Search

Background/purpose: Clinical implications of IL28B gene in Taiwanese chronic hepatitis C (CHC) patients remain unknown. We thus investigated the prevalence and clinical implications of IL28B rs8099917 genotypes in CHC patients with different hepatitis C virus (HCV) genotypes and healthy controls.Methods: A total of 200 HCV genotype 1 patients and 200 HCV genotype 2 patients who received liver biopsy, as well as 197 healthy controls were enrolled to determine the frequencies of IL28B rs8099917 genotypes. In addition, the association of IL28B rs8099917 genotype with baseline data, including HCV RNA level, HCV genotype, histological activity grade, fibrosis stage, and body mass index, were evaluated and further stratified by covariant factors.Results: Compared with healthy controls, CHC patients had a lower prevalence rate of favorable IL28B rs8099917 TT genotype (81.0% vs. 89.3%, p = 0.025). In addition, the prevalence rates of favorable TT genotype in patients with HCV genotypes 1 and 2 were 76.0% and 86.0%, respectively (p = 0.007). Using ordered logistic regression analysis, higher fibrosis stages were found to be associated with a lower prevalence of TT genotype (p = 0.033), but not histological activity grades (p = 0.748). The association with fibrosis stages was more pronounced in female patients (p = 0.024).Conclusion: In Taiwan, CHC patients have a lower frequency of favorable IL28B TT genotype than healthy controls. Among patients with CHC, the frequency of TT genotype is higher in HCV genotype 2 patients than in HCV genotype 1 patients. In addition, CHC patients with TT genotype, particularly females, have a lower likelihood of advanced fibrosis. [ABSTRACT FROM AUTHOR]

Copyright of Hepatology Research is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Adipocytokines play an important role in lipid metabolism and liver disease progression. However, the interactions between hepatitis B virus (HBV) infection and adipocytokines remain largely unknown. Aims: To investigate the association of HBV infection with adipocytokines in HBV-infected and noninfected subjects. In addition, the impact of adipocytokines on serum HBV DNA, HBsAg levels and liver fibrosis stage was also examined. Methods: A case-control analysis of patients with and without chronic HBV infection was performed. The HBV group consisted of 187 patients with chronic HBV infection, and the control group consisted of 184 age-, gender- and body mass index-matched subjects without HBV infection. Fasting blood glucose, lipid profiles, adiponectin, leptin and visfatin levels were compared between the two groups. APRI and FIB-4 were calculated to estimate the severity of liver fibrosis. Results: Most of the enrolled subjects had lower ALT levels [228 (57.7 %) ALT < ULN] and milder hepatic fibrosis [381 (96.5 %) APRI < 0.7; 307 (77.7 %) FIB4 < 1.45]. The HBV group had significantly higher serum adiponectin and visfatin but lower leptin levels than the control group. This difference remained significant after adjustment for age, sex, BMI and ALT levels ( p < 0.05). Serum adiponectin, leptin and visfatin levels were significantly associated with serum HBsAg and HBV DNA levels ( p < 0.05). In addition, a higher serum adiponectin level was associated with advanced liver fibrosis in elder male HBeAg-negative patients. Conclusions: Patients with chronic HBV infection have significantly higher serum adiponectin and visfatin but lower leptin levels than healthy controls. Serum adipocytokine levels independently correlate with HBV viremia, HBsAg levels and liver fibrosis stages. [ABSTRACT FROM AUTHOR]

Although hepatitis C virus infection is known to be linked with insulin resistance, dyslipidemia, and hepatic steatosis, the relationship between hepatitis B virus ( HBV) infection and metabolic factors remains unclear. HBV infection is a health problem worldwide, especially in endemic regions such as Asia and Africa. It induces liver decompensation, cirrhosis, hepatocellualr carcinoma, and premature mortality. The prevalence of metabolic syndrome continues to increase in parallel with the epidemic of obesity, which is closely associated with the development of diabetes, cardiovascular disease, or even cancer. The systemic review shows that chronic HBV infection protects against instead of promotes fatty liver. The mechanism is possibly due to a lower frequency of dyslipidemia profile in patients with chronic HBV infection. The association of HBV with metabolic syndrome, insulin resistance, and the risk of arteriosclerosis is still inconclusive. In addition, obesity, diabetes, and metabolic syndrome may accelerate the progression of liver disease in patients with chronic HBV infection and synergistically induce cirrhosis or even hepatocellualr carcinoma development. [ABSTRACT FROM AUTHOR]

Background and Aim Patients with hepatitis B virus ( HBV) genotype B infection experience hepatitis B e-antigen ( HBeAg) seroconversion at an earlier stage than do patients with genotype C infection. Therefore, this study investigated whether the differential phenotypes are related to HBV genomic evolution. Methods Thirty-three HBeAg-positive patients with a mean follow-up of 3.1 years were enrolled: 16 at the immune tolerance stage (group I) and 17 at the immune clearance stage (group II). The evolution rates of paired viral genomes at enrollment and at the final follow-up in the full-length genome (μf), nonoverlapping regions (synonymous [μs] and nonsynonymous [μa]), and overlapping regions (μ) were calculated. The evolution rates were then compared according to serum alanine aminotransferase ( ALT) levels and HBV genotype. Results The overall μf evolution rate was lower in group I than in group II (1.4 × 10−5 ± 3.3 × 10−5 vs 1.2 × 10−3 ± 1.2 × 10−3 nucleotide substitution/site/year, P < 0.001). We observed similar results for the μs, μa, and μ evolution rates. All evolution parameters were comparable between genotypes B and C. We determined a positive correlation between μa/y and the area under the average ALT time curve in genotype B (R2 = 0.6935, P < 0.0001), but not in genotype C (R2 = 0.1606, P = 0.124). Conclusion The evolution rate of the HBV genome is higher at the immune clearance stage than at the immune tolerance stage. Host immune selection might play a role in triggering evolution of genotype B. [ABSTRACT FROM AUTHOR]

Background: The clinical significance of serum microRNA-122 (miR-122) has been shown in viral hepatitis B and C, respectively. Specifically, miR-122 stimulates hepatitis C virus (HCV) replication but suppresses hepatitis B virus (HBV) replication. The profile and clinical significance of serum miR-122 in patients with dual chronic hepatitis B and C would be an interesting and important clinical issue. Methods: A total of 76 patients with HBV/HCV dual infection, 105 with HCV monoinfection and 39 with HBV monoinfection were enrolled. All patients received peginterferon alfa-2a (PEG-IFN)-based treatment. Serum miR-122 levels were quantified by using a sensitive hybridization-based assay. Results: At baseline, the serum miR-122 level was lower in HCV-monoinfected patients than in HBV-monoinfected patients, whereas HBV coinfection increased the expression of miR-122. In multivariate analysis, the serum miR-122 level was positively correlated with the serum HBsAg level in patients with HBV/HCV dual infection and those with HBV monoinfection. In dually infected patients who received PEG-IFN-based treatment, a high baseline miR-122 level was positively correlated with a greater reduction of the posttreatment serum HBsAg level. Conclusion: In summary, the serum miR-122 level is highly correlated with the HBsAg level in HBV/HCV dually infected patients and may serve as a biomarker to predict posttreatment HBsAg decline. [ABSTRACT FROM AUTHOR]

Background Occult hepatitis B virus ( HBV) infection ( OHB) may exist in patients experiencing hepatitis B surface antigen ( HBsAg) seroclearance. Aims We examined the clinical and virological features of OHB in patients who lost HBsAg post-treatment or spontaneously. Methods We collected 44 patients with HBsAg seroclearance: 15 patients with dual HBV/hepatitis C virus ( HCV) infection who lost HBsAg after peginterferon alfa-2a ( PEG- IFN) plus ribavirin therapy; 13 HBV mono-infected patients who lost HBsAg after various oral antiviral therapies; and 16 patients who lost HBsAg spontaneously. OHB was defined as detectable serum HBV DNA in the absence of HBsAg. Viral mutations associated with OHB were identified by comparison with matched controls that remained positive for HBsAg, and further characterized in vitro. Results The prevalence of OHB was 34.1% (15/44) in all patients, which was not significantly different among three groups. One mutation in surface promoter/polymerase region, C3050T (preS1T68I), was identified to be associated with the seroclearance of HBsAg in six cases. This mutation does not change the amino acid sequence of the polymerase protein. The S promoter activity was significantly lower in the construct containing C3050T mutation as compared with the wild-type ( P = 0.0008). However, this mutation did not affect HBV replication, transcription and translation in the context of the full-length HBV genome. OHB was not rare in patients with HBsAg seroclearance. Conclusions One mutation, C3050T (preS1T68I), decreased S promoter activity; nevertheless, other factors may play more important role in the clearance of HBsAg in these OHB patients. [ABSTRACT FROM AUTHOR]

Background and Aims The level of hepatitis B surface antigen ( HBsAg) has been shown to complement hepatitis B virus ( HBV)- DNA level in predicting disease progression in hepatitis B e antigen ( HBeAg)-negative patients, especially those with low viral loads. Whether this finding could be seen in spontaneous HBeAg seroconverters remains unclear. Methods A retrospective cohort of 390 Taiwanese spontaneous HBeAg seroconverters with a mean follow-up period of 7.4 years was enrolled. The relationships between HBV- DNA/ HBsAg levels and HBeAg-negative hepatitis/active viral replication ( HBV- DNA level ≥ 2000 IU/mL) were investigated. Results In the overall cohort, serum HBV- DNA level served as a better predictor for HBeAg-negative hepatitis compared with HBsAg level. However, in those with HBV- DNA level < 2000 IU/mL, a higher HBsAg level was associated with a higher risk of HBeAg-negative hepatitis ( P = 0.015). Multivariate analysis showed the hazard ratio of HBsAg level ≥ 1000 IU/mL versus < 1000 IU/mL was 4.1 (95% confidence interval: 1.3-13.6). When using the end-point of active viral replication, HBsAg ≥ 1000 IU/mL remained as an independent risk factor, with a hazard ratio of 2.5 (95% confidence interval: 1.1-5.9). Conclusions In spontaneous HBeAg seroconverters with HBV- DNA level < 2000 IU/mL, HBsAg level ≥ 1000 IU/mL is associated with increased risks of HBeAg-negative hepatitis and active viral replication. Combining HBV- DNA < 2000 IU/mL and HBsAg level < 1000 IU/mL may be used to define minimal viral activity. [ABSTRACT FROM AUTHOR]

Background: Serum hepatitis B surface antigen (HBsAg) level is important in the management of chronic hepatitis B (CHB). However, it is unclear whether serum HBsAg reflects its expression in liver and the hepatic HBsAg evolution following interferon therapy. Methods: Forty-five HBeAg-positive CHB patients receiving interferon-based therapy within a randomized, controlled, multicenter study during 1998-1999 were included. The hepatic HBsAg expressions were categorized into cytoplasmic, inclusion, marginal and negative patterns by immunohistochemical staining. The HBsAg-positive hepatocytes were quantified by image-based cytometry and correlated to HBV serological and virological profiles for clinical implications. The evolution of hepatic HBsAg levels was analyzed among 22 patients with paired liver biopsies before and after interferon therapy, sequentially. Results: There was a positive correlation between pretreatment serum HBsAg and hepatic HBsAg levels ( r = 0.67, P < 0.0001). The hepatic HBsAg expression pattern significantly evolved from cytoplasmic/inclusion pattern to marginal/negative pattern after interferon treatment. The serum HBV-DNA, HBsAg and hepatic HBsAg levels all decreased significantly after interferon therapy. Among 36 % patients with HBeAg loss after therapy, pretreatment hepatic HBsAg levels were significantly lower compared with those without HBeAg loss. After multivariate analysis, low pretreatment hepatic HBsAg levels rather than serum HBsAg titers were associated with a higher rate of HBeAg loss (OR: 4.97, 95 % CI: 1.12-22.00, P = 0.035). Conclusions: The serum HBsAg level positively reflects the HBsAg level in liver which evolves significantly after interferon therapy. A lower hepatic HBsAg level is associated with HBeAg loss after interferon treatment. Hepatic HBsAg may have clinical significance in CHB patients receiving interferon treatment. [ABSTRACT FROM AUTHOR]

Antiviral treatment criteria are based on disease progression risk, and hepatocellular carcinoma (HCC) surveillance recommendations for patients with chronic hepatitis B (CHB) without cirrhosis is based on an annual incidence threshold of 0.2%. However, accurate and precise disease progression estimate data are limited. Thus, we aimed to determine rates of cirrhosis and HCC development stratified by age, sex, treatment status, and disease activity based on the 2018 American Association for the Study of Liver Diseases and 2017 European Association for the Study of the Liver guidelines. We analyzed 18,338 patients (8914 treated, 9424 untreated) from 6 centers from the United States and 27 centers from Asia-Pacific countries. The Kaplan-Meier method was used to estimate annual progression rates to cirrhosis or HCC in person-years. The cohort was 63% male, with a mean age of 46.19 years, with baseline cirrhosis of 14.3% and median follow up of 9.60 years. By American Association for the Study of Liver Diseases criteria, depending on age, sex, and disease activity, annual incidence rates ranged from 0.07% to 3.94% for cirrhosis, from 0.04% to 2.19% for HCC in patients without cirrhosis, and from 0.40% to 8.83% for HCC in patients with cirrhosis. Several subgroups of patients without cirrhosis including males younger than 40 years of age and females younger than 50 years of age had annual HCC risk near or exceeding 0.2%. Similar results were found using European Association for the Study of the Liver criteria. There is great variability in CHB disease progression rates even among "lower-risk" populations. Future CHB modeling studies, public health planning, and HCC surveillance recommendation should be based on more precise disease progression rates based on sex, age, and disease activity, plus treatment status. [Display omitted] [ABSTRACT FROM AUTHOR]

LINKED CONTENT This article is linked to Kao et al and Liu et al papers. To view these articles, visit https://doi.org/10.1111/apt.16097 and https://doi.org/10.1111/apt.16132 [ABSTRACT FROM AUTHOR]

Background. The serum hepatitis B virus (HBV) surface antigen (HBsAg) level can predict hepatocellular carcinoma (HCC) development in hepatitis B e antigen (HBeAg)-negative patients with an HBV DNA level of <2000 IU/mL. However, little is known regarding how well the combination of both viral biomarkers stratifies HCC risk. Methods. A total of 2165 Taiwanese HBeAg-negative noncirrhotic patients were followed for 14.9 years. The predictive power of the HBsAg level for HCC was analyzed for different viral load ranges. Results. In patients with HBV DNA levels of 2000-19 999 IU/mL (intermediate viral load), a positive correlation between HBsAg level and HCC development was identified after adjustment for other risk factors (P = .002). In contrast, no association was found between HBsAg level and HCC in patients with higher viral loads. HBsAg level was subsequently included to stratify HCC risk in patients with low and intermediate viral loads. Receiver operating characteristic curve analysis showed that combining HBV DNA and HBsAg level better predicts 10-year HCC development as compared to using HBV DNA level alone in the overall cohort (P = .028). Conclusions. Serum HBsAg level helps stratify HCC risk in patients with intermediate viral loads. Combining HBV DNA and HBsAg levels better predicts HCC risk. [ABSTRACT FROM AUTHOR]

Using commercial quantitative assays, quantitative hepatitis B surface antigen (qHBsAg) has improved our understanding and management of chronic hepatitis B (CHB). The HBsAg level is highest in the immune tolerance phase, starts to decline during the immune clearance phase, and decreases slowly but progressively after hepatitis B e antigen (HBeAg) seroconversion. The HBsAg level is lowest in individuals with an inactive carrier state but higher in those who develop HBeAg-negative hepatitis. It has been shown that a reduction of HBsAg by 1 log IU/mL or more reflects improved host immune control of HBV infection. A combination of HBsAg <1000 IU/mL and HBV-DNA <2000 IU/mL can identify a 3-year inactive state in a genotype D HBeAg-negative carrier population. In the Asian-Pacific region, where HBV genotypes B and C are dominant, HBsAg levels of ≤10-100 IU/mL predict HBsAg loss over time. As to the prediction of disease progression, low-viremic carriers with HBsAg >1000 IU/mL have been shown to be at higher risks of HBeAg-negative hepatitis, cirrhosis, and hepatocellular carcinoma than those with HBsAg <1000 IU/mL. Although qHBsAg has been widely used in CHB patients receiving pegylated interferon therapy, the HBsAg decline is slow and does not correlate with HBV-DNA levels during nucleos(t)ide analogue (NUC) therapy. However, a rapid HBsAg decline during NUC therapy may identify patients who will finally clear HBsAg. A 6- to 12-monthly assessment of HBsAg level could be considered during NUC therapy. Taking these lines of evidence together, qHBsAg can complement HBV-DNA levels to optimize the management of CHB patients in our daily clinical practice. [ABSTRACT FROM AUTHOR]

Background. It is unclear whether hepatitis B e antigen (HBeAg) seroconversion induced by nucleos(t)ide analogues (NUC) has a prognosis that is similar to that of spontaneous HBeAg seroconversion.Methods. A total of 148 noncirrhotic NUC-induced HBeAg seroconverters were consecutively enrolled. A historical control of 407 noncirrhotic spontaneous HBeAg seroconverters was also recruited. We compared the rates of HBeAg seroreversion and HBV reactivation between these 2 cohorts.Results. There were 1652.8 and 465.2 person-years of follow-up for spontaneous and NUC-induced HBeAg seroconverters, respectively. Compared with NUC-induced seroconverters, spontaneous seroconverters were younger when achieving HBeAg seroconversion. We thus compared these 2 cohorts according to their age at HBeAg seroconversion. In patients achieving HBeAg seroconversion before 30 years of age, NUC-induced seroconverters had a higher 2-year HBeAg seroreversion rate than spontaneous seroconverters (12.0% vs 2.9%; P = .004) and were at a higher risk of HBV reactivation (hazard ratio, 4.6; 95% confidence interval, 1.5–14.4). Using multivariate analysis, NUC-induced HBeAg seroconversion remained a risk factor of both endpoints in young HBeAg seroconverters.Conclusion. NUC-induced HBeAg seroconverters may not have durable response after stopping therapy. For patients achieving HBeAg seroconversion before 30 years of age, the risk of HBeAg seroreversion and HBV reactivation is higher in NUC-induced seroconverters than spontaneous HBeAg seroconverters. [ABSTRACT FROM AUTHOR]

Purpose: Acute exacerbation (AE) of chronic hepatitis B virus (HBV) infection is common and negatively impacts the clinical outcome. Factors predicting outcomes after exacerbations were only partly clarified. We investigated the host immune parameters associated with long-term outcomes. Methods: We prospectively examined the profiles of serum cytokines and chemokines in 36 consecutive hepatitis B e antigen (HBeAg)-positive patients (male 72%, age 40.8 ± 9.9 years, genotype B/C 75%/25%) who developed AE in a medical center. The patients were followed up for a median of 4 years (range 2-6 years) post-AE. The impact of six cytokines (tumor necrosis factor alfa, interferon gamma, IL-2, IL-4, IL-6, and IL-10) and five chemokines (CXCL10/IP-10, CCL2/MCP-1, CXCL9/MIG, CCL5/RANTES, and CXCL8/IL-8) at the onset of AE activity on the long-term outcomes were analyzed. Results: Of 36 patients, 22 (61.1%) developed HBeAg seroconversion during follow-up (Group I), and the remaining 14 patients did not obtain HBeAg seroconversion (Group II). Baseline characteristics were generally similar between two groups of patients. In Group I patients, the frequency of undetectable serum IL-6 level (<3 pg/mL) at the onset of AE was significantly higher in comparison with Group II patients in multivariate analysis (86.4 vs. 42.9%, P = 0.016). Conclusions: Our findings indicate that undetectable serum IL-6 level at the early stage of AE correlated with the long-term outcomes and may serve as a useful clinical predictor. [ABSTRACT FROM AUTHOR]

Purpose: A significant portion of HBeAg-negative chronic hepatitis B patients have persistently normal serum alanine aminotransferase levels (PNALT). We thus investigated host genetic variants and virological features in HBeAg-negative hepatitis B carriers. Methods: Baseline clinical and virological features of 133 HBeAg-negative hepatitis B carriers (77 with PNALT and 56 with chronic hepatitis activity) with follow-up for more than 5 years were investigated. Three single nucleotide polymorphisms (SNPs) located within or around human leukocyte antigen ( HLA)- DPA1, HLA- DPB1, and interleukin ( IL) 28B loci were genotyped. Results: The genotype frequencies of these SNPs were comparable between hepatitis B carriers with PNALT and those with chronic hepatitis. Compared with hepatitis B carriers with PNALT, those with chronic hepatitis had significantly higher baseline serum HBV-DNA levels (4.96 vs. 4.04 log IU/ml, P = 0.001). Baseline serum HBV-DNA level > 2000 IU/ml (OR, 8.42; 95% CI, 2.74-25.90, P < 0.001) were the only independent factor associated with chronic hepatitis activity. Changes of serum HBV-DNA in 30 hepatitis B carriers with PNALT had showed a significant reduction of viral load from baseline to last visit (mean difference of paired HBV-DNA levels: −0.78 log IU/ml, 95% CI: −1.57 to −0.013, P = 0.047). In contrast, no significant reduction of viral load was found in 28 patients with chronic hepatitis. Conclusions: The results indicate that lower baseline serum HBV-DNA level and viral load reduction over time are associated with long-term biochemical remission in HBeAg-negative hepatitis B carriers. [ABSTRACT FROM AUTHOR]

Context: Chronic Hepatitis B virus (HBV) infection causes significant morbidity and mortality with widespread global distribution. Different genotypes display variations in pathogenesis, disease behavior, and treatment response. HBV/B and HBV/C are prevalent in Asia, but minimal data come from the Philippines. Objective: This study is aimed to determine the HBV genotypes of Filipino patients with Chronic HBV infection seen in Cebu City, Philippines and describe the age, sex, viral activity, alanine aminotransferase (ALT) levels and viral load patterns by genotype. Study design: Case series with prospective mode of data collection. Study setting: Gastroenterology specialty clinics, Cebu City, Philippines. Study population: Patients with Chronic HBV infection seen in 2008. Maneuvers: Chronic HBV infection was defined as HBsAg(+) for >6 months with persistent/intermittent ALT/aspartate aminotransferase levels (AST) elevations. Hepatitis panel and biochemical tests determined disease activity. Ultrasound documented liver cirrhosis with corresponding hypoalbuminemia and prolonged Prothrombin time. Hepatitis C virus (HCV) co-infection was a reactive anti-HCV test. Hepatocellular carcinoma was diagnosed by ultrasound or computed tomography (CT) scan with alpha-feto protein (AFP) > 500 ng/L. COBAS Taqman HBV Test determined HBV-DNA level. Polymerase chain reaction (PCR) genotyping was done using type-specific primers. Results: This study analyzed data from 50 patients, where 74% were males, and median age was 31 years (IR 25-40 years.). Chronic active hepatitis was seen in 76.6%. Only 18% had ALT levels >2 × ULN. Viral loads >20,000 IU/L were reported in 71% of HBeAg(+) patients. Viral loads >2,000 IU/L were seen in 73% of HBeAg(−) patients. Predominant genotypes identified were HBV/A (28%) and HBV/C (26%). No significant correlation between genotype and age ( p = 0.92) and ALT levels ( p = 0.58) was determined. Consistently high-DNA titers were reported for 83% of HBV/C patients and for all patients with >1 HBV genotypes. Hepatocelullar carcinoma was noted for one patient with HBV/A. Two patients with liver cirrhosis had HBV/C. Limitation: Possible significant associations between genotype and some patient-related parameters could not be determined due to scarcity of subjects. Conclusion: HBV/A and HBV/C genotypes are equally predominant among Filipino patients with Chronic HBV infection seen in two specialty clinics in Cebu City, Philippines. [ABSTRACT FROM AUTHOR]

Background Methods Results Conclusions Plain Language Summary Steatotic liver disease (SLD) is an emerging liver disease that has been associated with an increased risk for hepatocellular carcinoma (HCC). The impact of concurrent SLD on the prognosis of HCC remains unknown. This study investigates how concurrent SLD affects the outcomes of patients with HCC undergoing curative radiofrequency ablation (RFA) therapy.A retrospective analysis of patients with early‐stage HCC receiving curative RFA at a tertiary medical center was conducted. Laboratory data and HCC characteristics were recorded and analyzed by a Cox proportional hazards regression model to predict recurrence and all‐cause mortality after RFA.A total of 598 patients with HCC were included between 2005 and 2015, with 139 and 459 classified in SLD and non‐SLD groups, respectively. The SLD group exhibited a significantly better liver reserve and a lower cumulative incidence of HCC recurrence and liver‐related and all‐cause mortality after a median follow‐up of 51 months. After adjusting for metabolic dysfunction, liver reserve, and HCC characteristics, the presence of SLD reduced all‐cause mortality (adjusted hazard ratio [aHR], 0.67; 95% confidence interval [CI], 0.45–0.996; p = .048), which was supported by inverse probability weighting analysis (aHR, 0.65; 95% CI, 0.42–1.00; p = .049). Poor liver functional reserve (high albumin‐bilirubin grades) increased all‐cause mortality dose dependently. Barcelona Clinic Liver Cancer staging and a higher Fibrosis‐4 index were predictors for HCC recurrence, whereas SLD was not.Among patients with HCC undergoing curative RFA, those with concurrent SLD had a lower risk of all‐cause mortality compared to those with poor liver functional reserve. The present research demonstrated that patients with both liver cancer and steatotic liver disease who received curative radiofrequency ablation for liver cancer survived longer compared to those without steatotic liver disease. Maintaining good liver function is an important prognostic factor for survival. The present research demonstrated that patients with both liver cancer and steatotic liver disease who received curative radiofrequency ablation for liver cancer survived longer compared to those without steatotic liver disease.Maintaining good liver function is an important prognostic factor for survival. [ABSTRACT FROM AUTHOR]

Background and Aim Methods Results Conclusions Rituximab therapy is associated with a high risk of hepatitis B virus (HBV) reactivation. We aimed to assess whether the risk of reactivation differed among various underlying diseases and between hepatitis B surface antigen (HBsAg) carriers and patients with resolved HBV infection.We retrospectively analyzed patients with chronic or resolved HBV infection who received rituximab without prophylactic anti‐HBV therapy at a tertiary medical center. The risks of HBV reactivation, hepatitis, and hepatic decompensation were compared between the patients with hematologic and rheumatic diseases.There were 78 patients with hematologic diseases and 39 patients with rheumatic diseases included. Among them, 43 (59%) HBsAg‐positive patients and 24 (55%) patients with resolved HBV infection experienced HBV reactivation at a median of 14.6 months after rituximab therapy. After rituximab treatment, the 1‐year HBV reactivation rate among patients with hematologic and rheumatic diseases was 29% and 45% in HBsAg‐positive patients, respectively, while the rates were 38% and 17% in patients with resolved HBV infection. The reactivation risk continued to increase even 2 years after rituximab therapy and was comparable between hematologic and rheumatic patients. A higher baseline HBV DNA level (≥20 IU/mL vs <20 IU/mL) was an independent predictor for HBV reactivation (adjusted hazard ratio [aHR]: 10.9, 95% confidence interval [CI]: 1.1–107) and HBV‐associated hepatitis (aHR: 14.8, 95% CI: 1.4–158).Rituximab therapy is associated with a 50–64% risk of HBV reactivation regardless of underlying diseases and HBsAg status. HBV DNA levels should be assessed before initiating rituximab. [ABSTRACT FROM AUTHOR]