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Objectives: To determine the value of periportal hyperintensity sign from gadobenate dimeglumine (Gd-BOPTA)-enhanced hepatobiliary phase (HBP) magnetic resonance imaging (MRI) for predicting clinical outcomes in patients with decompensated cirrhosis. Methods: A total of 199 cirrhotic patients who underwent Gd-BOPTA-enhanced MRI were divided into control group (n = 56) and decompensated cirrhosis group (n = 143). The presence of periportal hyperintensity sign on HBP MRI was recorded. The Cox regression model was used to investigate the association between periportal hyperintensity sign and clinical outcomes. Results: There was a significant difference in the frequency of periportal hyperintensity sign on HBP between compensated and decompensated cirrhotic patients (p < 0.05). After a median follow-up of 29.0 months (range, 1.0–90.0 months), nine out of 143 patients (6.2%) with decompensated cirrhosis died. Periportal hyperintensity sign on HBP MRI was a significant risk factor for death (hazard ratio (HR) = 23.677; 95% confidence interval (CI) = 4.759–117.788; p = 0.0001), with an area under the curve (AUC) of 0.844 (95% CI = 0.774–0.899). Thirty patients (20.9%) developed further decompensation. Periportal hyperintensity sign on HBP MRI was also a significant risk factor for further decompensation (HR = 2.594; 95% CI = 1.140–5.903; p = 0.023). Conclusions: Periportal hyperintensity sign from Gd-BOPTA-enhanced HBP MRI is valuable for predicting clinical outcomes in patients with decompensated cirrhosis. Critical relevance statement: Periportal hyperintensity sign from gadobenate dimeglumine-enhanced hepatobiliary phase magnetic resonance imaging is a new noninvasive method to predict clinical outcomes in patients with decompensated cirrhosis. Key points: • There was a significant difference in the frequency of periportal hyperintensity sign on HBP between compensated and decompensated cirrhotic patients. • Periportal hyperintensity sign on the hepatobiliary phase was a significant risk factor for death in patients with decompensated cirrhosis. • Periportal hyperintensity sign on the hepatobiliary phase was a significant risk factor for further decompensation in patients with decompensated cirrhosis. [ABSTRACT FROM AUTHOR]

Simple Summary: Cirrhosis is the end-stage of chronic hepatitis, characterized by the replacement of hepatic parenchyma with fibrous tissue and regenerative nodules. In cirrhotic livers, reduced hepatic function and interference with portal blood flow cause sinusoidal portal hypertension, resulting in secondary complications such as varices, ascites, and hepatic encephalopathy. In human medicine, computed tomography (CT) is the most sensitive diagnostic imaging technique used to evaluate hepatic morphological change. However, there is limited information on the CT features of cirrhosis in dogs. This study aimed to describe the CT characteristics of histologically confirmed cirrhosis and to compare these characteristics between compensated and decompensated cirrhosis. The results of this study can aid clinicians in diagnosing cirrhosis and predicting the progression of cirrhosis to the decompensated phase. This study aimed to describe computed tomography (CT) characteristics of histologically confirmed cirrhosis and to compare these CT characteristics between compensated and decompensated cirrhosis. Sixteen dogs who underwent contrast CT and histopathological examinations were included; eleven dogs were assigned to the compensated group, and five dogs were assigned to the decompensated group. Irregular hepatic contours with a diffuse nodular distribution and hepatic lymph node enlargement are common concomitant features of cirrhotic livers on CT images. The enhancement patterns of the regenerative nodules and hepatic parenchyma were not significantly different from each other. Hypoattenuating areas with delayed contrast enhancement indicating fibrotic tissue were confirmed in 56.3% of cases. Hypoattenuating wedge-shaped area or nodule with minor or no contrast enhancement (histopathologically confirmed as focal necrosis) were confirmed in 37.5% of cases. Among CT variables, only normalized liver volume and portal vein-to-aorta ratio were significantly lower (p = 0.038 and 0.003, respectively) in the decompensated group. In conclusion, this study presented the CT features of cirrhosis and identified CT features that can discriminate between compensated and decompensated cirrhosis. Specifically, lower normalized liver volume and the portal vein-to-aorta ratio might be useful indicators for the progression of cirrhosis to the decompensated phase. [ABSTRACT FROM AUTHOR]

Introduction: This study aimed to investigate the liver-related outcomes of newly suggested metabolic dysfunction-associated steatotic liver disease (MASLD) and MASLD with increased alcohol intake (MetALD), as well as alcohol-associated liver disease (ALD). Methods: From a National Health Insurance Service Health Screening Cohort, we included 369,094 participants who underwent health checkups between 2009 and 2010 in South Korea. Steatotic liver disease (SLD) was defined as a fatty liver index ≥60. The risk of primary liver cancer (PLCa), hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (iCCA), incident cirrhosis, and decompensated cirrhosis was compared with no SLD. The subdistribution hazard ratio (SHR) was calculated using the Fine-Gray model regarding competing risks. Results: A total of 3,232 participants (0.9%) developed PLCa during the median follow-up of 3,227,176 person-years: 0.5% with no SLD, 1.1% with MASLD, 1.3% with MetALD, and 1.9% with ALD. Competing risk analysis revealed that compared with no SLD, MASLD (SHR: 1.65; 95% CI: 1.44−1.88), MetALD (SHR: 1.87; 95% CI: 1.52−2.29), and ALD (SHR: 1.86; 95% CI: 1.39−2.49) were associated with an increased risk of PLCa. MASLD (SHR: 1.96; 95% CI: 1.67−2.31), MetALD (SHR: 2.23; 95% CI: 1.75−2.84), and ALD (SHR: 2.34; 95% CI: 1.67−3.29) were associated with a higher risk of HCC. No significant difference was observed in the risk of iCCA. The risk of incident cirrhosis and decompensated cirrhosis increased in the order of no SLD, MASLD, MetALD, and ALD. Conclusion: MASLD, MetALD, and ALD have an increased risk of PLCa, HCC, incident cirrhosis, and decompensated cirrhosis but not iCCA. These findings may serve as a robust ground for the prognostic value of the newly suggested MASLD and MetALD. [ABSTRACT FROM AUTHOR]

There is no established rescue therapy for hepatitis C patients with decompensated cirrhosis who experience treatment failure on 12-week sofosbuvir (SOF)/velpatasvir (VEL) therapy that is the only approved regimen for decompensated cirrhosis in Japan. We experienced a patient with decompensated cirrhosis who showed virologic relapse at post-treatment week 7 following 12-week SOF/VEL therapy. She had resistance-associated substitutions (RASs) against VEL before therapy but did not achieve new RASs against VEL or SOF after therapy. We considered rescue therapy following strong demand from her and her family. The drug adherence of therapy was 100%, and the treatment was well tolerated. Because we prioritized the safety and drug adherence of the regimen, we performed prolonged 24-week SOF/VEL therapy without ribavirin at her own expense with the approval of the ethics board in the hospital where the first author belongs. Fortunately, a sustained virologic response 24 was achieved without any adverse events. Hepatocellular carcinoma that had developed after 12-week SOF/VEL therapy recurred and was treated near the end of rescue therapy, but hepatic functional reserve improved. Although this was a single case report and was assumed to be very rare, the same regimen might be effective for treatment failure with 12-week SOF/VEL therapy. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Clinical Hepatology / Linchuang Gandanbing Zazhi is the property of Journal of Clinical Hepatology 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.)

Objectives: To determine the value of periportal hyperintensity sign from gadobenate dimeglumine (Gd-BOPTA)-enhanced hepatobiliary phase (HBP) magnetic resonance imaging (MRI) for predicting clinical outcomes in patients with decompensated cirrhosis. Methods: A total of 199 cirrhotic patients who underwent Gd-BOPTA-enhanced MRI were divided into control group (n = 56) and decompensated cirrhosis group (n = 143). The presence of periportal hyperintensity sign on HBP MRI was recorded. The Cox regression model was used to investigate the association between periportal hyperintensity sign and clinical outcomes. Results: There was a significant difference in the frequency of periportal hyperintensity sign on HBP between compensated and decompensated cirrhotic patients (p < 0.05). After a median follow-up of 29.0 months (range, 1.0–90.0 months), nine out of 143 patients (6.2%) with decompensated cirrhosis died. Periportal hyperintensity sign on HBP MRI was a significant risk factor for death (hazard ratio (HR) = 23.677; 95% confidence interval (CI) = 4.759–117.788; p = 0.0001), with an area under the curve (AUC) of 0.844 (95% CI = 0.774–0.899). Thirty patients (20.9%) developed further decompensation. Periportal hyperintensity sign on HBP MRI was also a significant risk factor for further decompensation (HR = 2.594; 95% CI = 1.140–5.903; p = 0.023). Conclusions: Periportal hyperintensity sign from Gd-BOPTA-enhanced HBP MRI is valuable for predicting clinical outcomes in patients with decompensated cirrhosis. Critical relevance statement: Periportal hyperintensity sign from gadobenate dimeglumine-enhanced hepatobiliary phase magnetic resonance imaging is a new noninvasive method to predict clinical outcomes in patients with decompensated cirrhosis. Key points: • There was a significant difference in the frequency of periportal hyperintensity sign on HBP between compensated and decompensated cirrhotic patients. • Periportal hyperintensity sign on the hepatobiliary phase was a significant risk factor for death in patients with decompensated cirrhosis. • Periportal hyperintensity sign on the hepatobiliary phase was a significant risk factor for further decompensation in patients with decompensated cirrhosis. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Modern Medicine & Health is the property of Journal of Modern Medicine & Health 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: Hyponatremia portends a poor prognosis in decompensated cirrhosis and is an independent predictor of mortality. Multiple modalities have been evaluated in the management of hyponatremia, including albumin infusion. However, the effect of albumin infusion on the resolution of hyponatremia is unclear. We conducted a systematic review to explore the available literature on the use of albumin infusion in hyponatremia. Methods: We performed a comprehensive search up to 31st December 2022 using MEDLINE, EMBASE, and Scopus for studies reporting the effectiveness of albumin infusion in the resolution of hyponatremia. The impact of albumin infusion of any dose, administration frequency, and duration of therapy was recorded. The study protocol was prospectively registered (CRD42021245914). Results: The literature search yielded 1322 references after duplicate removal. Only seven studies (three randomized trials, three cohort studies, and one case series) satisfied the predefined selection criteria after a full-text review. While hyponatremia was clearly defined as serum sodium < 130 meEq/L in all studies, two studies explicitly defined hyponatremia resolution (serum sodium > 135 mEq/L). No differentiation was made between the types of hyponatremia. The strength of the albumin infusion used was 5% and 20%. All but one study reported significant improvement in hyponatremia with albumin infusion. A subgroup analysis showed albumin infusion improved 30-day survival (odds ratio 0.43, 95% CI 0.25–0.74, I2 = 0.) No studies reported adverse events or the impact of concomitant associations (diuretic withdrawal, lactulose use, sepsis). Conclusion: Despite available literature on the use of albumin infusion for the resolution of hyponatremia, the level of evidence remains low. Large prospective studies with pre-defined selection criteria and endpoints are required to generate the evidence. [ABSTRACT FROM AUTHOR]

Background and Aims: Decompensated‐cirrhosis encompasses several stages with different prognosis, such as bleeding, ascites and bleeding‐plus‐ascites. Development of further‐decompensation worsens survival, while non‐selective β‐blockers (NSBBs) can modify the risk. However, how this applies to each stage is uncertain. We aimed to investigate, in each stage of decompensated‐cirrhosis, the influence of further‐decompensation on mortality and whether changes in portal‐pressure (HVPG) under NSBBs influence these outcomes. Methods: Patients with variceal bleeding were consecutively included differentiating those with bleeding‐alone from those who also had ascites. Patients with ascites and high‐risk varices referred for primary‐prophylaxis were also investigated. A baseline haemodynamic study was performed and was repeated after 1‐3‐months under NSBBs. Outcomes were investigated by competing‐risk. Results: Totally 103 patients had bleeding‐alone, 186 bleeding‐plus‐ascites and 187 ascites‐alone. Mean follow‐up was 32‐months (IQR, 12–60). Patients with bleeding‐plus‐ascites had higher HVPG and were more hyperdynamic than patients with ascites‐alone and these than those with bleeding‐alone. At each stage, the mortality risk was more than twice in patients developing further‐decompensation vs. those without (p <.001). In each stage, HVPG‐decrease under NSBBs showed better discrimination to predict further‐decompensation than the baseline MELD, Child–Pugh or HVPG, by time‐dependent ROC‐curves (c‐statistic >70%). At each stage, patients without HVPG‐decreases, either ≥10% or ≥20% from the baseline, had higher risk of further‐decompensation (sHR from 2.43 to 6.73, p <.01) and worse survival. Conclusions: In each stage of decompensated cirrhosis, mortality risk significantly and very markedly increase with further‐decompensation. HVPG‐non‐response to NSBBs may adequately stratify the risk of further decompensation and death, in each stage. This suggests potential benefit with pre‐emptive therapies in HVPG‐non‐responders at each‐stage. [ABSTRACT FROM AUTHOR]

Key Clinical Message: We present a case of Cronkhite–Canada syndrome in a patient with decompensated cirrhosis who had successful induction of remission with nutritional supplementation alone. We propose that early institution of high‐protein, high‐energy enteral supplementation should be offered to all patients, especially those with compelling contraindications to immunosuppression. [ABSTRACT FROM AUTHOR]

Purpose of Review: The purpose of this review is to describe how implementation research methods can inform increased adoption of palliative care for patients with cirrhosis. Recent Findings: Research demonstrates that specialty palliative care consultation and care improve health and health service outcomes for patients with cirrhosis, yet few patients receive such care. Summary: Getting To Implementation (GTI) and other implementation process models can offer steps to improve the implementation of evidence-based hepatology care. Future work should identify the combinations of implementation strategies that can promote equitable implementation of palliative care services for this vulnerable population. [ABSTRACT FROM AUTHOR]

The current treatment approach to patients with liver cirrhosis relies on the individual management of complications. Consequently, there is an unmet need for an overall therapeutic strategy for primary and secondary prevention of complications. The clinical potential of long‐term albumin infusions supported by recent clinical trials has expanded its indications and holds promise to transform the management and secondary prevention of cirrhosis‐related complications. This renewed interest in albumin comes with inherent controversies, compounding challenges and pressing need for rigorous evaluation of its clinical potential to capitalize on its therapeutic breakthroughs. Australia is among a few countries worldwide to adopt outpatient human albumin infusion. Here, we summarize currently available evidence of the potential benefits of human albumin for the management of multiple liver cirrhosis‐related complications and discuss key challenges for wide application of long‐term albumin administration strategy in Australian clinical practice. Australian Gastroenterological week (AGW), organised by the Gastroenterological Society of Australia (GESA), was held between 9‐11 September 2022. A panel of hepatologists, advanced liver nurses and one haematologist, were invited to a roundtable meeting to discuss the use of long‐term albumin infusions for liver cirrhosis. management in Australia. In this review, we summarise the proceedings of this meeting in context of the current literature. [ABSTRACT FROM AUTHOR]

Type‐2 diabetes mellitus is a frequent comorbidity of cirrhosis independently associated with cirrhosis‐related complications and mortality. This post hoc analysis of the ANSWER trial database assessed the effects of long‐term human albumin (HA) administration on top of the standard medical treatment (SMT) on the clinical outcomes of a subgroup of 85 outpatients with liver cirrhosis, uncomplicated ascites and insulin‐treated diabetes mellitus type 2 (ITDM). Compared to patients in the SMT arm, the SMT + HA group showed a better overall survival (86% vs. 57%, p =.016) and lower incidence rates of paracenteses, overt hepatic encephalopathy, bacterial infections, renal dysfunction and electrolyte disorders. Hospital admissions did not differ between the two arms, but the number of days spent in hospital was lower in the SMT + HA group. In conclusion, in a subgroup of ITDM outpatients with decompensated cirrhosis and ascites, long‐term HA administration was associated with better survival and a lower incidence of cirrhosis‐related complications. [ABSTRACT FROM AUTHOR]

Chronic hepatitis B and C are among the most significant infectious diseases worldwide, and are major risk factors for liver cirrhosis and liver cancer. In Japan, comprehensive hepatitis measures are implemented for the testing and treatment of viral hepatitis, thus enabling the early diagnosis of liver cancer. Nevertheless, patients with decompensated cirrhosis and liver cancer often have unfavorable prognoses and require repetitive long‐term treatment. In fiscal year 2018, an integrated policy of medical expense subsidies and research was established in Japan that aimed to alleviate patients' financial burden and launch the clinical registry of advanced liver disease. Over time, updates to the eligibility for the subsidy increased access to patients and has led to an increased number of beneficiaries. Additionally, the accumulation of clinical data in the registry has revealed the treatment choices for these diseases. However, the disparities in efforts across prefectures have also become evident. Raising public awareness of the policy and tightening the multisector healthcare network are keys to success in supporting qualifying patients with advanced liver disease. [ABSTRACT FROM AUTHOR]

Cardiac morphology and function, which are conventionally evaluated by echocardiography, are often abnormal in decompensated cirrhosis. We aimed to evaluate the association of echocardiography-related parameters with prognosis in cirrhosis. This retrospective study included 104 decompensated cirrhotic patients, in whom cardiac structure and function were measured by echocardiography, including mitral inflow early diastolic velocity/mitral inflow late diastolic velocity (E/A), left atrium diameter, left ventricular end-diastolic dimension, interventricular septal thickness, left ventricular posterior wall thickness, right atrial transverse diameter, right atrial longitudinal diameter, right ventricular dimension (RVD), stroke volume, cardiac output, left ventricular ejection fraction, and fractional shortening. Cox regression and competing risk analyses and Kaplan-Meier and Nelson-Aalen cumulative risk curves were used to evaluate their associations with further decompensation and death in cirrhotic patients, if appropriate. Lower RVD was a predictor of further decompensation in Cox regression (adjusted by Child-Pugh score: p = 0.138; adjusted by MELD score: p = 0.034) and competing risk analyses (p = 0.003), and RVD ≤17 mm was significantly associated with higher cumulative incidence of further decompensation in Kaplan-Meier (p = 0.002) and Nelson-Aalen cumulative risk curves (p = 0.002). E/A ≤ 0.8 was a significant predictor of death in Cox regression (adjusted by Child-Pugh score: p = 0.041; adjusted by MELD score: p = 0.045) and competing risk analyses (p = 0.024), and E/A ≤ 0.8 was significantly associated with higher cumulative incidence of death in Kaplan-Meier (p = 0.023) and Nelson-Aalen cumulative risk curves (p = 0.024). Other echocardiography-related parameters were not significantly associated with further decompensation or death. RVD and E/A may be considered for the prognostic assessment of decompensated cirrhosis. [ABSTRACT FROM AUTHOR]

Background: Extracellular vesicles (EVs) modulate inflammation, coagulation and vascular homeostasis in decompensated cirrhosis. Aim: To characterize the profile of plasmatic EVs in patients with decompensated cirrhosis and bacterial infections and evaluate the association between EVs and the development of hemostatic complications. Methods: We measured the levels of EVs using high-sensitivity flow cytometry and phospholipid-dependent clotting time (PPL) in a prospective cohort of hospitalized patients with acutely decompensated cirrhosis with versus without bacterial infections. A separate cohort of patients with bacterial infections without cirrhosis was also enrolled. We measured endothelium-, tissue factor (TF)-bearing, platelet- and leukocyte-derived EVs. In patients with infections, EVs were reassessed upon resolution of infection. Bleeding and thrombotic complications were recorded during 1-year follow-up. Results: Eighty patients with decompensated cirrhosis were recruited (40 each with and without bacterial infections). Electron microscopy confirmed the presence of plasma EVs. Despite no difference in total EVs and PPL, patients with cirrhosis and infection had significantly higher TF+ EVs, P-Selectin+ EVs (activated platelet-derived), CD14+ EVs (monocyte/macrophages derived) and CD14+ TF+ EVs versus those with cirrhosis without infection. Upon infection resolution, levels of these EVs returned to those without infection. Patients with infections showed a significant association between reduced P-Selectin+ EVs and bleeding complications (HR 8.0 [95%CI 1.3-48.1]), whereas high levels of leukocyte-derived EVs (CD45+) and CD14+ EVs were significantly associated with thrombotic complications (HR 16.4 [95%CI 1.7-160] and 10.9 [95%CI 1.13-106], respectively). Results were confirmed in a validation cohort. Conclusion: Bacterial infections are associated with particular alterations of plasma EVs profile in decompensated cirrhosis. Bacterial infections trigger the release of EVs originating from various cell types, which may tip the precarious hemostatic balance of patients with acutely decompensated cirrhosis towards hyper- or hypocoagulability. [ABSTRACT FROM AUTHOR]

Patients with chronic hepatitis C virus (HCV) infection and decompensated cirrhosis are an important population for antiviral therapy yet under-represented in clinical trials. HCV direct-acting antiviral (DAA) therapies, unlike interferon-containing regimens, can be safely utilized in decompensated patients. Per guidelines from the American Association for the Study of Liver Diseases (AASLD), therapy of choice in HCV and decompensated cirrhosis is sofosbuvir, an HCV polymerase inhibitor, combined with a replication complex inhibitor (NS5A inhibitor) with or without ribavirin. Combination therapy with a HCV protease inhibitor and an NS5A inhibitor is effective in this population but is specifically not recommended in AASLD guidelines due to safety concerns. Important risk factors for further decompensation during DAA therapy are serum albumin < 3.5 g/dL, MELD (Model for End-Stage Liver Disease) score > 14, or HCV genotype 3 infection. Although sustained virologic response (SVR) is achieved less often in patients with decompensated vs compensated cirrhosis, in clinical studies response rates are > 80%. Both Child-Turcotte-Pugh Class at baseline and viral genotype can affect these response rates. Achieving SVR lowers risk of mortality, but to a lesser extent than in individuals with compensated cirrhosis. Likewise, treating patients for HCV infection along with successful treatment for hepatocellular carcinoma improves risks of both liver-related and overall mortality. In fewer than one third of cases, treating transplant-eligible, HCV-infected patients pre-transplant enables their delisting from transplant wait lists. [ABSTRACT FROM AUTHOR]

Objective: To determine the incidence of decompensated cirrhosis and associated risk factors in people hospitalised with non-alcoholic fatty liver disease (NAFLD) or non- alcoholic steatohepatitis (NASH) with or without cirrhosis. Design: Retrospective cohort study; analysis of linked Queensland Hospital Admitted Patient Data Collection, Queensland Registry of Births, Deaths and Marriages, and Queensland Cancer Register data. Setting, participants: Queensland residents aged 20 years or older admitted to Queensland hospitals with NAFLD/NASH during 1 July 2009 - 31 December 2018. Main outcome measures: Progression to decompensated cirrhosis (ascites, hepatic encephalopathy, or oesophageal variceal bleeding). Results: We included data for 8006 patients in our analysis (10 082 admissions), including 4632 women (58%) and 2514 people with diabetes mellitus (31%); median follow- up time was 4.6 years (interquartile range, 2.7-7.2 years). Three hundred and fifty- one people (4.4%) experienced decompensated cirrhosis during the follow- up period. Of the 6900 people without cirrhosis, 4.5% (95% confidence interval [CI], 3.6-5.7%) experienced decompensated cirrhosis within ten years (mean, 0.5% per year; 95% CI, 0.4-0.6% per year); risk of progression was greater for people aged 70 years or older (v 20-39 years: adjusted hazard ratio [aHR], 4.7; 95% CI, 2.0-11.0) and those who had extrahepatic cancers (aHR, 5.0; 95% CI, 3.0-8.2), history of major cardiovascular events (aHR, 1.9; 95% CI, 1.2-3.1), or diabetes mellitus (aHR, 2.8; 95% CI, 2.0-3.9). Of the 1106 people with cirrhosis, 32.4% (95% CI, 27.2-38.3%) experienced decompensated cirrhosis within ten years (mean, 5.5% per year; 95% CI, 4.8-6.3% per year); risk of progression was greater for those with portal hypertension (aHR, 1.8; 95% CI, 1.3-2.7), extrahepatic cancer (aHR, 1.8; 95% CI, 1.1-2.9), or diabetes mellitus (aHR, 1.5; 95% CI, 1.1-2.0). Compared with people who had neither cirrhosis nor diabetes mellitus, the risk of decompensation was greater for people with cirrhosis (aHR, 10.7; 95% CI, 7.6-15.0) or cirrhosis and diabetes mellitus (aHR, 14.4; 95% CI, 10.1-20.6). Conclusions: Given the greater risk of progression to cirrhosis decompensation in people with diabetes mellitus, a disorder common in people with NAFLD/NASH, identifying advanced fibrosis and providing appropriate treatment for averting disease progression is vital. [ABSTRACT FROM AUTHOR]

Aim: To determine the outcomes concerning portal venous blood flow and portosystemic shunts in patients with decompensated cirrhosis due to hepatitis C virus (HCV) infection who achieved sustained viral response (SVR) following antiviral therapy. Methods: Portal hypertension‐related events and liver function were evaluated in 24 patients achieving SVR following sofosbuvir plus velpatasvir therapy. Results: Serum albumin level (median; g/dL) increased from 2.9 at baseline to 3.5 at 12 weeks after the end of treatment (EOT) (p = 0.005), while liver volumes (cm3) decreased from 1260 to 1150 (p = 0.0002). Portal hypertension‐related events developed in 10 patients (41.7%), and the cumulative occurrence rates after the EOT were 29.2%, 33.3%, and 46.1% at 24, 48, and 96 weeks, respectively. Multivariate logistic regression analysis revealed that the maximal diameter of the shunts (p = 0.0235) was associated with the development of the events, with a cut‐off value of 8.3 mm (p = 0.0105). Meanwhile, multiple linear regression analysis revealed that portal venous blood flow, liver volume, serum albumin, and bilirubin levels at baseline were associated with serum albumin levels at 12 weeks after EOT (p = 0.0019, p = 0.0154, p = 0.0010, and p = 0.0350, respectively). Conclusion: In patients with decompensated cirrhosis due to HCV infection, the baseline portal venous blood flow and liver volume and function were predictive of liver function following SVR, while the maximal diameter of portosystemic shunts predicted the occurrence of portal hypertension‐related events. [ABSTRACT FROM AUTHOR]

Follicular cholangitis (FC) is a rare non-neoplastic biliary tract disease first reported in 2003. A 74-year-old woman underwent extended left hepatectomy with a diagnosis of intrahepatic cholangiocarcinoma. Histopathological examination of the surgical specimen demonstrated no malignant findings, and lymphocytic infiltration with lymphoid follicles was observed within the bile duct wall. Along with immunohistochemical findings, the patient was diagnosed with FC. More than 3 years after surgery, the patient exhibited elevated hepatobiliary enzymes and total bilirubin. Endoscopic retrograde cholangiography revealed stricture and dilation from the extrahepatic bile duct to the right intrahepatic bile duct. Histopathological findings uncovered lymphocytic infiltration without malignant results. It was concluded that bile duct stricture due to FC had newly developed in her remnant liver. Subsequently, the patient developed hypoalbuminemia, and abdominal computed tomography revealed atrophy of the remnant liver and ascites accumulation. Esophagogastroduodenoscopy exposed the development of esophageal varices, which were not observed preoperatively. The patient was diagnosed with decompensated liver cirrhosis accompanied by portal hypertension. This case strongly suggests that long-term follow-up after surgery may be required for patients with FC for screening of potential new bile duct stricture and progression to liver cirrhosis due to cholestasis. [ABSTRACT FROM AUTHOR]

A fixed-dose combination of sofosbuvir/velpatasvir (SOF/VEL) plus weight-based ribavirin (RBV) for 12 weeks is recommended for the treatment of patients with hepatitis C virus (HCV)-associated decompensated cirrhosis. However, large global studies, while confirming the effectiveness of SOF/VEL in a broad range of patients, often exclude these patients. This Phase 2, single-arm, open-label study in adult patients with HCV-associated decompensated cirrhosis in France and the USA aimed to provide further data on the safety and efficacy of SOF/VEL plus RBV for 12 weeks in this population. Patients were treated with a fixed-dose combination of SOF 400 mg/VEL 100 mg plus weight-based RBV once daily for 12 weeks. The inclusion criteria were chronic HCV infection (≥6 months), quantifiable HCV RNA at screening, Child–Turcotte–Pugh class B or C cirrhosis, and liver imaging within 6 months of Day 1 to exclude hepatocellular carcinoma. Among 32 patients who initiated treatment, 78.1% achieved sustained virologic response 12 weeks after the end of treatment (SVR12). Failure to achieve SVR12 was due to non-virologic reasons (investigator discretion, n = 1; death, n = 6). All 25 patients in the per-protocol population achieved SVR12 and all but one achieved sustained virologic response 24 weeks after the end of treatment. Adverse events (AEs) were as expected for a patient population with advanced liver disease. All Grade 3–4 and serious AEs and deaths were deemed unrelated to treatment. In patients with HCV-associated decompensated cirrhosis, SOF/VEL plus RBV achieved high SVR12 rates and was generally well tolerated. [ABSTRACT FROM AUTHOR]

Objective: To determine the incidence of decompensated cirrhosis and associated risk factors in people hospitalised with non‐alcoholic fatty liver disease (NAFLD) or non‐alcoholic steatohepatitis (NASH) with or without cirrhosis. Design: Retrospective cohort study; analysis of linked Queensland Hospital Admitted Patient Data Collection, Queensland Registry of Births, Deaths and Marriages, and Queensland Cancer Register data. Setting, participants: Queensland residents aged 20 years or older admitted to Queensland hospitals with NAFLD/NASH during 1 July 2009 – 31 December 2018. Main outcome measures: Progression to decompensated cirrhosis (ascites, hepatic encephalopathy, or oesophageal variceal bleeding). Results: We included data for 8006 patients in our analysis (10 082 admissions), including 4632 women (58%) and 2514 people with diabetes mellitus (31%); median follow‐up time was 4.6 years (interquartile range, 2.7–7.2 years). Three hundred and fifty‐one people (4.4%) experienced decompensated cirrhosis during the follow‐up period. Of the 6900 people without cirrhosis, 4.5% (95% confidence interval [CI], 3.6–5.7%) experienced decompensated cirrhosis within ten years (mean, 0.5% per year; 95% CI, 0.4–0.6% per year); risk of progression was greater for people aged 70 years or older (v 20–39 years: adjusted hazard ratio [aHR], 4.7; 95% CI, 2.0–11.0) and those who had extrahepatic cancers (aHR, 5.0; 95% CI, 3.0–8.2), history of major cardiovascular events (aHR, 1.9; 95% CI, 1.2–3.1), or diabetes mellitus (aHR, 2.8; 95% CI, 2.0–3.9). Of the 1106 people with cirrhosis, 32.4% (95% CI, 27.2–38.3%) experienced decompensated cirrhosis within ten years (mean, 5.5% per year; 95% CI, 4.8–6.3% per year); risk of progression was greater for those with portal hypertension (aHR, 1.8; 95% CI, 1.3–2.7), extrahepatic cancer (aHR, 1.8; 95% CI, 1.1–2.9), or diabetes mellitus (aHR, 1.5; 95% CI, 1.1–2.0). Compared with people who had neither cirrhosis nor diabetes mellitus, the risk of decompensation was greater for people with cirrhosis (aHR, 10.7; 95% CI, 7.6–15.0) or cirrhosis and diabetes mellitus (aHR, 14.4; 95% CI, 10.1–20.6). Conclusions: Given the greater risk of progression to cirrhosis decompensation in people with diabetes mellitus, a disorder common in people with NAFLD/NASH, identifying advanced fibrosis and providing appropriate treatment for averting disease progression is vital. [ABSTRACT FROM AUTHOR]

Purpose of Review: Hepatorenal syndrome (HRS), the severe manifestation of renal injury in patients with cirrhosis and acute on chronic liver failure (ACLF), is characterized by decreased renal blood flow and glomerular filtration rate. Manuscript will elaborate how acute kidney injury (AKI) is different in ACLF and cirrhosis. Recent Findings: We have role of biomarkers in differentiating HRS AKI from chronic kidney disease (CKD) in cirrhosis as well as ACLF patients. Medical therapy, timing of extracorporeal therapies, and role of liver transplant in patients of cirrhosis and ACLF. Summary: ACLF patients usually have structural form of AKI as compared to functional-volume responsive AKI in patients with cirrhosis. Combination of terlipressin and albumin augments renal recovery faster than other vasopressor therapies. But, liver transplant always remain the definitive treatment of progressive renal failure in patients with cirrhosis as well as ACLF. [ABSTRACT FROM AUTHOR]

Our study aimed to investigate the prognostic value of neutrophil count to albumin ratio (NAR) in predicting short-term mortality of patients with decompensated cirrhosis (DC). A total of 623 DC patients were recruited from a retrospective observational cohort study. They were admitted to our hospital from January 2014 to December 2015. NAR of each patient was calculated and analyzed for the association with 90-day liver transplantation-free (LT-free) outcome. The performance of NAR and the integrated model were tested by a receiver-operator curve (ROC) and C-index. The 90-day LT-free mortality of patients with DC was 10.6%. NAR was significantly higher in 90-day non-survivors than in survivors (The median: 1.73 vs 0.76, P < 0.001). A threshold of 1.40 of NAR differentiated patients with a high risk of death (27.45%) from those with a low risk (5.11%). By multivariate analysis, high NAR was independently associated with poor short-term prognosis (high group: 5.07 (2.78, 9.22)). NAR alone had an area under the ROC curve of 0.794 and C-index of 0.7789 (0.7287, 0.8291) in predicting 90-day mortality. The integrated MELD–NAR (iMELD) model had a higher area under the ROC (0.872) and C-index (0.8558 (0.8122, 0.8994)) than the original MELD in predicting 90-day mortality. NAR can be used as an independent predictor of poor outcomes for patients with DC during short-term follow-up. [ABSTRACT FROM AUTHOR]

Background Platelet (PLT)-based biomarkers have been studied for the evaluation of liver fibrosis and cirrhosis. There are no data regarding their prognostic significance in decompensated cirrhosis. Methods We studied 525 stable decompensated patients from the 2 Greek transplant centers. We measured PLT values, mean PLT volume (MPV), red cell distribution width, γ-globulins, and calculated PLT-based scores: aspartate aminotransferase-to-PLT ratio index (APRI), γ-globulinto- PLT model, and γ-glutamyl transpeptidase-to-PLT ratio (GPR). Results We followed our cohort for 12 (range: 1-84) months. Baseline mean model for end-stage liver disease (MELD) and Child-Turcotte-Pugh (CTP) scores were 15±6 and 8±2, respectively. On univariate analysis, MPV/PLT (hazard ratio [HR] 3.75, 95% confidence interval [CI] 1-14.5; P=0.05), APRI (HR 1.03, 95%CI 1.006-1.06; P=0.016), GPR (HR 1.096, 95%CI 1.016-1.182; P=0.017) were significantly associated with our patients' outcome (survival vs. death or liver transplantation). In a multivariate model without MELD and CTP scores, APRI was the only significant factor associated with the outcome (HR 1.054, 95%CI 1.009-1.101; P=0.018). APRI had good discriminative ability for the outcome (area under the curve 0.723 vs. 0.675 and 0.656 for MELD and CTP scores, respectively). The optimal cutoff point was 1.3 (sensitivity 71%, specificity 65%). There were 200 patients (38%) with APRI scores <1.3 who had better survival than patients with APRI >1.3 (log rank 22.4, P<0.001). Conclusions This study found a prognostic role for APRI in stable decompensated cirrhosis, regardless of the underlying etiology of chronic liver disease. This suggests new perspectives for PLT-based noninvasive scores to discriminate patients' outcomes. [ABSTRACT FROM AUTHOR]

Summary: Background: Aetiological therapy improves liver function and may enable hepatic recompensation in decompensated cirrhosis. Aims: We explored the potential for recompensation in patients with decompensated primary biliary cholangitis (PBC) – considering a biochemical response to ursodeoxycholic acid (UDCA) according to Paris‐II criteria as a surrogate for successful aetiological treatment. Methods: Patients with PBC were retrospectively included at the time of first decompensation. Recompensation was defined as (i) resolution of ascites and hepatic encephalopathy (HE) despite discontinuation of diuretic/HE therapy, (ii) absence of variceal bleeding and (iii) sustained liver function improvement. Results: In total, 42 patients with PBC with decompensated cirrhosis (age: 63.5 [IQR: 51.9–69.2] years; 88.1% female; MELD‐Na: 13.5 [IQR: 11.0–15.0]) were included and followed for 41.9 (IQR: 11.0–70.9) months after decompensation. Seven patients (16.7%) achieved recompensation. Lower MELD‐Na (subdistribution hazard ratio [SHR]: 0.90; p = 0.047), bilirubin (SHR per mg/dL: 0.44; p = 0.005) and alkaline phosphatase (SHR per 10 U/L: 0.67; p = 0.001) at decompensation, as well as variceal bleeding as decompensating event (SHR: 4.37; p = 0.069), were linked to a higher probability of recompensation. Overall, 33 patients were treated with UDCA for ≥1 year and 12 (36%) achieved Paris‐II response criteria. Recompensation occurred in 5/12 (41.7%) and in 2/21 (9.5%) patients with vs. without UDCA response at 1 year, respectively. Recompensation was linked to a numerically improved transplant‐free survival (HR: 0.46; p = 0.335). Nonetheless, 4/7 recompensated patients presented with liver‐related complications after developing hepatic malignancy and/or portal vein thrombosis and 2 eventually died. Conclusions: Patients with PBC and decompensated cirrhosis may achieve hepatic recompensation under UDCA therapy. However, since liver‐related complications still occur after recompensation, patients should remain under close follow‐up. [ABSTRACT FROM AUTHOR]

Background: Patients with decompensated cirrhosis face poor prognosis and increased mortality risk. Rifaximin, a non‐absorbable antibiotic, has been shown to have beneficial effects in preventing complications and improving survival in these patients. However, the underlying mechanisms of rifaximin's effects remain unclear. Methods: We obtained fecal samples from decompensated cirrhotic patients undergoing rifaximin treatment and controls, both at baseline and after 6 months of treatment. Shotgun metagenome sequencing profiled the gut microbiome, and untargeted metabolomics analyzed fecal metabolites. Linear discriminant and partial least squares discrimination analyses were used to identify differing species and metabolites between rifaximin‐treated patients and controls. Results: Forty‐two patients were enrolled and divided into two groups (26 patients in the rifaximin group and 16 patients in the control group). The gut microbiome's beta diversity changed in the rifaximin group but remained unaffected in the control group. We observed 44 species with reduced abundance in the rifaximin group, including Streptococcus_salivarius, Streptococcus_vestibularis, Haemophilus_parainfluenzae, etc. compared to only four in the control group. Additionally, six species were enriched in the rifaximin group, including Eubacterium_sp._CAG:248, Prevotella_sp._CAG:604, etc., and 14 in the control group. Furthermore, rifaximin modulated different microbial functions compared to the control. Seventeen microbiome‐related metabolites were altered due to rifaximin, while six were altered in the control group. Conclusion: Our study revealed distinct microbiome‐metabolite networks regulated by rifaximin intervention in patients with decompensated cirrhosis. These findings suggest that targeting these specific metabolites or related bacteria might be a potential therapeutic strategy for decompensated cirrhosis. [ABSTRACT FROM AUTHOR]

The development and progression of ascites represent a crucial event in the natural history of patients with cirrhosis, predisposing them to other complications and carrying a heavy impact on prognosis. The current standard of care for the management of ascites relies on various combinations of diuretics and large-volume paracenteses. Periodic long-term albumin infusions on top of diuretics have been recently shown to greatly facilitate the management of ascites. The insertion of a transjugular intrahepatic portosystemic shunt (TIPS), an artificial connection between the portal and caval systems, is indicated to treat patients with refractory ascites. TIPS acts to decrease portal hypertension, thus targeting an upstream event in the pathophysiological cascade of cirrhosis decompensation. Available evidence shows a significant benefit on ascites control/resolution, with less clear results on patient survival. Patient selection plays a crucial role in obtaining better clinical responses and avoiding TIPS-related adverse events, the most important of which are hepatic encephalopathy, cardiac overload and failure, and liver failure. At the same time, some recent technical evolutions of available stents appear promising but deserve further investigations. Future challenges and perspectives include (i) identifying the features for selecting the ideal candidate to TIPS; (ii) recognizing the better timing for TIPS placement; and (iii) understanding the most appropriate role of TIPS within the framework of all other available treatments for the management of patients with decompensated cirrhosis. [ABSTRACT FROM AUTHOR]

Background and aims: A complete understanding of disease pathophysiology in advanced liver disease is hampered by the challenges posed by clinical specimen collection. Notably, in these patients, a transjugular liver biopsy (TJB) is the only safe way to obtain liver tissue. However, it remains unclear whether successful sequencing of this extremely small and fragile tissue can be achieved for downstream characterization of the hepatic landscape. Methods: Here we leveraged in-house available single-cell RNA-sequencing (scRNA-seq) and single-nucleus (snRNA-seq) technologies and accompanying tissue processing protocols and performed an in-patient comparison on TJB's from decompensated cirrhosis patients (n = 3). Results: We confirmed a high concordance between nuclear and whole cell transcriptomes and captured 31,410 single nuclei and 6,152 single cells, respectively. The two platforms revealed similar diversity since all 8 major cell types could be identified, albeit with different cellular proportions thereof. Most importantly, hepatocytes were most abundant in snRNA-seq, while lymphocyte frequencies were elevated in scRNA-seq. We next focused our attention on hepatic myeloid cells due to their key role in injury and repair during chronic liver disease. Comparison of their transcriptional signatures indicated that these were largely overlapping between the two platforms. However, the scRNA-seq platform failed to recover sufficient Kupffer cell numbers, and other monocytes/macrophages featured elevated expression of stressrelated parameters. Conclusion: Our results indicate that single-nucleus transcriptome sequencing provides an effective means to overcome complications associated with clinical specimen collection and could sufficiently profile all major hepatic cell types including all myeloid cell subsets. [ABSTRACT FROM AUTHOR]

(1) Background: The aim was to evaluate the effectiveness of the probiotic containing Saccharomyces boulardii in the treatment of small intestinal bacterial overgrowth (SIBO) in patients with decompensated cirrhosis. (2) Methods: This was a blinded, randomized, placebo-controlled study. (3) Results: After 3 months of treatment, SIBO was absent in 80.0% of patients in the probiotic group and in 23.1% of patients in the placebo group (p = 0.002). The patients with eliminated SIBO had decreased frequency of ascites and hepatic encephalopathy, the increased platelets and albumin levels, the decreased blood levels of total bilirubin, biomarkers of bacterial translocation (lipopolysaccharide [LPS]) and systemic inflammation (C-reactive protein), and positive changes in markers of hyperdynamic circulation compared with the state at inclusion. There were no significant changes in the claudin 3 level (the intestinal barrier biomarker) in these patients. No significant changes were observed in the group of patients with persistent SIBO. The serum level of nitrate (endothelial dysfunction biomarker) was lower in patients with eradicated SIBO than in patients with persistent SIBO. One (5.3%) patient with eradicated SIBO and six (42.9%) patients with persistent SIBO died within the first year of follow-up (p = 0.007). (4) Conclusions: SIBO eradication was an independent predictor of a favorable prognosis during the first year of follow-up. [ABSTRACT FROM AUTHOR]

This study aimed to characterize serum lipid metabolism and identify potential biomarkers for compensated cirrhosis (CC) predicting and decompensated cirrhosis (DC) discrimination using targeted quantitative lipidomics and machine learning approaches. Serum samples from a cohort of 120 participants was analyzed, including 90 cirrhosis patients (45 CC patients and 45 DC patients) and 30 healthy individuals. Lipid metabolic profiling was performed using targeted LC-MS/MS. Two machine learning methods, least absolute shrinkage and selection operator (LASSO), and random forest (RF) were applied to screen for candidate metabolite biomarkers. The metabolic profiling analysis showed a significant disruption in patients with CC and DC. Compared to the CC group, the DC group exhibited a significant upregulation in the abundance of glycochenodeoxycholic acid (GCDCA), glyco-ursodeoxycholic acid (GUDCA), glycocholic acid (GCA), phosphatidylethanolamine (PE), N-acyl-lyso-phosphatidylethanolamine (LNAPE), and triglycerides (TG), and a significant downregulation in the abundance of ceramides (Cer) and lysophosphatidylcholines (LPC). Machine learning identified 11 lipid metabolites (abbreviated as BMP11) as potential CC biomarkers with excellent prediction performance, with an AUC of 0.944, accuracy of 94.7 %, precision of 95.6 %, and recall of 95.6 %. For DC discrimination, eight lipids (abbreviated as BMP8) were identified, demonstrating strong efficacy, with an AUC of 0.968, accuracy of 92.2 %, precision of 88.0 %, and recall of 97.8 %. This study unveiled distinct lipidomic profiles in CC and DC patients and established robust lipid-based models for CC predicting and DC discrimination. [ABSTRACT FROM AUTHOR]

Background & aims: Ascites is a frequent complication of cirrhosis. In intensive care units, initial hemodynamic assessment is frequently performed by echocardiography. This study evaluated the feasibility and usefulness of early hemodynamic assessment in the gastroenterology ward. Methods: This observational cohort study prospectively included all patients admitted to a teaching hospital's gastroenterology unit for decompensated cirrhosis. A gastroenterologist with minimal training and an intensivist both performed an echocardiography exam. The primary outcome was inter-rater agreement and reliability for three echocardiography parameters: visual LVEF (Left Ventricular Ejection Fraction), subaortic VTI (velocity time integral) and E wave velocity. Secondary outcomes were agreement for presence of pleural effusion, description of 3 hemodynamics profiles (hypovolemic, hyperkinetic and intermediate), and 28-day mortality.Results: From March 2018 to March 2020, 53 patients were included. The median age was 62 years and 81% were men. Patients presented mostly advanced liver disease, with 43% Child-Pugh C and median MELD score of 15.2. The limits of agreement between intensivists and gastroenterologists for subaortic VTI were − 6.6 to 7.2 cm, and ranged from − 0.6 to 0.37 m.s-1 for E wave velocity. Clinically significant differences between intensivists and gastroenterologists were found in 22% for subaortic VTI and 24.5% for E wave velocity. Reliability was good for subaortic VTI (ICC: 0.79, 95% CI [0.58; 0.9;]) and moderate for E wave velocity (0.53, 95% CI [0.19; 0.74]). The three hemodynamics profiles had different prognosis, with a 28-day mortality for Hypovolemic, Intermediate and Hyperkinetic group of 31, 18, and 4%, respectively.Conclusion: Reliability of hemodynamic assessment by gastroenterologists was good, while agreement was unsatisfactory, advocating for further training. Transthoracic echocardiography can differentiate hypovolemia from hyperkinetic states. The role of transthoracic echocardiography in managing decompensated cirrhosis requires further study. Clinical trial number: NCT03650660. Lay Summary: Echocardiographic hemodynamic evaluation can be performed by gastroenterologists after a short training. Transthoracic echocardiography evaluation by intensivists defined three hemodynamic profiles in patients with decompensated cirrhosis: Hypovolemic, Hyperkinetic and intermediate, with distinct prognosis. [ABSTRACT FROM AUTHOR]

Background: Cirrhosis is associated with sarcopaenia and fat wasting, which drive decompensation and mortality. Currently, nutritional status, through body composition assessment, is not routinely monitored in outpatients. Given the deleterious outcomes associated with poor nutrition in decompensated cirrhosis, there is a need for remotely monitoring this to optimise community care. Methods: A retrospective analysis was conducted on patients monitored remotely with digital sensors post hospital discharge, to assess outcomes and indicators of new cirrhosis complications. 15 patients had daily fat mass measurements as part of monitoring over a median 10 weeks, using a Withing's bioimpedance scale. The Clinical Frailty Score (CFS) was used to assess frailty and several liver disease severity scores were assessed. Results: 73.3% (11/15) patients were male with a median age of 63 (52–68). There was a trend towards more severe liver disease based on CLIF-Consortium Acute Decompensation (CLIF-C AD) scores in frail patients vs. those not frail (53 vs 46, p = 0.072). When the cohort was split into patients who gained fat mass over 8 weeks vs. those that lost fat mass, the baseline CLIF-C AD scores and WBC were significantly higher in those that lost fat (58 vs 48, p = 0.048 and 11.2 × 109 vs 4.7 × 109, p = 0.031). Conclusions: This proof-of-principle study shows feasibility for remote monitoring of fat mass and nutritional reserve in decompensated cirrhosis. Our results suggest fat mass is associated with greater severity of acute decompensation and may serve as an indicator of systemic inflammatory response. Further prospective studies are required to validate this digital biomarker. [ABSTRACT FROM AUTHOR]

Introduction: There are a lack of data describing outcomes and follow-up after hospital discharge for patients with newly diagnosed cirrhosis with complication on index admission. This study examines factors that influence outcomes such as readmission, follow-up, and mortality for patients with newly diagnosed cirrhosis. Methods: We conducted a single-center retrospective chart review study of 230 patients with newly diagnosed cirrhosis from January 1st, 2020 through December 31st, 2021. We obtained demographics, clinical diagnoses, admission, and discharge MELD-Na, disposition, mortality, appointment requests rate, appointment show rate, and readmission. Results: The primary complications on admission were GI bleed (27%), ascites (25.7%), and hepatic encephalopathy (HE) (10.4%). Overall, the median length of stay (LOS) was 6 days, and the readmission rate was 27%. Out of 230 patients, 25 (10.9%) patients died while hospitalized while another 43 (18.6%) died after initial discharge within the two-year study period. Although there was a significant reduction of the MELD-Na from admission to discharge (p < 0.05), admission MELD-Na did not correlate with LOS and discharge MELD-Na did not predict readmission. Patients with HE had the highest median LOS, while patients with ascites had the highest readmission rate. The median time to an appointment was 32 days. When comparing discharge destinations, most patients were discharged to home (63%), to facilities (13.9%), or expired (10.9%). The average appointment show rate was 38.5%, although 70% of patients had appointment requests. Readmission rate and mortality did not differ based on appointment requests. No significant differences in outcomes were observed based on race, sex, or insurance status. Conclusion: New diagnosis of decompensated was found to have high mortality and high readmission rates. Higher MELD-Na score was seen in patients who died within 30 days. Routine appointment requests did not significantly improve readmission, mortality, increase appointment show rate, or decrease time to appointment. A comprehensive and specialized hepatology-specific program may have great benefits after cirrhotic decompensation, especially for those with newly diagnosed cirrhosis. [ABSTRACT FROM AUTHOR]

Background and aim: Since hepatocytes produce majority of serum proteins, patients with cirrhosis display substantial alterations in the serum proteome. The aim of the current study was to characterize these changes and to study the prognostic utility of hepatocellular proteins available in routine clinical testing. Methods: Sera from 29 healthy controls and 43 patients with cirrhosis were subjected to untargeted proteomic analysis. Unsupervised hierarchical clustering was performed with Perseus software and R. Ingenuity pathway analysis (IPA) suggested upstream regulators that were validated in liver tissues. The behavior and prognostic usefulness of selected biomarkers was investigated in 61 controls and 285 subjects with decompensated cirrhosis. Results: Proteomics uncovered 65 and 16 hepatocellular serum proteins that are significantly downregulated or upregulated in patients with cirrhosis vs. controls. Hierarchical clustering revealed two main clusters and six sub-clusters. IPA identified HNF4α and IL-6 as the two major upstream regulators that were confirmed by hepatic gene expression analyses. Among pseudocholinesterase, transferrin, transthyretin, albumin, and apolipoprotein AI (Apo-AI), Apo-AI was the best predictor of 90-days transplant-free survival (AUROC 0.678; p = 0.0001) and remained an independent predictor in multivariable Cox independently of the presence of acute-on-chronic liver failure. Conclusion: Our study reveals cirrhosis-associated changes in hepatocellular serum proteins and underlying transcription factors. Serum apolipoprotein AI may constitute a useful prognostic adjunct in patients with decompensated cirrhosis. [ABSTRACT FROM AUTHOR]

Background: HBV-associated decompensated cirrhosis (HBV-DC) is hallmarked by high short-term mortality. Accurate non-invasive prognostic tools for these patients are urgent clinical need. Thus, we aimed to explore the relationship between the plasma D-dimer to lymphocyte ratio (DLR) and mortality in HBV-DC patients. Methods: A retrospective analysis was conducted on 152 patients with HBV-DC. To estimate disease severity and outcomes, the Model for End-Stage Liver Disease (MELD) score was utilized. The predictive value of the DLR in assessing mortality risk was assessed using multivariate logistic regression analysis and receiver operating characteristic curve analysis. Results: During the 30-day follow-up period, 20 patients died. The DLR was markedly different between non-survivors and survivors and higher DLR was found to be linked with adverse consequences. Furthermore, logistic regression demonstrated DLR as an independent predictive factor of 30-day mortality in HBV-DC patients and the prognostic value of DLR was very similar to that of MELD score, the combinations of DLR and MELD score show a better predictive value than that of a single index. Conclusions: The DLR was a reliable tool to predict 30-day mortality in HBV-DC patients. [ABSTRACT FROM AUTHOR]

Background and aims: Recompensation between patients with ascites and bleeding was unknown in treatment-naïve HBV-related decompensated cirrhosis. Methods: In this retrospective multi-center study, treatment-naïve HBV-related decompensated patients were enrolled at first decompensating event of ascites and/or variceal bleeding. Further complications and clinical characteristics were collected using standard case report form every 6 months to year-5 of antiviral treatment. Recompensation was defined as maintaining free of decompensation for one year and achieving liver function within Child–Pugh A and/or MELD < 10. Results: Totally, 170 (170/298, 57.0%) patients in ascites group of 298 (298/383, 77.8%) treatment-naïve decompensated patients and 33 (33/85, 38.8%) in bleeding group of 85 (85/383, 22.2%) patients, achieved recompensation. Ascites group had higher 5-year rate of recompensation than bleeding group (63.3% vs. 46.5%, p = 0.012), respectively. Patients achieving recompensation in ascites group maintained lower rate of second decompensation than these in bleeding group (at year-5: 26.7% vs. 43.3%, p = 0.032). Specifically, recompensated patients in ascites group had predominantly 5-year rate of further ascites (24.0%) and lower rate of further bleeding (6.0%), which differed from the pattern of these in bleeding group, with lower rate of further ascites (16.0%, p = 0.599) and significantly higher rate of further bleeding (33.9%, p < 0.001). Both patients had superior long-term prognosis (death/LT rate at year-5: 0.6% vs. 3.0%, p = 0.196). Conclusion: Ascites patients could achieve higher rate of recompensation through antiviral therapy than bleeding patients. Recompensated patients in ascites group had better prognosis in terms of preventing further bleeding. [ABSTRACT FROM AUTHOR]

Patients with decompensated cirrhosis are at risk of developing acute kidney injury (AKI). Studies have suggested that inhibition of the Renin-Angiotensin System (RAS) has certain nephro- and hepatoprotective effects in patients with compensated liver disease. This study aimed to investigate the clinical impact of RAS-Inhibitors in individuals with decompensated liver cirrhosis. Overall, 1181 consecutive hospitalized patients with ascites that underwent paracentesis were considered for this retrospective study. In total, 667 patients with decompensated cirrhosis fulfilled the inclusion criteria and were finally analyzed. RAS-Inhibitor intake was documented in 41 patients (7%). First, 28-day incidences of AKI and grade III AKI of all patients with RAS-Inhibitors were compared to those without intake. Afterwards, propensity score matching was conducted in a 3:1 manner. Here, incidence of further renal endpoints such as need of hemodialysis were analyzed in detail. In the unmatched setting, intake of RAS-Inhibitors was not associated with an increased 28 day-incidence of AKI (P = 0.76) or LTx-free survival (P = 0.60). However, 28 day-incidence of grade III AKI was significantly lower in patients with RAS-Inhibitor intake (P < 0.001). In the matched setting, 28 day-incidence of AKI did not differ (P = 0.81), while grade III AKI was significantly less frequent in the RAS-Inhibitor group (P < 0.001). Need for hemodialysis was also significantly lower in patients with RAS-Inhibitors (P = 0.03) and LTx-free survival was comparable between both groups (P = 0.52). Thus, this study suggests that intake of RAS-Inhibitors is associated with decreased incidences of grade III AKI and need of hemodialysis in patients with decompensated liver disease. [ABSTRACT FROM AUTHOR]

Background: Patients with decompensated cirrhosis are well known to experience morbidity and mortality. Aim: We assessed clinical characteristics, health‐care utilization, and economic burden according to the type, number, and combination of decompensation‐related complications. Methods: We used recent nationally representative sample data from 2016 to 2018, covering approximately 13% of hospitalized patients in South Korea annually. Decompensation‐related complications included ascites, hepatic encephalopathy (HE), gastroesophageal variceal (GEV) bleeding, and hepatorenal syndrome (HRS). Results: Among 14 601 patients with decompensated cirrhosis, 11 201 (76.7%) experienced ≥ 1 decompensation‐related complications, and approximately three‐quarters underwent hospitalization. The most prevalent decompensation‐related complications were ascites (54.8%), GEV bleeding (33.2%), HE (27.4%), and HRS (3.6%). Patients with GEV bleeding exhibited the highest hospitalization rate (95.7%), and patients with HE or HRS underwent hospitalization for 4 weeks/year due to decompensated cirrhosis. Hospitalization costs were 1.9 times higher in patients with HRS than in those with ascites alone ($9022 vs $4673; P < 0.01). Once patients developed decompensation‐related complications, 41.3% had ≥ 2 types of decompensation‐related complications. As the number of decompensation‐related complications increased from 0 to ≥ 3, health‐care utilization and economic burden significantly increased in a stepwise manner; patients with ascites, GEV bleeding, and HE visited medical institutions 2.2 times more (11 vs 5/year; P < 0.01) and incurred 6.4 times greater medical expenditure ($11 060 vs $1728/year; P < 0.01) than those with ascites only. Conclusion: A substantial proportion of patients had multiple decompensation‐related complications and socioeconomic burdens for decompensated cirrhosis considering admission rate, hospital stay, and costs increased markedly, depending on the number of decompensation‐related complications. [ABSTRACT FROM AUTHOR]

Introduction: Infections in patients with cirrhosis are associated with high morbidity and mortality. Rifaximin is an antibiotic used to treat and prevent hepatic encephalopathy (HE); however, it has been suggested that it may play a crucial role in reducing infections in these populations. Aim: To evaluate the role of rifaximin in preventing frequent cirrhosis-related infections [spontaneous bacterial peritonitis, pneumonia, urinary tract infection (UTI), and bacteremia], Clostridioides difficil e infection, and all-cause mortality, as well as determining adverse effects and adherence to the drug. Methods: A retrospective cohort study was conducted on decompensated cirrhotic patients with history of HE between January 2017 and November 2022 at a university center. Patients with cirrhosis, regardless of their etiology and severity, were included in the study, encompassing both hospitalized and outpatient cases. The statistical analysis included adjusted general linear models, Poisson regressions, and propensity score matching. Results: We included 153 patients. The mean age in the cohort was 60.2 ± 12.3 years and 67 (43.8%) were women. The main cause of cirrhosis was metabolic dysfunction-associated steatotic liver disease 52 (38%), and the median Model of End-Stage Liver Disease sodium was 16.5 (7–32). In the cohort, 65 (45%) patients used rifaximin. The mean follow-up was 32 months. Eighty-five patients with infectious events were recorded, and a total of 164 infectious events were registered. The main infectious events were UTIs (62, 37.8%) and pneumonia (38, 23.2%). The use of rifaximin was associated with lower infection rates, displaying an incidence rate ratio (IRR) of 0.64 [95% confidence interval (CI) (0.47–0.89); p = 0.008]. However, no discernible impact on mortality outcome was observed [IRR 1.9, 95% CI (0.9–4.0); p = 0.09]. There were no reported adverse effects, and no patient discontinued the therapy due to adverse effects. Conclusion: The use of rifaximin significantly reduces infections in patients with cirrhosis and HE. Despite rifaximin was associated with a decreased all-cause mortality, this impact was not statistically significant in the adjusted analysis. Plain language summary: Assessing the impact of rifaximin on infections in cirrhosis This study aimed to investigate the role of rifaximin, an antibiotic commonly used to treat hepatic encephalopathy, in preventing infections and mortality in patients with cirrhosis. The retrospective cohort study included 153 decompensated cirrhotic patients with a history of hepatic encephalopathy, covering the period from January 2017 to November 2022 at a university center. Results showed that 45% of the patients in the cohort used rifaximin, and the mean follow-up duration was 32 months. A total of 164 infectious events were recorded during the study, with urinary tract infections (37.8%) and pneumonia (23.2%) being the most common. The use of rifaximin was associated with a significant reduction in infection rates, with an incidence rate ratio of 0.64 (95% CI [0.47-0.89]; p=0.008). However, there was no statistically significant impact on all-cause mortality (IRR 1.9, 95% CI [0.9-4.0]; p=0.09). Notably, no adverse effects were reported, and no patient discontinued rifaximin therapy due to adverse effects. In conclusion, rifaximin demonstrated a noteworthy reduction in infections among cirrhotic patients with hepatic encephalopathy. Although a decrease in all-cause mortality was observed with rifaximin use, this effect did not reach statistical significance in the adjusted analysis. The study supports the potential benefits of rifaximin in preventing infections in this vulnerable patient population without apparent adverse effects. Further research may provide additional insights into the long-term impact of rifaximin on mortality outcomes in cirrhotic patients. [ABSTRACT FROM AUTHOR]

Introduction: The synergistic impact of coexistent malnutrition and sarcopenia on morality in hospitalized patients with decompensated cirrhosis remains elusive. This prospective cohort study aimed to delineate the prevalence concerning coexistence of malnutrition and sarcopenia and the prognosticating role on long-term mortality among cirrhosis. Methods: Adult cirrhotic patients with decompensated episodes between 2019 and 2021 were consecutively enrolled. Malnutrition and sarcopenia were diagnosed according to the Global Leadership Initiative on Malnutrition (GLIM) criteria and the European Working Group on Sarcopenia in Older People (EWGSOP2) algorithm, respectively. The entire cohort was divided into three groups: non-malnutrition and non-sarcopenia (NN), malnutrition or sarcopenia, and coexistent malnutrition and sarcopenia (MS). Log-rank test and multivariate Cox regression model were utilized to evaluate survival status and independent risk factors for mortality, respectively. Results: Our findings indicated that malnutrition manifested in 44.6% of inpatients with decompensated cirrhosis, while sarcopenia presented in 16.4% of the entire cohort, indicative of a prevalence of 14.7% regarding coexistent malnutrition and sarcopenia. The Kaplan-Meier graphic demonstrated a significant difference regarding survival curves among the three groups, referring to the MS group presented with the lowest survival rate (log-rank test: p < 0.001). Moreover, coexistent malnutrition and sarcopenia were associated with nearly 4 times higher mortality risk (model 1: hazard ratio [HR] = 3.31, 95% confidence interval [CI]: 1.20–9.13, p = 0.020; model 2: HR = 4.34, 95% CI: 1.52–12.4, p = 0.006) in comparison with patients without any condition (NN group). Conclusions: Malnutrition and sarcopenia had superimposed negative impacts on inpatients with decompensated cirrhosis. It is imperative to identify this vulnerable subset to provide prompt therapeutic intervention for better prognosis. [ABSTRACT FROM AUTHOR]

Background and Aims: Decompensated liver cirrhosis has a poor prognosis, with a median overall survival of two to four years, which is worse than for many oncological disorders. These patients are highly susceptible to infections due to increased systemic inflammation leading to kidney failure and death. The aim was to study the efficacy of albumin in reducing episodes of decompensation, preventing bacterial infection, kidney dysfunction and mortality. Method: Study involved patients with Child B or C cirrhosis with an albumin level below 3.0 g/dL, who were administered 20% human albumin weekly with standard medical treatment (SMT) for three months or till serum albumin levels were 4.0 g/dL (whichever is earlier) and compared with age and sex-matched controls who received only SMT. The primary end-point was six-month mortality and the secondary end-points were reduction in infections, kidney dysfunction, ascites recurrence, hepatic encephalopathy (HE), gastrointestinal (GI) bleed and complications of cirrhosis. Results: From September 2021 to January 2023, 88 cases and 86 controls were taken and followed up for six months. Overall, six-month survival was not statistically significant between groups (95.1% vs. 91.9%; p = 0·330). The incidence of recurrence of ascites (34.09% vs. 59.3%, p < 0.001), kidney dysfunction (6.8% vs. 24.4%, p < 0.001), HE (15.9% vs, 37.2%, p = 0.015), spontaneous bacterial peritonitis (SBP) (3.4% vs 17.4%, p = 0.002) and non-SBP infections (7.9% vs. 18.6%, p = 0.038) were significantly less in cases as compared with controls; however, GI bleed (14.8% vs. 17.4%, p = 0.632) was not statistically significant. Conclusion: Long-term human albumin acts as a disease-modifying treatment in patients with decompensated cirrhosis. [ABSTRACT FROM AUTHOR]