Background/Objectives: Carbohydrate antigen 125 (CA125) is a glycoprotein commonly overexpressed in epithelial ovarian cancer and widely recognized as a tumor marker. However, elevated CA125 levels are also observed in various non-malignant conditions, including diseases affecting mucosal surfaces, pleural or peritoneal effusions, cirrhosis (with or without ascites), endometriosis, uterine fibroids, adenomyosis, pelvic inflammatory disease, and pregnancy. This review aims to explore the role of CA125 in non-malignant serous effusions, highlighting its diagnostic and prognostic potential beyond the realm of oncology. Methods: A comprehensive literature search was conducted across multiple databases and clinical trial registries. Eligible studies included full-text original research articles, reviews, and case reports published in English over the past 10 years. Inclusion criteria were limited to studies involving human subjects and focused on the role of CA125 in non-malignant serous effusions. Results: CA125 is produced by coelomic epithelial cells lining the ovary, pleura, pericardium, and peritoneum. Its serum concentration is not significantly influenced by age, body weight, or renal function, even in the advanced stages of the disease. In peritoneal conditions, CA125 is synthesized by mesothelial cells and serves as a potential marker of peritoneal involvement. The prevailing pathophysiological mechanism suggests that mechanical stretching of mesothelial cells due to ascitic pressure stimulates CA125 release. Similarly, in heart failure, mesothelial cells of the pericardium produce CA125, which correlates with congestion severity, supports risk stratification, and may inform diuretic therapy. Conclusions: While a threshold of 35 U/mL is established for malignancy, no standardized cutoff exists for CA125 in non-malignant conditions. The utility of CA125 measurement in peritoneal, pleural, or pericardial effusions—and cardiovascular diseases such as acute heart failure—for purposes of differential diagnosis, treatment guidance, or prognostication warrants further investigation through prospective clinical trials.

Background: Pregnancy induces a physiological prothrombotic state. The highest risk period for venous thromboembolism and pulmonary embolism in pregnant women is during the postpartum period. Materials and Methods: We present the case of a young woman who gave birth 2 weeks before admission and was transferred to our clinic for edema. She had an increased temperature in her right limb, and a venous Doppler of the limb confirmed thrombosis of the right femoral vein. From the paraclinical examination, we obtained a CBC with leukocytosis, neutrophilia, and thrombocytosis, and a positive D-dimer test. Thrombophilic tests were negative for AT III, lupus anticoagulant negative, and protein S and C, but were positive for heterozygous PAI-1, heterozygous MTHFR A1298C, and EPCR with A1/A2 alleles. After 2 days of UFH with therapeutic APTT, the patient had pain in her left thigh. We performed a venous Doppler, which revealed bilateral femoral and iliac venous thrombosis. During the computed tomography examination, we assessed the venous thrombosis extension on the inferior cava, common iliac, and bilateral common femoral veins. Thrombolysis was initiated with 100 mg of Alteplase given at a rate of 2 mg/h; however, this did not lead to a considerable reduction in the thrombus. Additionally, the treatment with UFH was continued under therapeutic APTT. After 7 days of UFH and triple antibiotic therapy for genital sepsis, the patient had a favorable evolution with remission of venous thrombosis. Results: Alteplase is a thrombolytic agent that is created with recombinant DNA technology, and it was successfully used to treat thrombosis that occurred in the postpartum period. Conclusions: Thrombophilias are associated with a high VTE risk but also with adverse pregnancy outcomes, including recurrent miscarriages and gestational vascular complications. In addition, the postpartum period is associated with a higher VTE risk. A thrombophilic status with heterozygous PAI-1, heterozygous MTHFR A1298C, and EPCR with A1/A2 positive alleles is associated with a high risk of thrombosis and cardiovascular events. Thrombolysis can be successfully used postpartum to treat VTEs. Thrombolysis can be used successfully in VTE developed in the postpartum period.

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.

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: 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 and Objectives: To find low-cost markers that can identify the hepatitis C virus cirrhotic patients that are at risk for long-term severe adverse liver effects (ascites, ascites or upper gastrointestinal bleeding, hepatocellular carcinoma), after treatment. There is established evidence for the benefits of treating hepatitis C virus cirrhotic patients, but there is still some need for clarification concerning the real impact on the long-term evolution after achieving sustained virological response; there is no general consensus in the literature about identifying the patients that do not improve post-treatment. Materials and Methods: Our retrospective analysis investigated the long-term (2 years) evolution of 46 patients with cirrhosis with thrombocytopenia, previously infected with VHC, treated and who obtained an SVR after DAA treatment. Results: Despite the overall improvement, 8.7% patients developed hepatocellular carcinoma and 6.5% patients ascites/upper GI bleeding. We found that FIB-4, MELD and AFP changes at 1 year were the most significant predictors for these outcomes. Additionally, a drop in leukocyte count after 1 year seemed to indicate a risk for hepatocellular carcinoma, but this was not consistent. Conclusions: It might be beneficial to intensify the surveillance for post-treatment adverse liver effects for the patients with these marker changes at 1 year.