Controversies exist regarding the classification of the different clinical phases of chronic hepatitis B (CHB) because hepatitis B virus (HBV) DNA and alanine aminotransferase levels fluctuate over time.<sup>1,2</sup> To improve the distinction of clinical phases and the associated spectrum of clinical outcome,<sup>3,4</sup> hepatitis B surface antigen (HBsAg) levels may be of help.<sup>5-7</sup> We hypothesize that HBV genotype specific HBsAg levels are needed for the identification of different clinical HBV disease phases.<sup>7</sup>.
In part 2, participants were required to have HBeAg-positive or HBeAg-negative chronic HBV infection, with serum HBV DNA concentrations of at least 2 × 10<sup>4</sup> IU/mL (HBeAg-positive) or 2 × 10<sup>3</sup> IU/mL (HBeAg-negative) and serum alanine aminotransferase concentrations less than seven times the upper limit of normal.
Using well-characterized cohort of treatment-naïve patients with chronic HBV infection in The Gambia, we evaluated the accuracy of serum HBcrAg to diagnose HBV DNA levels, and to indicate treatment eligibility determined by the American Association for the Study of Liver Diseases, based on the reference tests (HBV DNA, HBV e antigen (HBeAg), alanine transaminase (ALT), liver histopathology and/or FibroScan).
The primary efficacy outcome was a virological response (VR), and the secondary efficacy outcomes were hepatitis B e antigen (HBeAg) seroconversion and alanine aminotransferase (ALT) normalization.
Through intracellular IFN-γ and TNF-α staining, HBV-specific CD4 T cells were analyzed in 68 patients with chronic HBV infection and alanine aminotransferase (ALT) <2x the upper limit of normal (ULN), and 28 patients with a hepatitis B flare.
At the end of follow-up, 8.8% of patients progressed to cirrhosis, the average estimate values of hepatitis B virus DNA and alanine aminotransferase demonstrated a downward trend, the aspartate aminotransferase/alanine aminotransferase ratio showed a flat trend overall.
For chronic hepatitis B patients, hepatitis B e antigen (HBeAg) seroclearance signals a transition from an immunologically active phase to an inactive carrier state with a reduction in hepatitis B virus (HBV) DNA levels and a reduced risk of hepatocellular carcinoma (HCC).<sup>1</sup> Predictors of HBeAg seroclearance include lower HBV DNA levels, viral genotype, the precore mutation, and higher serum alanine aminotransferase (ALT) levels.<sup>2</sup>.
Furthermore, a nomogram, including tumor size, alanine aminotransferase (ALT) level, white blood cell counts, Barcelona Clinic Liver Cancer grade, and APRI was built for DFS, while factors including hepatitis B surface antigen, tumor size, ALT, microvascular invasion, and APRI was built for TTR.
HBV group had higher alanine transaminase (60.9 ± 85.7 U/L vs. 48.0 ± 52.1 U/L; p = 0.003), hemoglobin (12.7 ± 2.28 g/dL vs. 12.0 ± 2.46 g/dL, p < 0.001), albumin (32.9 ± 6.8 g/L vs. 31.3 ± 7.7 g/L; p = 0.007), and prothrombin time (13.2 ± 2.95 s vs. 12.7 ± 2.01 s, p = 0.023), as compared to the cryptogenic group.
In the subgroup of hepatitis B e antigen-negative patients with HBV DNA levels from 2000 to 19,999 IU/mL (intermediate viral load [IVL]) and normal levels of alanine aminotransferase, HBcrAg levels of 10 KU/mL or more identified patients at increased risk of HCC (hazard ratio, 6.29; confidence interval, 2.27-17.48).
At reactivation, the median HBV DNA level was 3.89 × 10<sup>4</sup> IU/mL (range, 1.80 × 10<sup>3</sup>-6.00 × 10<sup>7</sup> IU/mL); five had HBV-related hepatitis and one exhibited increasing HBV DNA level without alanine transaminase elevation.No HBV-related fatal events occurred.
Baseline parameters including hepatitis B virus DNA, hepatitis B surface antigen (HBsAg), hepatitis B core antibody (HBcAb), and alanine aminotransferase level were quantified.
The cumulative rates of undetectable hepatitis B virus DNA (HBV-DNA, < 2.1 log copies/mL), alanine aminotransferase (ALT) normalization, hepatitis B e antigen (HBeAg) seroclearance, hepatitis B surface antigen (HBsAg) seroclearance, and viral breakthrough of 1094 nucleos(t)ide analogue-naïve CHB patients (HBeAg-positive: 47%) who were on continuous entecavir treatment for 10 years were calculated.
Chronic HBeAg-negative phases were classified at yearly visits and defined as 'infection' (HBV DNA ≤10 000 copies/mL and normal alanine aminotransferase [ALT]) or 'hepatitis' (HBV DNA >10 000 copies/mL and/or above normal ALT).
In this study, hepatitis B surface antigen (HBsAg), hepatitis B e-antigen (HBeAg), alanine transaminase (ALT), aspartate transaminase (AST), and hs HBV DNA titers in serum of 5611 cases with suspected HBV infection were reviewed.
The incidence and outcomes of alanine aminotransferase (ALT) flares during the natural history of chronic HBV infection has not been determined in a large, racially heterogeneous group of patients in North America.
The primary end point was the degree of decline of plasma hepatitis B virus (HBV) DNA levels at week 48 and the secondary endpoints were viral suppression, normalization of alanine aminotransferase (ALT) levels, hepatitis B surface antigen (HBsAg)/HBeAg loss or seroconversion, and virological breakthrough.
To evaluate the efficacy and safety of telbivudine (LdT) and tenofovir (TDF) for preventing hepatitis B virus (HBV) vertical transmission for HBV-positive pregnant women.Pregnant women (n = 145) from January 2013 to June 2017 were enrolled when they met inclusion criteria, which included HBV DNA ≥1.0 × 10 copies/mL and increased alanine aminotransferase (ALT) levels.
Child-Pugh score, alanine aminotransferase, total bilirubin level, status of hepatitis B e antigen, and serum hepatitis B virus DNA level were compared between groups.
Subgroup analysis showed that in patients with negative hepatitis B surface antigen, Edmonson's histology grade < 3, and aspartate transaminase > alanine transaminase, the <i>ALDH</i>2-rs671-GG genotype was associated with both shorter time-to-metastasis and shorter overall survival.
At Year 10, 118/118 (100%) of HBeAg-negative patients and 78/80 (98%) of HBeAg-positive patients with available data achieved hepatitis B virus (HBV) DNA < 69 IU/mL, while 88/106 (83%) and 60/77 (78%) patients achieved ALT normalisation, respectively.