Rare presentations are surprising and may disturb the day-to-day routine of a medical unit; however, they are expected (not as individual entities, but as a group of “uncommon causes”). While reviewing the literature in relation to three clinical cases of upper gastrointestinal bleeding (UGIB) encountered in our institution—gastric metastases of breast cancer (GMB), pyloric gland adenoma, and gastrointestinal stromal tumor (GIST)—we identified seven and 29 case reports for the first two entities, and over 100 publications addressing GIST. This prompted a shift in focus from novel reporting to diagnostic contextualization. We found it difficult to obtain an overview of the spectrum of UGIB etiologies, as most publications refer to a few individual entities or to a subgroup of rare causes. The narrative review we conducted arose from this particular research methodology. Based on a broad literature search, UGIB etiologies were organized in five categories (lesions of the mucosa, neoplasms, vascular causes, bleeding predisposition, and external sources of bleeding). In the management of patients with UGIB, the underlying etiology deviates from the classic peptic ulcer disease/esophageal varices dyad in approximately half of the cases. This underscores the need for heightened clinical vigilance, particularly in complex scenarios, where endoscopic findings, imaging results, and histopathological interpretations may be unexpected or prone to misinterpretation. As an illustration, we conducted two systematic reviews of case reports of bleeding GMB and PGA. Our findings support a proactive diagnostic and research mindset and advocate for improved awareness of uncommon UGIB etiologies.

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: 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.

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.

Portal vein thrombosis (PVT) refers specifically to the presence of a thrombus within the main portal vein trunk or its intrahepatic branches. In contrast, portal vein occlusion encompasses a broader spectrum of conditions, including tumor invasion, external compression and disorders that predispose to thrombosis, such as thrombophilia or inflammatory states. Advanced liver disease, particularly cirrhosis, is the most common cause of PVT, primarily due to portal hypertension, altered hemostasis and hemodynamic changes, followed by malignancies and inherited or acquired thrombophilic conditions. In contrast to these common etiologies, our clinical experience has highlighted rare causes of portal vein obstruction associated with typical presentations, which pose diagnostic challenges. Examples include acute PVT during transjugular intrahepatic portosystemic shunt (TIPS) placement and non-thrombotic porto-mesenteric obstruction related to portal venous gas. While these events may appear unexpected, they represent a recognizable group of uncommon causes rather than isolated incidents. PVT can present as an acute or chronic condition: acute thrombosis is characterized by recent thrombus formation and potential intestinal ischemia, whereas chronic thrombosis is associated with long-standing obstruction, cavernous transformation and portal hypertension. This narrative review integrates a comprehensive literature search with clinical experience, with particular emphasis on uncommon etiologies of portal vein obstruction.

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.