Background: Atrial fibrillation (AF) is frequently associated with cardiometabolic comorbidities, and increasing evidence suggests a close relationship between AF and liver disease, particularly metabolic dysfunction-associated steatotic liver disease (MASLD); however, the clinical patterns, hepatic phenotypes, and clinical implications of this association remain insufficiently characterized. Therefore, the aim of the present study was to characterize hepatic involvement in patients with paroxysmal AF by integrating a structured literature review with original clinical data. Methods: We performed a retrospective analysis of 253 patients admitted with paroxysmal AF between 2015 and 2025. Demographic data and associated diagnoses were collected with a specific focus on hepatic pathology. Patients were stratified according to the presence and type of liver disease, and descriptive statistics, bivariate analyses, and multivariate logistic regression were used to identify associations and independent predictors. Results: Liver disease was identified in 65.2% of patients, most commonly hepatic steatosis (46.2%), followed by liver cirrhosis or advanced liver disease (19.0%). Patients with liver disease had higher prevalences of type 2 diabetes mellitus, dyslipidemia, obesity, and alcohol consumption. Dyslipidemia (OR 4.51) and obesity (OR 2.54) were independent predictors of hepatic steatosis, whereas liver cirrhosis was inversely associated with age and serum lipid levels. Conclusions: Liver pathology is highly prevalent among patients with paroxysmal AF and is closely associated with adverse metabolic and clinical profiles. Recognition of distinct hepatic phenotypes may support improved risk stratification and multidisciplinary management in patients with AF.

Background: Decompensated cirrhosis is associated with high in-hospital mortality, influenced by disease severity and underlying etiology. The COVID-19 pandemic may have altered both the etiological spectrum and clinical presentation of hospitalized patients. This study aimed to assess longitudinal changes in etiology and identify predictors of in-hospital mortality over a 10-year period. Methods: We conducted a retrospective cohort study including 812 patients hospitalized with decompensated liver cirrhosis between 2015 and 2025. Patients were grouped into pre-COVID-19 (2015–2019), COVID-19 (2020–2021) and post-COVID-19 (2022–2025) periods. Etiological factors and mortality rates were compared using chi-square tests. Independent predictors were identified through multivariate analysis. A clinical risk score based on Child–Pugh stage, platelet count and age was developed and evaluated using ROC analysis. Results: Alcohol-related cirrhosis increased significantly from 51.2% (pre-COVID-19) to 90.4% (COVID-19) and remained high post-COVID-19 (86.3%) (p < 0.001), while HCV decreased from 34.4% to 13.5% and stabilized at 14.8% (p < 0.001). HBV showed no significant variation. All-cause in-hospital mortality increased from 19.7% pre-COVID-19 to 42.3% during COVID-19 and remained elevated post-COVID-19 at 34.5% (p < 0.001). Independent predictors of all-cause in-hospital mortality included advanced Child–Pugh stage, thrombocytopenia and age above 70 years. The risk score (0–7 points) showed good discrimination (AUC = 0.752), with mortality rates of 2.8%, 24.0% and 45.7% across increasing risk categories. A score <5 had a negative predictive value of 84.3%. Conclusions: A significant etiological shift from HCV to alcohol was observed, accompanied by persistently increased mortality after COVID-19. Thrombocytopenia remains an important predictor of mortality. The proposed score enables simple and effective risk stratification.

Background and Objectives: Ascites is associated with substantial symptom burden and increased healthcare utilization, and it is observed in patients with advanced disease across multiple etiologies. However, because ascites is a clinical sign rather than a diagnosis category, it can be challenging to study using routine health reporting. In routinely collected hospital administrative data, ascites is commonly captured using International Classification of Diseases, Tenth Revision (ICD-10) code R18, an etiologically non-specific classification whose outcome implications are less documented. We aimed to evaluate the incremental association of R18-coded ascites with length of stay (LOS), readmission burden, and in-hospital mortality in the Gastroenterology and Internal Medicine inpatient department, beyond comorbidity burden and other coded decompensation proxies. Materials and Methods: We conducted a single-center retrospective study using routinely collected administrative discharge data from adult inpatient admissions (2015–2023) in the Gastroenterology and Internal Medicine department of a Romanian tertiary-care hospital. Admissions were classified by the presence of ICD-10 R18-coded ascites. Outcomes were LOS, readmission burden (count of subsequent admissions), and in-hospital mortality. Multivariable models adjusted for age, sex, and comorbidity burden (Charlson Comorbidity Index), with additional models incorporating ICD-10-derived decompensation proxies to assess overlap in administrative severity signal. LOS was further examined within Charlson strata to evaluate incremental stratification. Results: Coded ascites was associated with higher hospital burden, including longer LOS and greater readmission burden, and with higher in-hospital mortality in partially adjusted models. Within each CCI stratum, LOS remained higher among admissions with R18-coded ascites, supporting incremental stratification beyond comorbidity alone. Furthermore, mobility impairment was an important predictor of LOS. Age-stratified analyses suggested a high-burden phenotype among younger patients and infrequent R18 coding among the very elderly in this cohort. Conclusions: These findings support the potential utility of R18-coded ascites as a pragmatic administrative marker for risk adjustment and service planning.

Liver cirrhosis represents the end stage of chronic liver disease arising from diverse etiologies and is characterized by persistent hepatic injury, architectural distortion, extensive fibrosis, and nodular regeneration. While decompensated cirrhosis is commonly associated with overt, life-threatening complications such as hepatic encephalopathy, hepatorenal syndrome and gastrointestinal bleeding, less apparent manifestations—including sarcopenia and metabolic disturbances—have emerged as major determinants of prognosis. Sarcopenia, defined by the progressive loss of skeletal muscle mass and function, is highly prevalent in cirrhotic patients and is closely linked to frailty, increased morbidity, mortality, and adverse liver transplantation outcomes. Increasing data support the role of gastrointestinal dysfunction in the pathogenesis of sarcopenia in liver cirrhosis. In chronic liver disease, intestinal dysfunction is exacerbated by portal hypertension, which promotes increased intestinal permeability and bacterial translocation. Furthermore, gut dysbiosis, a key feature of advanced liver disease, contributes to impaired digestion, malabsorption of macro- and micronutrients, increased intestinal permeability, malnutrition and systemic inflammation. These alterations promote negative energy balance, reduce muscle protein synthesis and enhance muscle catabolism, thereby accelerating muscle wasting. Despite increasing recognition of the individual roles of gut dysbiosis, malabsorption, and sarcopenia in cirrhosis, their complex interrelationship has not been comprehensively addressed. This narrative review synthesizes current evidence on the interplay between gut dysbiosis, malabsorption and sarcopenia in patients with liver cirrhosis. We discuss underlying pathophysiological mechanisms, clinical implications and potential therapeutic strategies, while highlighting existing knowledge gaps and future research directions. Improved understanding of the gut-liver-muscle axis may offer novel opportunities for early intervention and optimization of outcomes in this high-risk patient population.

Background: Liver cirrhosis, particularly in its decompensated stages, is associated with high short-term mortality among hospitalized patients. Although the prognostic value of the Child–Pugh classification is well established, its independent impact on survival in real-world tertiary emergency settings requires further evaluation. This study aimed to assess the prognostic role of Child–Pugh stage and other clinical factors on short- and mid-term survival in hospitalized cirrhotic patients over a 10-year period. Methods: We conducted a retrospective cohort study including 2831 patients hospitalized for liver cirrhosis between 2015 and 2025. Among them, 631 patients with complete Child–Pugh staging were included in the survival analysis. Survival time was defined as the interval between the first hospitalization and the last recorded discharge or in-hospital death. Survival differences were assessed using Kaplan–Meier curves and log-rank tests, while independent predictors of mortality were identified using multivariate Cox proportional hazards regression. A complementary logistic regression model was used to evaluate predictors of mortality as a binary outcome. Results: Among the 631 staged patients, 13.5% were classified as Child–Pugh A, 31.9% as Child–Pugh B and 54.7% as Child–Pugh C. In-hospital mortality increased significantly across stages (1.2%, 9.0% and 46.7%, respectively; p < 0.001). One-year survival was 98.7% for Child–Pugh A, 83.6% for Child–Pugh B and 40.7% for Child–Pugh C (log-rank p < 0.001). In multivariate Coxregression analysis, the strongest predictor of mortality was mixed cirrhosis type (HR = 8.58, 95% CI: 4.81–15.32, p < 0.001). Child–Pugh C was also independently associated with a markedly increased mortality risk compared with Child–Pugh A (HR = 25.11, 95% CI: 3.44–183.29, p = 0.002). Alcohol-related etiology (HR = 1.81, 95% CI: 1.09–3.01, p = 0.023) and age (HR = 1.18 per SD increase, 95% CI: 1.00–1.39, p = 0.050) were additionalindependent predictors. The Cox model demonstrated good discrimination (C-statistic ≈ 0.80). In the logistic regression model, mixed cirrhosis type (OR = 13.28, p < 0.001) and Child–Pugh stage (OR = 8.66, p < 0.001) were the strongest predictors of mortality, while ascites showed an inverse association after adjustment (OR = 0.62, p = 0.036). The logistic model showed excellent discrimination (AUC = 0.865). Conclusions: Child–Pugh stage remains a strong and independent predictor of survival in hospitalized patients with decompensated cirrhosis. The marked survival gradient across stages, particularly the substantially reduced survival observed in Child–Pugh C patients, highlights thecontinued clinical utility of this simple classification for early risk stratification intertiary emergency hospital settings.

Background: Advanced chronic kidney disease (CKD) and cardiovascular comorbidities frequently coexist in patients with multiple myeloma and are particularly common among hospitalized patients. However, the relationship between common cardiovascular comorbidities and advanced CKD in routine clinical practice remains incompletely characterized. Methods: We conducted a retrospective single-center cohort study including 137 hospitalized patients diagnosed with multiple myeloma between January 2015 and February 2026. Demographic, clinical, and laboratory data were extracted from electronic medical records. Advanced CKD was defined as eGFR < 30 mL/min/1.73 m², calculated using the CKD-EPI 2021 equation. Patients with isolated acute kidney injury were excluded. Cross-sectional associations between cardiovascular comorbidities and advanced CKD were assessed using logistic regression models. Results: The median age was 69 years (IQR 63–77), and 56.9% of patients were women. Renal impairment was common, with a median creatinine level of 2.82 mg/dL and a median eGFR of 22.4 mL/min/1.73 m². Advanced CKD was identified in 55 of 116 patients (47.4%) with available CKD classification. Cardiovascular comorbidities were common, including hypertension (42/55, 76.4%), diabetes mellitus (18/55, 32.7%), myocardial ischemia (41/55, 74.5%), and heart failure (25/55, 45.5%). In univariate analysis, atrial fibrillation showed a significant cross-sectional association with advanced CKD (OR 4.43, 95% CI 1.30–15.07, p = 0.017), as was myocardial ischemia (OR 2.89, 95% CI 1.07–7.80, p = 0.039). In multivariable analysis, atrial fibrillation demonstrated a trend toward an association with advanced CKD but did not remain statistically significant after adjustment. Conclusions: Advanced CKD and cardiovascular comorbidities frequently coexist in hospitalized patients with multiple myeloma. Atrial fibrillation and myocardial ischemia were associated with advanced CKD in univariate analyses; however, these associations were attenuated after multivariable adjustment. Overall, these findings provide insight into the coexistence of advanced CKD and cardiovascular comorbidities in hospitalized patients with multiple myeloma.