HBV-related Decompensated Cirrhosis Research Articles

Elevated neutrophil-to-hemoglobin ratio as an indicator of poor survival in hepatitis B virus-related decompensated cirrhosis.

Aim: Our goal was to explore the prognostic value of the neutrophil-to-hemoglobin ratio (NHR) in HBV-related decompensated cirrhosis (HBV-DC) patients. Methods: 172 HBV-DC patients were enrolled. Multivariate analyses were used to identify risk factors influencing 30-day mortality. Results: The 30-day mortality was 12.8% (22/172). nonsurvivors exhibited a higher NHR than survivors. On multivariate analysis, NHR and model for end-stage liver disease (MELD) score were the only independent predictors of mortality. Notably, the predictive capabilities of NHR were found to be comparable to those of the MELD score. Conclusion: High NHR was associated with poor prognosis in HBV-DC patients, and NHR can serve as an effective and readily available indicator for the prediction of mortality in these patients.

D-dimer-to-platelet count ratio as a novel indicator for predicting prognosis in HBV-related decompensated cirrhosis

BackgroundHepatitis B virus-related decompensated cirrhosis (HBV-DC) is a critical illness with a low survival rate. Timely identification of prognostic indicators is crucial for risk stratification and personalized management of patients. The present study aimed to investigate the potential of the D-dimer-to-platelet count ratio (DPR) as a prognostic indicator for HBV-DC. MethodsA retrospective review of medical records was conducted for 164 patients diagnosed with HBV-DC. Baseline clinical and laboratory characteristics were extracted for analysis. The endpoint was 30-day mortality. Disease severity was assessed by the Model for End-stage Liver Disease (MELD) score. A multivariate logistic regression model and receiver operating characteristic curve analysis (ROC) were used to evaluate the predictive value of DPR for mortality. ResultsDuring the 30-day follow-up period, 30 (18.3%) patients died. Non-survivors exhibited significantly higher DPR values than survivors, and a high DPR had a strong association with increased mortality. Importantly, DPR was identified as an independent risk factor for mortality in HBV-DC patients after adjustments for confounding factors (Odds ratio = 1.017; 95% Confidence interval, 1.006–1.029; p = 0.003). The cut-off value of DPR as a predictor of mortality was>57.6 (sensitivity = 57%, specificity = 86%, p < 0.001). The area under ROC curve for DPR for 30-day mortality was 0.762, comparable to the MELD score (p = 0.100). Furthermore, the combined use of DPR and MELD score further increased the area under the ROC curve to 0.897. ConclusionElevated DPR was demonstrated to have a correlation with unfavorable outcomes in HBV-DC patients, suggesting its potential utility as an effective biomarker for assessment of prognosis in these patients.

Risk of HCC decreases in HBV-related patients with cirrhosis acquired recompensation: A retrospective study based on Baveno VII criteria.

Antiviral therapy improves the clinical outcomes of patients with HBV-related cirrhosis. In this study, we aimed to evaluate the incidence rate of HCC in patients with HBV-related recompensated, compensated, or decompensated cirrhosis based on the latest Baveno VII criteria. In this two-center retrospective study, HBV-related patients with cirrhosis were enrolled and treated with first-line nucleos(t)ide analogues therapy for at least 12 months. Participants were classified into 3 groups: (1) compensated group, (2) decompensated group, or (3) recompensated group according to Baveno VII criteria. Multivariate regression models and propensity score matching were used to identify the predictors of HCC. Of the 404 patients recruited, during a median follow-up of 44.5 months (interquartile range 26.8, 57.0 months), 233 (57.7%), 100 (24.8%), and 71(17.6%) patients had compensated, recompensated, and decompensated cirrhosis. In total, 38 developed HCC. The cumulative incidence of HCC development at 2, 4, and 6 years was 1.3%, 5.4%, and 20.0% in the compensated group, 1.2%, 5.2%, and 24.5% in the recompensated group, and 2.1%, 23.6%, and 41.8% in the decompensated group, respectively. In the multivariate Cox regression model, compared with the recompensated group, the decompensated group had a significant increased risk for the development of HCC (aHR 2.55; 95% CI: 1.240-5.240; p = 0.027), while the compensated group had similar HCC risk for the development of HCC (aHR 1.41; 95% CI: 0.540-3.730; p = 0.835). Propensity score-matching analysis between the recompensated and compensated groups (84 pairs) and propensity score-matching analysis between the recompensated and decompensated groups (62 pairs) showed similar results. Achieving recompensation reduced the risk of HCC in patients with HBV-related decompensated cirrhosis, while the risk remained comparable to that of compensated cirrhosis.

A new model predicts hepatocellular carcinoma in patients with HBV-related decompensated liver cirrhosis and long-term antiviral therapy: a prospective study.

We aimed to evaluate the prediction values of non-invasive models for hepatocellular carcinoma (HCC) development in patients with HBV-related liver cirrhosis (LC) and long-term NA treatment. Patients with compensated or decompensated cirrhosis (DC), who achieved long-term virological response, were enrolled. DC and its stages were defined by the complications including ascites, encephalopathy, variceal bleeding, or renal failure. Prediction accuracy of several risk scores, including ALBI, CAMD, PAGE-B, mPAGE-B and aMAP, was compared. The median follow-up duration was 37 (28-66) months. Among the 229 patients, 9 (9.57%) patients in the compensated LC group and 39 (28.89%) patients in the DC group developed HCC. The incidence of HCC was higher in the DC group ( 2 = 12.478, P < 0.01). The AUROC of ALBI, aMAP, CAMD, PAGE-B and mPAGE-B scores were 0.512, 0.667, 0.638, 0.663, 0.679, respectively. There was no significant difference in AUROC between CAMD, aMAP, PAGE-B and mPAGE-B (all P > 0.05). Univariable analysis showed that age, DC status and platelet were associated with HCC development, and multivariable analysis showed that age and DC status (both P < 0.01) were independent risk factors for HCC development, then Model (Age_DC) was developed and its AUROC was 0.718. Another model, Model (Age_DC_PLT_TBil) consisting of age, DC stage, PLT, TBil was also developed, and its AUROC was larger than that of Model (Age_DC) (0.760 vs. 0.718). Moreover, AUROC of Model (Age_DC_PLT_TBil) was larger than the other five models (all P < 0.05). With an optimal cut-off value of 0.236, Model (Age_DC_PLT_TBil) achieved 70.83% sensitivity, 76.24% specificity. There is a lack of non-invasive risk scores for HCC development in HBV-related DC, and a new model consisting of age, DC stage, PLT, TBil may be an alternative.

Low Prealbumin Levels Were Associated with Increased Frequency of Hepatic Encephalopathy in Hepatitis B Virus (HBV)-Related Decompensated Cirrhosis.

BACKGROUND The role of nutritional parameter prealbumin in predicting the incidence of hepatic encephalopathy (HE) remains unclear. This study was designed to assess the diagnostic performance of prealbumin in predicting the incidence of HE in hepatitis B virus (HBV)-related decompensated liver cirrhosis patients. MATERIAL AND METHODS A retrospective cohort of 262 patients with HBV-related decompensated liver cirrhosis was involved in this study. Prealbumin, albumin, and other indicators were collected at admission, and independent factors were identified by logistic regression analysis. The Mann-Whitney U test and receiver operating characteristic (ROC) curves were used to compare the groups and indicators. RESULTS A total of 262 patients were enrolled in the study, including 197 men and 65 women. In patients with HBV-related decompensated liver cirrhosis accompanied by HE, the model for end-stage liver disease (MELD) scores, and prothrombin time (PT) and international normalized ratio (INR) values were significantly increased, while prealbumin and albumin levels were significantly decreased. Multivariate analysis showed that only serum prealbumin level (P=0.014) was independently related to the incidence of HE. Moreover, prealbumin level was negatively correlated with MELD (r=-0.63, P<0.001) and Child-Turcotte-Pugh (r=-0.35, P<0.001) scores. ROC curves were performed, and prealbumin showed the highest area under the ROC curve (0.781) compared with MELD and Child-Turcotte-Pugh scores. CONCLUSIONS Low prealbumin levels were associated with increased frequency of hepatic encephalopathy in HBV-related decompensated cirrhosis, which showed better performance than traditional models.

The clinical effect of antiviral therapy in patients with hepatitis B virus-related decompensated cirrhosis and undetectable DNA.

Antiviral therapy (AVT) is the mainstay of hepatitis B virus (HBV) management. We investigated whether AVT improves the outcomes of HBV-related decompensated cirrhosis and undetectable HBV-DNA. Between 2000 and 2017, treatment-naïve patients with HBV-related decompensated cirrhosis and undetectable HBV-DNA were recruited from two tertiary hospitals. The endpoints included death and hepatocellular carcinoma (HCC). A total of 429 patients were analyzed (50 and 379 patients in the AVT and non-AVT groups, respectively). Patients in the AVT group were significantly younger and had higher alanine aminotransferase and alpha-fetoprotein levels than those in the non-AVT group (all P<0.05). During follow-up (median 49.6months), 98 patients died and 105 developed HCC. The cumulative incidence rates of death (2.0%, 4.1%, and 6.4%, and 4.9%, 7.2%, and 10.2% at 6months, 1year, and 2years, respectively) and HCC (8.6%, 15.8%, and 26.4% vs 1.6%, 7.7%, and 24.4% at 1, 2, and 5years, respectively) were statistically comparable between the AVT and non-AVT groups (all P>0.05). Using Cox regression analysis, AVT was not significantly associated with death nor HCC (all P>0.05). Similar results were observed after balancing baseline characteristics with inverse probability of treatment weighting. In the non-AVT group, the cumulative incidence rates of HBV-DNA detection at 6months, 1year, and 2years were 2.0%, 3.1%, and 6.4%, respectively. Antiviral therapy did not attenuate the risk of death nor HCC in patients with HBV-related decompensated cirrhosis and undetectable HBV-DNA.

Ascites re-compensation in HBV-related first decompensated cirrhosis after anti-viral therapy.

Effective antiviral therapy can significantly improve the long-term prognosis of HBV-related decompensated patients, and re-compensation may be achieved in part of the patients. To explore the re-compensation of ascites after HBV suppression and the risk factors, the clinical outcomes of 196 consecutive patients with HBV-related first decompensated cirrhosis of ascites treated with nucleos(t)ide analogue (NUC) were analyzed retrospectively. Among these patients, the median serum HBV DNA level was 5.0 (IQR, 3.0-6.0) log10 IU/mL before treatment. Most patients were given NUC with high barrier to resistance including ETV (152), TDF (1) and TAF (1). Initial combination of LAM plus ADV and LdT plus ADV was used in 41 patients and 1 patients, respectively. After NUC treatment, the percentage of patients with ascites regression was 77.6%, 81.4%, 70.5%, 93.8%, 80.8% at 12, 24, 36, 48, 60 months, respectively (P<0.001). The distribution of ascites severity showed that the patients' ascites improved, with the proportion of no ascites and mild ascites gradually increased. The proportion of re-compensation of ascites defined as negative HBV DNA, improved liver function and ascites regression (off diuretics) was 59.7%, 70.0%, 52.3%, 59.4%, 46.2% at 12, 24, 36, 48, 60 months (P<0.001). The rate of ascites regression was higher in viral response (VR) cohort when compared with that in non-VR cohort. Univariate and multivariable analysis showed that level of serum ALT (OR:0.988, 95%CI, p=0.029) and load of serum HBV DNA (OR:0.78895%CI, p=0.044) at baseline were risk factors of re-compensation of ascites. This study demonstrated that antiviral therapy could reverse decompensation of ascites in HBV-related first decompensated cirrhosis and the level of ALT and HBV DNA were risk factors of ascites re-compensation.

Blood Urea Nitrogen-To-Albumin Ratio is a Predictor of Poor Outcomes in HBV-Related Decompensated Cirrhosis.

This study was conducted to explore the predictive role of blood urea nitrogen-to-albumin ratio (BAR) in HBV-related decompensated cirrhosis (HBV-DC). A total of 163 HBV-DC patients were enrolled. The prognostic performance of BAR for predicting 30-day mortality was evaluated. The mortality was 16.0%. BAR levels were obviously different between survivors and non-survivors and BAR levels were significantly correlated with Model for End-Stage Liver Disease score (MELDs). Both BAR and MELDs were identified as independent prognostic indicators of mortality by multivariate analysis. The discriminatory ability for mortality of BAR was similar to that of MELDs, and the combination of BAR and MELDs could improve prognostic accuracy. Elevated BAR was correlated with worse prognosis in HBV-DC patients.

Circulating tumour cell combined with DNA methylation for early detection of hepatocellular carcinoma.

Background: The inadequate early detection strategies makes hepatocellular carcinoma (HCC) patients with poor prognisis. Therefore, more effective detection methods are urgently needed for early detection and early intervention of HCC. Methods: 17 cases of suspected HCC patients and 11 cases of HBV-related decompensated cirrhosis (HBV-DeCi) patients were enrolled. For each patient, 5ml blood sample was separated into circulating tumor cells (CTCs) and plasma, CTCs were stained with Diff staining for counting. Plasma was used for extracting cell free DNA (cfDNA) and then analyzed by qMSP assay. Ct values were recorded for GNB4 and Riplet as target genes and β-actin as an endogenous reference gene. Finally, clinical efficacy of CTC count combined with GNB4/Riplet methylation detection for early diagnosis of HCC was analyzed. Results: The CTC of HCC patients has pleomorphic characteristics, but it is difficult to distinguish from other blood cells with non-obviously pleomorphic of CTC. Although a small number of CTCs can also be detected in HBV-DeCi patients (control group), the number is significantly lower than that in HCC patients, the sensitivity and specificity of CTC for HCC detection were 70.6% and 90.9% (AUC = 0.81). The Ct values of GNB4 and Riplet methylation were significantly different between HCC patients and control group patients. When CTC combined with two genes, the AUC value was significantly increased to 0.98, the sensitivity was 88.2%, and the specificity was 100%. Conclusion: Our study has developed a novel test that CTC count combined with GNB4/Riplet methylation detection and showed its high performance for early diagnosis of HCC.

Use of serum Golgi protein 73 for screening chronic hepatitis B virus infection patients needing antiviral therapy in the community.

Use of serum Golgi protein 73 for screening chronic hepatitis B virus infection patients needing antiviral therapy in the community.

Two-year free of complications during antiviral therapy predicts stable re-compensation in immediate-treatment HBV-related decompensated cirrhosis

Background and aims Disease progression could be altered or even reversed in decompensated patients with HBV-related cirrhosis once they initiate antiviral therapy. However, little is known about the stable re-compensation in these patients. Methods In this retrospective study, HBV-related liver cirrhosis patients were consecutively enrolled at the first decompensated event of ascites or variceal hemorrhage (VH), and divided into immediate-treatment, on-treatment and delayed/no treatment groups. Patients were followed up to at least presence of second decompensation event or to June 2021. Re-compensation was defined as patients who did not occur second (further) decompensation during follow-up. Results A total of 130 HBV-related decompensated cirrhotic patients were included with a median follow-up of 61.0 (41.6, 72.0) months. The cumulative incidence of re-compensation at year 6 was 39.0, 9.8 and 6.6 in immediate-treatment, on-treatment and delayed/no treatment group (p = 0.001). Among 87 patients in immediate-treatment group, thirty-seven (37/87, 42.5%) were recognized as stable re-compensation. Seventy percent (35/50) of second decompensated events occurred in the first 2 years. In patients free of 2-year decompensated complications, about 71.2% (37/52) maintained stable re-compensation. The cumulative incidence of death (and/or transplantation) and HCC in patients free of 2-year decompensated complications or not was 2.9 vs. 27.3% (HR 9.4, 95% CI 2.2–40.0, p = 0.002) and 12.6 vs. 37.7% (HR 4.5, 95% CI 1.5–13.3, p = 0.006), respectively. Conclusions In decompensated patients with HBV-related cirrhosis, about 40% in immediate-treatment group maintained stable re-compensation during 6 years of antiviral therapy. Two-year free of complications could predict stable re-compensation.

Trends in decompensated cirrhosis and hepatocellular carcinoma among people with a hepatitis B notification in New South Wales

Background & AimsPopulation-level trends and factors associated with HBV-related decompensated cirrhosis (DC), hepatocellular carcinoma (HCC), and liver-related mortality are crucial to evaluate the impacts of therapeutic interventions.MethodsTrends in HBV-DC and -HCC diagnoses and liver-related mortality in New South Wales, Australia, were determined through linkage of HBV notifications (1993-2017) to hospital admissions (2001-2018), mortality (1993-2018), and cancer registry (1994-2014) databases. Late HBV notification was defined as notification at or within 2 years of a DC or HCC diagnosis. Cox proportional-hazards regression and multivariable logistic regression analyses were performed to evaluate associated factors.ResultsAmong 60,660 people with a HBV notification, 1,276 (2.0%) DC and 1,087 (1.8%) HCC diagnoses, and 1,219 (2.0%) liver-related deaths were documented. Since the early 2000s, the number of DC and HCC diagnoses increased; however, age-standardised incidence decreased from 2.64 and 1.95 in 2003 to 1.14 and 1.09 per 1,000 person-years in 2017, respectively. Similarly, age-standardised liver mortality decreased from 2.60 in 2003 to 1.14 per 1,000 person-years in 2017. Among people with DC and HCC diagnoses, late HBV notification declined from 41% and 40% between 2001-2009 to 29% and 25% in 2010-2018, respectively. Predictors of DC diagnosis included older age (birth <1944, adjusted hazard ratio [aHR] 2.06, 95% CI 1.57–2.69), alcohol use disorder (aHR 4.82, 95% CI 3.96–5.87) and HCV co-infection (aHR 1.88, 95% CI 1.53–2.31). Predictors of HCC diagnosis included older age (birth <1944, aHR 3.94, 95% CI 2.91–5.32) and male sex (aHR 3.79, 95% CI 3.05–4.71).ConclusionIn an era of improved antiviral therapies, the risk of HBV-related liver morbidity and mortality has declined. HCV co-infection and alcohol use disorder are key modifiable risk factors associated with the burden of HBV.Lay summaryRising hepatitis B-related morbidity and mortality is a major public health concern. However, the development of highly effective medicines against hepatitis B virus (HBV) has brought renewed optimism for its elimination by 2030. This study shows a steady decline in HBV-related liver morbidity and mortality in New South Wales, Australia. Moreover, late hepatitis notification has also declined, allowing individuals with HBV to have access to timely antiviral treatment. Despite this, hepatitis C co-infection and alcohol use disorder are key modifiable risk factors associated with HBV disease burden. To attain the desired benefits from highly effective antiviral treatment, managing comorbidities, including hepatitis C and high alcohol use, must improve among individuals with hepatitis B.

Platelets, mean platelet volume, lymphocytes, leukocytes, and ratios of them altered in patients with hepatitis B virus‐related decompensated cirrhosis

Blood routine examination is an inexpensive, routinely performed clinical project, which includes many blood parameters. Hepatitis B virus (HBV) infection may have significant effects on blood parameters in decompensated patients with hepatitis B cirrhosis. However, details were not quite clear yet. A total of 207 HBV-related decompensated cirrhosis (HBV-DeCi) patients were included in this retrospective analysis. The included patients were subdivided into three groups: 44 patients with HBsAg, HBeAg, and HbcAb positive were set as Group I; 122 patients with HBsAg, HBeAb, and HbcAb positive were set as Group II; 41 patients with HBsAb, HBeAb, and HbcAb positive were set as Group III. Blood parameters, including platelet (PLT) count, mean platelet volume (MPV), lymphocyte count, leukocyte count and MPV/lymphocyte ratio (MPVLR), lymphocyte/ leukocyte ratio (LLR), platelet/leukocyte ratio (PLR) were analyzed respectively. The correlation between mentioned parameters and the HBV infection were characterized respectively. The values of PLT, MPVLR, and PLR in Group I and II were lower than that in Group III. Group II has a much higher LLR than that in Group I and III. HBV does have significantly effect on blood parameters in HBV-DeCi patients. Effective treatment must be applied to achieve cirrhosis recompensation promptly.

Chloride intercellular channel 3 suppression‐mediated macrophage polarization: a potential indicator of poor prognosis of hepatitis B virus‐related acute‐on‐chronic liver failure

Patients with hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) are characterized by immune paralysis and susceptibility to infections. Macrophages are important mediators of immune responses can be subclassified into two main phenotypes: classically activated and alternatively activated. However, few studies have investigated changes to macrophage polarization in HBV-related liver diseases. Therefore, we investigated the functional status of monocyte-derived macrophages (MDMs) from patients with mild chronic hepatitis B (n = 226), HBV-related compensated cirrhosis (n = 36), HBV-related decompensated cirrhosis (n = 40), HBV-ACLF (n = 62) and healthy controls (n = 10), as well as Kupffer cells (KCs) from patients with HBV-ACLF (n = 3). We found that during the progression of HBV-related liver diseases, the percentage of CD163+ CD206+ macrophages increased, while the percentage of CD80+ human leukocyte antigen-DR+ macrophages decreased significantly. MDMs and KCs mainly exhibited high CD163+ CD206+ expression in patients with HBV-ACLF, which predicted poor clinical outcome and higher liver transplantation rate. Transcriptome sequencing analysis revealed that chloride intracellular channel-3 (CLIC3) was reduced in patients with HBV-ACLF, indicating a poor prognosis. To further study the effect of CLIC3 on macrophage polarization, human monocytic THP-1 cell-derived macrophages were used. We found that classical and alternative macrophage activation occurred through nuclear factor kappa B (NF-κB) and phosphoinositide 3-kinase/protein kinase B pathways, respectively. CLIC3 suppression inhibited NF-κB activation and promoted the alternative activation. In conclusion, macrophage polarization gradually changed from classically activated to alternatively activated as HBV-related liver diseases progressed. Both CLIC3 suppression and increased alternatively activated macrophage percentage were potential indicators of the poor prognosis of patients with HBV-ACLF.

Efficacy and Safety of Yanggan Jian in Hepatitis B Virus-related Decompensated Cirrhosis: A Randomized, Double-blind, Controlled Trial.

The aim was to evaluate the efficacy and safety of Yanggan Jian (YGJ) in HBV-infected patients with decompensated cirrhosis. This randomized, double-blind controlled trial enrolled 160 patients with HBV-related decompensated cirrhosis who were already receiving or about to start antiviral therapy. Patients were randomly assigned to receive YGJ or placebo for 24 weeks, and were followed-up to 36 weeks. The primary outcome was the proportion of patients with a ≥2 point reduction in Child-Turcotte-Pugh (CTP) score from baseline at week 24. Secondary outcomes were CTP class and score, serum liver function indices, mortality, incidence of hepatocellular carcinoma and variceal bleeding. The proportion of patients with a CTP score reduction ≥2 was significantly greater in the YGJ than in the placebo group (p=0.009); the percentage of patients with CTP class C was significantly less than that in the placebo group (p<0.05), and the YGJ group had a significantly greater mean change from baseline in CTP score at week 24 (p=0.034). The improvement in measured values and change from baseline of prothrombin time, serum albumin, platelets, cholinesterase, international normalized ratio, and activated partial thromboplastin time were significantly better with YGJ than with placebo. Between-group differences in cumulative rates of variceal bleeding, hepatocellular carcinoma, death, or the frequency of any adverse event (AE), AEs related to treatment, or discontinuation because of AEs were not significant. YGJ significantly improved CTP scores and hepatic synthetic and reserve function in patients with HBV-related decompensated cirrhosis, and was safe and well tolerated.

Low Hemoglobin-to-Red Cell Distribution Width Ratio Is Associated with Mortality in Patients with HBV-Related Decompensated Cirrhosis.

Background The prognostic role of hemoglobin-to-red blood cell distribution width ratio (HRR) in HBV-related decompensated cirrhosis (HBV-DeCi) has not been established. The present study is aimed at determining the potential of HRR as a predictive factor for the prognosis of HBV-DeCi patients. Methods The study included 177 HBV-DeCi patients. The clinical outcome was death at 30 days. Multivariate regression analysis and receiver operating characteristic curve analysis were applied to assess the predictive value of HRR for poor outcomes. Results A total of 26 patients (14.7%) had died by 30 days. Patients with unfavorable outcomes had lower HRR than patients with favorable outcomes. Multivariate analysis revealed that HRR and Model for End-Stage Liver Disease (MELD) score were independently associated with poor outcomes. Combination of HRR and MELD score may improve prognostic accuracy in HBV-DeCi. Conclusions The present findings indicate that low HRR may be a promising predictor for mortality in HBV-DeCi patients.

Determinants of re-compensation in patients with hepatitis B virus-related decompensated cirrhosis starting antiviral therapy.

Despite antiviral therapy, liver function often fails to recover in patients with hepatitis B virus (HBV)-related decompensated cirrhosis. To establish a prognostic model to predict re-compensation in patients starting potent nucleos(t)ide analogue (NUC) therapy METHODS: We analysed 311 consecutive patients with HBV-related decompensated cirrhosis treated with entecavir or tenofovir. The primary outcome was re-compensation, defined as recovery to a Child-Pugh score of 5. The BC2AID score was developed from a cohort of 152 subjects based on competing risk models and validated in another cohort of 159 subjects. Re-compensation occurred in 57.2% and 66.7% of the subjects in the derivation and validation cohorts, respectively. Six independent predictors for re-compensation were identified in the derivation cohort and these comprised the BC2AID score: bilirubin ≤5mg/dL (adjusted sub-distribution hazard ratio [aSHR] 2.18), absence of severe complications (aSHR 2.78), alpha-fetoprotein (AFP) ≥50ng/mL (aSHR 2.54), alanine aminotransferase ≥200IU/L (aSHR 2.62), international normalised ratio ≤1.5 (aSHR 2.37) and ≤6months from initial decompensation until initiation of NUCs (aSHR 4.79). In the validation cohort, the area under the receiver operating characteristic curve of the BC2AID score for re-compensation within 1year of NUC therapy was significantly higher than that of the Child-Pugh, MELD, MELDNa and BE3A scores (0.813 vs 0.691, 0.638, 0.645 and 0.624, respectively; all P<0.05). Six clinical parameters, including AFP and the timing of antiviral therapy, were combined into a scoring system to accurately predict early re-compensation in patients with HBV-related decompensated cirrhosis.

Serum potassium levels and prognosis in HBV-associated decompensated cirrhosis.

BackgroundSerum potassium disorders are commonly seen in patients with advanced cirrhosis and have a detrimental effect on clinical outcome, but its role in HBV‐related decompensated cirrhosis (DeCi) is remained to be illustrated. We aim to assess the effects of serum potassium on outcomes in HBV‐DeCi patients.MethodsRetrospective study included 155 subjects. Multivariate analysis was used to determine the independent prognostic factor. Predictive ability of mortality for variables was determined using the receiver operating characteristics curves.ResultsThe 30‐day in‐hospital mortality was 12.9%. Serum potassium levels differed markedly between survivors and non‐survivors. On multivariate analysis, Model for End‐Stage Liver Disease (MELD) score and serum potassium level were identified as independent predictors of outcomes in HBV‐DeCi patients. The combination of serum potassium and MELD score could improve prognostic accuracy in these patients.ConclusionsOur findings suggest that serum potassium is an effective predictor for poor outcomes in HBV‐DeCi patients.

Long-term prognosis with or without nucleot(s)ide analogue therapy in hepatitis B virus-related decompensated cirrhosis.

The development of nuleos(t)ide analogues (NAs) has dramatically changed the natural history of chronic hepatitis B virus (HBV) infection. In this study, we compared patients with HBV-related decompensated cirrhosis with and without NA therapy in terms of hepatocarcinogenesis and all-cause, liver-related, and non-liver-related mortality. This study enrolled 160 patients with decompensated cirrhosis, 78 of whom were treated with NA therapy (NA group) and 82 of whom were not (non-NA group). Propensity score matching and inverse probability weighting were performed to adjust the baseline characteristics in the NA and non-NA groups. Liver-related and non-liver-related mortality were analysed using the competing risks IPW cumulative incidence functions estimator. The Cox proportional hazards model and the Fine and Gray proportional hazards model were used to analyse factors associated with hepatocarcinogenesis and all-cause, liver-related, and non-liver-related mortality. HBV DNA ≥20,000IU/ml (adjusted hazard ratio [aHR], 8.440) and dyslipidemia (aHR, 0.178) were independently associated with hepatocarcinogenesis. HBV DNA ≥20,000IU/ml (aHR, 4.360) and non-NA group (aHR, 4.802) were independently associated with all-cause mortality. Diabetes mellitus (aHR, 4.925), FIB-4 score >3.6 (aHR, 4.151), non-NA group (aHR, 9.180), presence of dyslipidemia (aHR, 0.182) and male gender (aHR, 3.045) were independently associated with liver-related mortality. HBV DNA ≥20,000IU/ml (aHR, 3.216) and high age (aHR, 2.692) were independently associated with non-liver-related mortality. Although the cumulative incidence rate of hepatocarcinogenesis and non-liver-related mortality was not reduced by NA therapy, viral suppression reduced liver-related mortality in patients with DC.

Anemia Predicts Poor Outcomes in Patients with HBV-Related Decompensated Cirrhosis.

Anemia is common in patients with severe chronic liver disease, but its role in HBV-related decompensated cirrhosis (DeCi) is still unclear. We therefore aimed to assess the impact of anemia on prognosis in HBV-DeCi patients. One hundred thirty-three patients diagnosed with HBV-DeCi were retrospectively collected. A total of 113 (85.0%) patients suffered from anemia in our cohort. The low hemoglobin (Hb) level group exhibited a significantly increased 28-day mortality rate compared with the high Hb group. Hb level was a predictor of 28-day mortality in HBV-DeCi patients. Reduced Hb levels were associated with unfavorable prognosis in HBV-DeCi patients, and more attention should be paid to anemia in routine clinical assessments of liver cirrhosis.