In two cases deep prosthesis infection occurred leading to the removal of the implant. In the remaining eight patients the mean AOFAS score improved significantly from 21.5 to 68.0 points (P < 0.0005), the VAS score decreased significantly from 7.6 to 1.9 points (P < 0.0005). ROM increased from 23.2 to 25.0 degrees (P = 0.51). At final follow-up all patients without any complications were satisfied with the postoperative results. Radiographic examination did not reveal any signs of prosthetic loosening.

TAR is a viable surgical treatment option in patients with end-stage Y-27632 molecular weight ankle osteoarthritis due to haemophilia. It provides significant pain relieve and high patient satisfaction. However, due to the increased risk of infection and lack of long-term results, TAR particularly in patients with severe haemophilia and virus infections should be indicated carefully. “
“Summary.  The development of inhibitors is a complication of replacement treatment in Haemophilia. Loss of factor VIII-specific memory B cells in the spleen is associated with down regulation of antibodies in mice treated with high doses of FVIII, but changes in B cell memory have not been described in haemophilic patients. The aim of this study was to evaluate the phenotype of circulating

lymphocytes in severe haemophilia A. Twenty patients with inhibitors (PI), 22 without Ruxolitinib purchase inhibitors (P), nine patients during immune tolerance induction (ITI) treatment and 20 healthy donors (HD) were included. Peripheral blood lymphocytes were examined using flow cytometry. Anti-FVIII antibodies were measured using Bethesda and flow cytometry. Percentages of T subsets and B lymphocytes were similar in all groups. In contrast, memory B cells (CD27+) were decreased in PI and P compared with HD, but the level of significance was higher in PI (P = 0.001) than P (P = 0.01). PI with high level of anti-FVIII antibodies presented the lowest B memory values. CD70 expression was also lowest in PI. Non-switched

CD27+ subpopulation MCE (IgD+) was prevalent in PI, but did not show statistical significance. When ITI failed, the percentages of CD27+ B cells after 12 months of ITI were lowest. In a longitudinal study performed in four patients, an increased percentage of CD27+ and CD70+ B cells during ITI was found. This work suggests that different peripheral lymphocyte markers, such as CD27 and CD70 on B cells, may be helpful to evaluate anti-FVIII response and to monitor the success of ITI. “
“Summary.  The Spanish Epidemiological Study in Haemophilia carried out in 2006 enrolled 2400 patients [2081–86.7% with haemophilia A (HA) and 319–13.3% with haemophilia B]; 465 of them (19.4%) were on prophylaxis. These rates were higher in patients with severe haemophilia (45.4%) and severe paediatric cases (72.5%).

Reduced expression of Glut2 in mouse liver due to reduced hepatic entry of THs and activation of hepatic TR is likely to be the cause of aberrant glucose homeostasis. Importantly, expression of Glut2 in pancreatic islet cells of wild-type and Slco1b2−/− mice did not reveal any STA-9090 cell line differences, because Oatp1b2 is a liver-specific transporter, further strengthening our hypothesis that Oatp1b2 is linked to hepatic Glut2 expression. An important question we addressed was whether the observed murine phenotype predicts the human situation. Oatp1b2 is an ortholog of the human OATP1B subfamily. OATP1B1 has been studied extensively, and its polymorphisms are associated with impaired drug transport

activity.3, 4 To more fully delineate the clinical relevance of our findings, OATP1B1 and OATP1B3 expression was correlated to that INCB018424 in vivo of known TH target genes in a bank of human liver tissue samples. The highest correlation among 34,266 profiled genes was between OATP1B1 and GLUT2. Similar results were obtained for GLUT2 and OATP1B1 protein expression. We then hypothesized that if OATP1B1 is critical to GLUT2 expression, then known functional SNPs in this transporter would alter GLUT2 expression. Previous studies have shown that the SLCO1B1 c.521C>T polymorphism can result in marked differences in plasma levels of substrate drugs2 and predict statin-induced myotoxicity.6 Therefore, in a subset of OATP1B1 genotype–defined liver

samples, we determined GLUT2 expression. Consistent with our hypothesis, the expressed level

of GLUT2 was nearly three-fold lower in livers of individuals harboring SLCO1B1 c.521T>C SNP (haplotypes *5 and *15) (Table 1). Ironically, it appears that patients carrying this SNP would obtain less benefit from statin therapy due to reduced hepatic entry,5 whereas at the same time, be at greater risk for exhibiting aberrant glucose and cholesterol levels due to reduced hepatic TH entry and thus most likely to be prescribed statins. It will be MCE公司 important to determine the role of OATP1B1 in the hepatic entry of TH mimetic agents such as eprotirome32 targeting the liver, and resulting in reduced efficacy for carriers of OATP1B1 polymorphisms. In conclusion, we report a physiological role of hepatic OATP1B transporters in regulating cholesterol and glucose metabolism revealed through the systematic examination of a newly created Slco1b2−/− mouse model. Oatp1b2 in rodents and OATP1B1 in humans appear to be tightly linked to hepatic TR signaling pathways that govern glucose and cholesterol homeostasis; a proposed network is depicted in Fig. 6C. Accordingly, decreased activity of OATP1B1, whether due to intrinsic genetic variation or inhibition of the transporter by concomitant ingestion of an OATP1B1 inhibitor drug,1, 2 alters TH response and signaling pathways in liver and is a heretofore unrecognized determinant of chronic diseases such as hyperlipidemia and diabetes.

Conclusion:  The epidemiology of gastric cancer in the experience of Hospital “José Carrasco Arteaga” corresponds to result of international data published in several studies. It should make new guidelines for asymptomatic patients older than 40 years taking into account genetic factors, educational, food, refrigeration of food, drinking water, and increase the detection rate of early gastric cancer of 7.1% to 50% as it is in Japan. Conducting check details annual checkups funded by the state and private enterprise in this way private employees and provide certificates updated every one or two years. Determination by histopathology, tumor type, and marker KI67 ploidies

of pre-neoplastic lesions such as polyps, villous tubules, low-grade dysplasia, metaplasia intestinal secretory type II B sulphomucins

to determine the degree of histological damage, and the presence of infection by H. pylori, since in our setting this is present in more than 50% in children under 10 years of age, especially the differentiated histological type. Key Word(s): 1. gastric cancer; 2. histopatology; 3. early cancer; 4. advanced cancer; Presenting Author: SHANJIN ZHANG Corresponding Author: SHANJIN ZHANG Affiliations: people’s hospital of yichun city Objective: To explore the causes of the common complications and its treatment and prevention measures through the retrospective analysis of 203 cases of ERCP examination. AP24534 purchase Methods: Through reviewing and summarizing 203 cases of clinical data from the diagnostic and therapeutic ERCP examinations from April 2007 to April 2007, analyzing the cause of the complications and treatment methods, effective preventive measures were explored. Results: 9 cases of complications were in 203 cases of ERCP examination (4.43%), and the incidence of diagnostic ERCP was 3.84% (5/130), complicating with acute pancreatitis in 4 cases, hemorrhage

in 1 case; the incidence of therapeutic ERCP was 5.47% (4/73), complicated with hemorrhage MCE公司 in 2 cases, acute pancreatitis in 1 case, debris basket in 1 case. In 9 cases of complications, 5 cases with the medical therapy (55.56%), 4 cases with the surgical treatment (44.44%). Conclusion: Therapeutic ERCP complications were significantly higher than diagnostic ERCP, may due to a long time of operation and many equipments. The most common complications of diagnostic ERCP was acute pancreatitis, which related with reiterative development, difficult intubation, excessive contrast agents and high pressure. The most common complication of therapeutic ERCP was bleeding, relating with technical operation, accompanying with jaundice, and diabetes. Most of complications after the medical therapy were alleviated, and only a few severe complications required surgical treatment. Key Word(s): 1. ERCP complications; 2. treatment; 3.

The nucleotide HCV polymerase inhibitor sofosbuvir (SOF) in combination with ribavirin (RBV) has provided high rates of response in treatment-naïve and treatment experienced patients with HCV GT 2 or 3. Methods: We conducted 2 phase 3 studies in patients infected with HCV GT 2 and 3. In the POSITRON study, patients who were

interferon-ineligible, -intolerant or -unwilling were randomly assigned (3:1) to receive SOF 400 mg daily and RBV 1000–1200 mg daily for 12 weeks or placebo. In the FUSION study, patients who had failed prior interferon therapy were randomly assigned (1:1) to receive 12 or 16 weeks of SOF 400 mg daily and ribavirin 1000–1200 mg daily. The primary efficacy end point was sustained virologic see more response (SVR) 12 weeks after the end of treatment.

Results: In POSITRON, 207 patients (53% GT 2, 47% GT BVD-523 purchase 3) were randomized to SOF+RBV and 71 (48% GT 2, 52% GT 3) received placebo; 54% were male, 16% had compensated cirrhosis, and 45% carried the IL28B CC genotype. In the FUSION study, 103 patients (35% GT 2, 62% GT 3) were randomized to receive SOF +RBV for 12 weeks and 98 patients (33% GT 2, 64% GT 3) were randomized to receive SOF +RBV for 16 weeks; 70% were male, 34% had compensated cirrhosis,

and 30% carried the IL28B CC genotype. SVR12 rates are given in table. Extending MCE treatment duration to 16 weeks improved SVR12 rate in patients with genotype 3 HCV infection, whereas the SVR12 rates for patients with GT 2 infection were similar in the 12- and 16-week arms. Relapse accounted for all virologic failure and no S282T variant was observed in patients with relapse. SOF with RBV for 12 or 16 weeks had a safety profile similar to that expected for RBV. There were few SAEs, and rates of discontinuation of the treatment regimen due to adverse events was 1–2%. Conclusions: SOF+RBV for 12 or 16 weeks was well tolerated and effective in patients with HCV GT 2 and 3 who are interferon-ineligible, -intolerant or -unwilling or who have failed prior treatment. Prolonging treatment duration for HCV GT3 enhances response. Table 1. Outcomes Response POSITRON FUSION Placebo SOF + RBV × 12 wk SOF + RBV × 12 wk SOF + RBV × 16 wk (n = 71) (n = 207) (n = 100)* (n = 95)* *The efficacy analysis of FUSION excludes 6 patients (3 in each arm) who were found to have GT 1 infection after randomization.

To characterize data from all voxels in an ROI without temporal filtering, 4-dimensional (4D) fMRI scans were motion corrected using FSL MCFLIRT (using the first scan of the volume as the reference scan for alignment) and spatially smoothed (using a Gaussian kernel of 8.0 mm FWHM). These volumes were then masked by the individual ROI created in TBV, and a timecourse of mean intensities from all voxels in the ROI was extracted. To characterize data using parameters approximate to the TBV settings, the 4D fMRI scans were motion corrected using

FSL MCFLIRT (using the first scan of the volume as the reference scan for alignment). These volumes were then masked by the individual ROI created in TBV. An FSL FEAT analysis was Nivolumab mw then run on the masked data using preprocessing (spatial smoothing using a Gaussian kernel of 8.0 mm FWHM and high-pass temporal filtering with 44 seconds cutoff) and statistical analysis (GLM with temporal derivative). A timecourse of signal intensities was created from the voxel with the highest z-score. For both time series extraction approaches, intensity values were converted to PSC using baseline defined as the average of volumes 51-60 (end of first REST period). The hemodynamic response to the “IMAGINE” period was temporally defined by the average time series (from the voxel

with the highest z-score) of the no feedback ROI selleck screening library localizer scans (positive PSC values, less one volume as the intermittent imagine period was one volume shorter). For each condition of feedback type (continuous or intermittent), the average PSC per block was compared pairwise for each participant between real feedback and false feedback. Slopes for each scan were calculated as the change in PSC over the 11 blocks, and slopes were compared pairwise between real feedback and false feedback for feedback methods (continuous MCE or intermittent). For each scan, a standard FSL FEAT analysis was performed using preprocessing (motion correction, brain extraction using FSL BET, spatial smoothing using a Gaussian kernel of 8.0 mm FWHM, high-pass temporal filtering with 44 seconds cutoff) statistical analysis (FILM prewhitening, motion parameters

added to model, and GLM with temporal derivative). Two conditions were defined for the no feedback ROI localizer and continuous scans (rest and imagine), and 3 conditions were defined for the intermittent scans (rest, imagine, and feedback). Higher level analysis were performed in FSL using fixed effects for within-subject comparisons and mixed effects (FLAME 1 + 2) for between-subject comparisons. All statistical results were thresholded using clusters determined by Z > 2.3 and a corrected cluster significance of P= .05. Fifteen participants (8 men and 7 women) enrolled in the study, but scanning was not completed for 1 male (due to claustrophobia) and 1 female (nausea during scanning). The average age of the 13 included participants was 31.6 years (SD = 10.7 years).

To characterize data from all voxels in an ROI without temporal filtering, 4-dimensional (4D) fMRI scans were motion corrected using FSL MCFLIRT (using the first scan of the volume as the reference scan for alignment) and spatially smoothed (using a Gaussian kernel of 8.0 mm FWHM). These volumes were then masked by the individual ROI created in TBV, and a timecourse of mean intensities from all voxels in the ROI was extracted. To characterize data using parameters approximate to the TBV settings, the 4D fMRI scans were motion corrected using

FSL MCFLIRT (using the first scan of the volume as the reference scan for alignment). These volumes were then masked by the individual ROI created in TBV. An FSL FEAT analysis was selleck chemicals llc then run on the masked data using preprocessing (spatial smoothing using a Gaussian kernel of 8.0 mm FWHM and high-pass temporal filtering with 44 seconds cutoff) and statistical analysis (GLM with temporal derivative). A timecourse of signal intensities was created from the voxel with the highest z-score. For both time series extraction approaches, intensity values were converted to PSC using baseline defined as the average of volumes 51-60 (end of first REST period). The hemodynamic response to the “IMAGINE” period was temporally defined by the average time series (from the voxel

with the highest z-score) of the no feedback ROI PLX4032 ic50 localizer scans (positive PSC values, less one volume as the intermittent imagine period was one volume shorter). For each condition of feedback type (continuous or intermittent), the average PSC per block was compared pairwise for each participant between real feedback and false feedback. Slopes for each scan were calculated as the change in PSC over the 11 blocks, and slopes were compared pairwise between real feedback and false feedback for feedback methods (continuous MCE or intermittent). For each scan, a standard FSL FEAT analysis was performed using preprocessing (motion correction, brain extraction using FSL BET, spatial smoothing using a Gaussian kernel of 8.0 mm FWHM, high-pass temporal filtering with 44 seconds cutoff) statistical analysis (FILM prewhitening, motion parameters

added to model, and GLM with temporal derivative). Two conditions were defined for the no feedback ROI localizer and continuous scans (rest and imagine), and 3 conditions were defined for the intermittent scans (rest, imagine, and feedback). Higher level analysis were performed in FSL using fixed effects for within-subject comparisons and mixed effects (FLAME 1 + 2) for between-subject comparisons. All statistical results were thresholded using clusters determined by Z > 2.3 and a corrected cluster significance of P= .05. Fifteen participants (8 men and 7 women) enrolled in the study, but scanning was not completed for 1 male (due to claustrophobia) and 1 female (nausea during scanning). The average age of the 13 included participants was 31.6 years (SD = 10.7 years).

In addition, our results suggest that neutralizing antibodies contribute to the initial protection after reexposure CYC202 datasheet with homologous HCV, probably by interfering with the early steps of the HCV life cycle such as viral binding and entry. However, despite the evidence for crossreactivity of these antibodies, they appear to not to provide protection against the heterologous HCV strain. Development of an effective preventive vaccine and immunotherapeutics would have to target multiple pathways of immune response for an optimal effect. The authors thank E. Soulier (Inserm U748, University Strasbourg, France) for excellent technical assistance.

Additional Supporting Information may be found in the online version of this article. “
“The PNPLA3 rs738409 C>G polymorphism (encoding for I148M) has recently been identified as a susceptibility factor for steatosis-mediated liver damage. We evaluated the influence of this polymorphism on hepatocarcinogenesis in patients with chronic hepatitis C (CHC) virus infection. We genotyped the rs738409 single Navitoclax nucleotide polymorphism in 358 hepatitis C-associated hepatocellular

carcinoma (HCC) patients and correlated the age at onset of HCC and the interval between hepatitis C virus (HCV) infection and the development of HCC in patients with each genotype. The frequencies of CC, CG and GG genotypes were 27.9% (100/358), 49.2% (176/358) and 22.9% (82/358), respectively, and were in Hardy–Weinberg equilibrium. MCE公司 The median age at onset of HCC for the GG genotype was significantly younger compared to for non-GG genotypes (67.81 vs 69.87 years, P < 0.001), and the median interval between HCV infection and the development of HCC was significantly shorter in patients with the

GG genotype (39.96 vs 40.85 years, P = 0.008). PNPLA3 GG genotype was also associated with a higher aspartate aminotransferase level (69.5 vs 59.0 IU/L, P = 0.02), lower prothrombin time (73.0% vs 78.0%, P = 0.008) and a higher prevalence of histological steatosis (40.0% vs. 22.2%, P = 0.01) at the time of HCC onset. The PNPLA3 genotype GG may be associated with accelerated hepatocarcinogenesis in CHC patients through increased steatosis in the liver. HEPATITIS C VIRUS (HCV) infection is a major health burden, with 130–170 million people infected, representing nearly 3% of the world’s population.[1] HCV infection is one of the major causes of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma (HCC).[2] In epidemiological studies of chronic HCV infection (CHC), age, duration of infection, alcohol consumption, co-infection with HIV, low CD4 count, male sex and HCV genotype 3 have been shown to be associated with histological activity.[3-8] We also reported higher body mass index (BMI) as an independent risk factor for HCC development in CHC patients.[9] Although these factors explain part of the extreme variability seen in fibrosis progression among HCV-infected patients, they do not completely account for the differences.

Statistical analyses were performed using Mann-Whitney’s U test (nonequal distribution) and the unpaired Student t test (equal distribution), respectively. Data are presented as means ± standard error of the mean (SEM). A P value <0.05 was considered significant. We used new TRAIL fusion proteins in which three TRAIL protomers were expressed as a single-polypeptide chain (scTRAIL) that were further fused to a humanized single-chain Fv fragment RGFP966 of the anti-EGFR Ab, cetuximab (αEGFR-scTRAIL). In initial experiments, we investigated EGFR expression in liver cancer (Huh7) cells and PHHs by flow cytometry. We also compared EGFR expression in HCC to healthy liver tissues using immunohistochemistry (IHC). Almost no EGFR

expression click here was found in PHH, whereas in Huh7 cells, EGFR was strongly up-regulated (Fig. 1A, B). Similarly, in healthy liver (n = 8), we found no EGFR expression, whereas HCC patients (n = 12) revealed strong EGFR expression on the cell membrane of tumor cells (Fig. 1C, D). This observation, in line with previous reports demonstrating increased EGFR expression in the majority

of HCC tissues,27 therefore suggests that EGFR is a valid tumor target in HCC. We next compared the apoptotic activity of nontargeted scTRAIL with the construct targeting human EGFR (αEGFR-scTRAIL). Because HCC cells, as with many solid tumor cells, reveal a weak TRAIL sensitivity, sensitizing agents, such as proteasome inhibitors, have been suggested to overcome TRAIL resistance.24 Therefore, we additionally analyzed the effects

of both TRAIL proteins in combination with the proteasome inhibitor BZB in Huh7 HCC cells and PHHs. Initial dose-finding experiments revealed a concentration of 100 ng/mL of the two TRAIL proteins to be the most effective for inducing apoptotic caspase-3 activation, when combined with a nontoxic concentration of BZB (500 ng/mL). Compared to BZB alone, which showed almost no effect on caspase activity, scTRAIL significantly increased caspase-3 activation (5.21- ± 1.01-fold) in Huh7 cells, which was further enhanced by BZB (17.06- ± 2.34-fold; Fig. 2A). In contrast to HCC cells, no significant MCE caspase-3 activity was induced by treatment of PHHs with either scTRAIL alone or in combination with BZB. Compared to scTRAIL, EGFR-targeted scTRAIL even more potently increased caspase-3 activity in HCC cells (6.24- ± 1.07-fold, compared to untreated control), which was most strongly enhanced by cotreatment with BZB (50.63- ± 13.97-fold, P < 0.01; Fig. 2B). Importantly, neither αEGFR-scTRAIL alone nor its combination with BZB significantly induced caspase-3 activation in PHHs (2.19- ± 0.76- and 1.88- ± 0.77-fold; Fig. 2B). In contrast, CD95L, which served as a positive control, induced strong caspase-3 activation in PHHs (38.87- ± 10.51-fold; Fig. 2C). We then compared apoptosis induction by nontargeted and EGFR-targeted scTRAIL in the presence or absence of BZB.

Statistical analyses were performed using Mann-Whitney’s U test (nonequal distribution) and the unpaired Student t test (equal distribution), respectively. Data are presented as means ± standard error of the mean (SEM). A P value <0.05 was considered significant. We used new TRAIL fusion proteins in which three TRAIL protomers were expressed as a single-polypeptide chain (scTRAIL) that were further fused to a humanized single-chain Fv fragment AZD1208 of the anti-EGFR Ab, cetuximab (αEGFR-scTRAIL). In initial experiments, we investigated EGFR expression in liver cancer (Huh7) cells and PHHs by flow cytometry. We also compared EGFR expression in HCC to healthy liver tissues using immunohistochemistry (IHC). Almost no EGFR

expression selleck chemicals llc was found in PHH, whereas in Huh7 cells, EGFR was strongly up-regulated (Fig. 1A, B). Similarly, in healthy liver (n = 8), we found no EGFR expression, whereas HCC patients (n = 12) revealed strong EGFR expression on the cell membrane of tumor cells (Fig. 1C, D). This observation, in line with previous reports demonstrating increased EGFR expression in the majority

of HCC tissues,27 therefore suggests that EGFR is a valid tumor target in HCC. We next compared the apoptotic activity of nontargeted scTRAIL with the construct targeting human EGFR (αEGFR-scTRAIL). Because HCC cells, as with many solid tumor cells, reveal a weak TRAIL sensitivity, sensitizing agents, such as proteasome inhibitors, have been suggested to overcome TRAIL resistance.24 Therefore, we additionally analyzed the effects

of both TRAIL proteins in combination with the proteasome inhibitor BZB in Huh7 HCC cells and PHHs. Initial dose-finding experiments revealed a concentration of 100 ng/mL of the two TRAIL proteins to be the most effective for inducing apoptotic caspase-3 activation, when combined with a nontoxic concentration of BZB (500 ng/mL). Compared to BZB alone, which showed almost no effect on caspase activity, scTRAIL significantly increased caspase-3 activation (5.21- ± 1.01-fold) in Huh7 cells, which was further enhanced by BZB (17.06- ± 2.34-fold; Fig. 2A). In contrast to HCC cells, no significant medchemexpress caspase-3 activity was induced by treatment of PHHs with either scTRAIL alone or in combination with BZB. Compared to scTRAIL, EGFR-targeted scTRAIL even more potently increased caspase-3 activity in HCC cells (6.24- ± 1.07-fold, compared to untreated control), which was most strongly enhanced by cotreatment with BZB (50.63- ± 13.97-fold, P < 0.01; Fig. 2B). Importantly, neither αEGFR-scTRAIL alone nor its combination with BZB significantly induced caspase-3 activation in PHHs (2.19- ± 0.76- and 1.88- ± 0.77-fold; Fig. 2B). In contrast, CD95L, which served as a positive control, induced strong caspase-3 activation in PHHs (38.87- ± 10.51-fold; Fig. 2C). We then compared apoptosis induction by nontargeted and EGFR-targeted scTRAIL in the presence or absence of BZB.

Pearson’s correlation coefficient was used to assess the correlation between HBV DNA and HBsAg. All statistical tests were two-sided. Statistical significance was taken as Luminespib in vivo P < 0.05. Overall, 49 patients had positive HBeAg and 68 patients had negative HBeAg at the first visit (Table 1). HBeAg-negative

patients were generally older than HBeAg-positive patients. All patients had compensated disease and only four patients had ultrasonic features of liver cirrhosis. HBeAg-positive patients had higher HBV DNA and ALT levels than HBeAg-negative patients. There was a relative predominance of genotype C HBV infection among HBeAg-positive patients. The mean duration of follow-up was 99 months in both HBeAg-positive patients (median 106, range 47-127 months) and HBeAg-negative patients (median 102, range 47-117 Ferrostatin-1 research buy months). At the first visit, HBeAg-positive patients had higher serum HBsAg levels than HBeAg-negative

patients (Table 1). All HBeAg-positive patients had HBsAg > 1 log IU/mL, 41 (84%) patients had HBsAg > 3 log IU/mL, and 28 (57%) patients had HBsAg > 4 log IU/mL. On the other hand, 60 (88%) of the HBeAg-negative patients had HBsAg > 1 log IU/mL, 40 (59%) patients had HBsAg > 3 log IU/mL, and only three (4%) patients had HBsAg > 4 log IU/mL. HBeAg-positive patients also had lower HBsAg/HBV DNA than HBeAg-negative patients (Table 1). There was no statistical difference in the age, sex ratio, and HBV genotypes among HBeAg-positive patients with persistently normal ALT (Group 1, 上海皓元医药股份有限公司 N = 7), elevated ALT (Group 2, N = 25), and sustained HBeAg seroconversion (Group 3, N = 17).

At the first visit, Group 1 patients had higher HBV DNA and HBsAg levels than those in the other two groups. There was no difference in HBV DNA and HBsAg levels between patients in Group 2 and Group 3. Patients in Group 1 had the highest HBV DNA and HBsAg levels among all five groups of patients throughout the entire follow-up period (Table 2). The mean HBV DNA level of Group 1 patients stayed at approximately 8 log IU/mL and HBsAg at approximately 5 log IU/mL at all time points of assessment (Fig. 1A). The median reduction in HBsAg per year was −0.006 (range −0.02 to 0.03) log IU/mL. Patients in Group 2 and Group 3 had lower HBV DNA and HBsAg levels than Group 1 patients throughout the follow-up, but there was no difference in the HBsAg levels between Group 2 and Group 3 at all time points of assessment (Table 2). The mean HBV DNA of patients in Group 2 stayed at approximately 6-7 log IU/mL and HBsAg at approximately 3-4 log IU/mL at all time points of assessment (Fig. 1A). Although there was some fluctuation in serum HBsAg levels during the follow-up, the median reduction of HBsAg per year was 0.021 (range −0.21 to 0.19) log IU/mL. Twenty-two (88%) patients in Group 2 had HBsAg reduction less than 1 log IU/mL at the last visit (Fig. 2).