52 weeks.
In this random and control study, the efficacy of Telbivudine and Entecavir treatments were compared in 180 patients with HBeAg positive chronic hepatitis B.The patients were randomly assigned to a daily 600 mg Telbivudine treatment group or daily 0.5 mg Entecavir group for 52 weeks.
At week 52, HBV DNA undetectable rate was better in the Entecavir-treated group than in the Telbivudine-treated group, but didn't reach statistical significance. The viral breakthrough rates were significantly lower in the Entecavir-treated group than in the Telbivudine-treated group (x2 = 4.09, P <0.05). The clearance and seroconversion of HBeAg and the mean reductions of HBeAg from baseline at week 52 were significantly greater in the telbivudine-treated group than in the entecavir-treated group (x(2) clearance = 4.63, x(2) seroconversion = 4.80, (t-mean) reductions = 2.02; P < 0.05). The HBeAg seroconversion rates were not associated with both baseline ALT and baseline HBV DNA in both groups (P more than 0.05). In Telbivudine-treated group, the HBeAg decline is more than 2 log at week 24, HBeAg decline is more than 1 log at week 12 and the HBeAg baseline were independent factors correlated to HBeAg seroconversion rates at week 52 by Binary Logistic analysis, and also in entecavir-treated group the HBeAg decline is more than 2 log at week 24, HBeAg decline is more than 2 log at week 36 and the HBeAg decline is more than 2 log at week 12 were independent factors correlated to HBeAg seroconversion rates at week 52.
Significant difference of HBeAg seroconversion rates at week 52 existed between Telbivudine-treated group and Entecavir-treated group. Entecavir is significantly superior to Telbivudine with less resistance to nucleosides. HBeAg decline is more than 2 log at week 24 is the best predicting factor for HBeAg seroconversion at week 52.
Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 03/2011; 19(3):178-81.
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ABSTRACT: To establish standard serum proteomic pattern for early liver cancer and explore its value in early liver cancer diagnosis.
The serum samples were obtained from 12 healthy subjects and 12 patients with early liver cancer. After removal of serum albumin and IgG, 300 µg serum sample was mixed with the hydrating solution for two-dimensional gel electrophoresis. Each experiment was repeated for 3 times. With silver staining and image analysis, the differentially expressed proteins were identified to establish the standard proteomic pattern for early liver cancer. The proteomics pattern was then tested in the diagnosis of 13 cases of chronic liver disease and 10 healthy individuals in a double-blind manner.
Thirty-eight differentially expressed protein spots were identified. Eleven protein spots with differential expressions by over 5 folds were analyzed to establish the standard proteomics pattern for early liver cancer, which showed a sensitivity of 92% and specificity of 90% in early diagnosis of liver cancer.
The standard serum 2-DE proteomic pattern for early liver cancer shows distinct differences from that of healthy subjects. The differentially expressed proteins and their specific combination pattern may have the potential for diagnosis and prognostic evaluation of early liver cancer.
Nan fang yi ke da xue xue bao = Journal of Southern Medical University 02/2011; 31(2):341-3.
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ABSTRACT: To study individualized treatment of chronic hepatitis C (CHC) genotype 1 patients using respond guided therapy (RGT) of peginterferon α-2a in combination with ribavirin.
140 patients with CHC genotype 1 received peginterferon α-2a 180 microg injection once a week in combination with ribavirin 800-1200 mg/d. Patients achieved RVR after 4 weeks treatment (group A) were randomized into 2 subgroups and proceeded with 24 and 48 weeks treatments (subgroups A1 and A2) respectively. Patients who had not received RVR but achieved cEVR at week 12 (group B) were further divided into 2 subgroups randomly and treated for 48 and 72 weeks (subgroups B1 and B2), respectively. Patients with PVR at week 24 were treated for 72 weeks (group C1), while patients without PVR at week 24 discontinued treatment (group C2). All Patients were followed-up for 24 weeks after the end of treatment.
For patients treated for 24 weeks, the ETR rate was 100%, the SVR rate was 65.9%, and the relapse rate was 34.1%. For those treated for 48 weeks, the ETR, SVR and relapse rate were 95.3% , 82.8% and 12.5% respectively. For those treated for 72 weeks, the above rates were 82.1%, 67.9% and 14.3% respectively. SVR rates of subgroup A1 and A2 were 65.9% and 84.4% respectively and the difference was statistically significant (P<0.00). The HCV RNA loads were less than 1x10(6) copy/ml in group A and the SVR were 72.7% and 100% respectively with 24 and 48 weeks treatment, and the difference was insignificant statistically (P>0.05). SVR in subgroup B1 and B2 were 78.9% and 73.7% respectively and the difference was statistically insignificant (P>0.05). The SVR in group C1 was raised to 55. 6%.
RVR and cEVR were respond guided prediction factors for CHC treatment. SVR among patients with RVR was higher in 48-week treatment than those with 24 weeks treatment. For patients with baseline virus load less than 1x10(6) copy/ml and achieved RVR, treatment duration can be shortened to 24 weeks. Treatment extension to 72 weeks can not result in SVR increase among patients without RVR but with cEVR. However, treatment extension to 72 weeks can increase SVR among those patients with PVR.
Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology 08/2010; 18(8):585-9.
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ABSTRACT: To survey the status of Helicobacter pylori (Hp) infection in the liver of patients with liver cancer and explore the correlation between Hp infection and liver cancer.
Liver specimens were obtained 30 patients with chronic liver disease (CLD), 30 with liver cancer, and 30 healthy control subjects. The specimens were cultured in Colombian agar medium in microaerophilic condition for isolation of Hp. The presence of Hp was also identified by biochemical test, urease test, immunohistochemistry, and PCR and sequence analysis.
Hp was found in none of the liver specimens by culture tests. One out of the 30 patients with liver cancer (3%) was positive for Hp by urease tests. Immunohistochemical staining identified Hp positivity in 9 liver cancer tissue (30.0%), but in none of control or CLD cases (P<0.05). PCR detected Hp 16S rRNA in 18 out of the 30 patients with liver cirrhosis (60.0%) and in none of the control or chronic hepatitis cases. Sequencing analysis of Hp 16S rRNA in liver tissue showed a 98.8% homology with the Hp16S rRNA gene.
A greater incidence of Hp infection in the liver is identified in patients with liver cancer than in healthy subjects and CLD patients, suggesting a potential correlation between Hp infection to liver cancer.
Nan fang yi ke da xue xue bao = Journal of Southern Medical University 05/2010; 30(5):1028-30.
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ABSTRACT: To investigate the infection of Helicobacter pylori (Hp) in the liver tissue of patients with chronic liver disease and the association between Hp and chronic liver disease.
Liver tissue samples were obtained by liver biopsy and surgical resection from 30 healthy subjects, 30 patients with chronic hepatitis, 30 with cirrhosis and 30 with liver cancer. All the samples were confirmed by pathological examination. The gene fragment coding for 16SrRNA were amplified by PCR with sequence analysis.
The PCR product of the 16SrRNA gene was 109 bp in length. Hp 16SrRNA was detected in 18 out of 30 liver biopsy samples from patients with primary cancer (60.0%), in 14 samples from patients with liver cirrhosis (47.0%), and in none of the samples from normal subjects or patients with chronic hepatitis. Sequencing analysis of Hp 16SrRNA gene in the liver tissue showed a 98.8% homology with the gene fragment encoding Hp 16SrRNA.
Hp is identified in the liver tissue of patients with chronic liver disease, suggesting the possible correlation between Hp infection and hepatocellular carcinoma.
Nan fang yi ke da xue xue bao = Journal of Southern Medical University 01/2010; 30(1):131-2.
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ABSTRACT: HepG2 cells were treated with Helicobacter pylori (Hp) at different concentrations and the cell killing and apoptosis of the cells were measured with MTT assay and Hoechst 33258 staining technique. The results showed that with the increment of cagA (+) Hp concentration, HepG2 cell killing and apoptosis rate increased in a concentration-dependent manner, but cagA (-) Hp did not significantly impacted on the proliferation and apoptosis of HepG2.
Nan fang yi ke da xue xue bao = Journal of Southern Medical University 09/2006; 26(8):1219-21.
