The patient was a 54-year-old male. He underwent invasive seminoma resection, bypass grafting from the left subclavian vein to the right atrial appendage, and patch plasty of the superior vena cava(SVC) 18 years ago in 1990. In 1992, graft obstruction was demonstrated, and in 1994, subsequent downhill esophageal varices developed. Varices deteriorated to grade F3 with a red-colored sign in 2008. Therefore, bypass grafting from bilateral subclavian veins to the right atrial appendage was performed to prevent rupture. Endoscopy performed two weeks after surgery showed that the varices had improved to grade F1. The patient was discharged without adverse events. In 2023, the graft remained patent and the varices did not worsen. After SVC reconstruction, strict follow-up is necessary because fatal event in esophageal varices can occur owing to graft obstruction.

Cirrhosis represents the end stage of chronic liver injury, characterized by progressive fibrosis and architectural distortion that precipitate portal hypertension and systemic complications. Recent evidence positions gut microbiota dysbiosis and nitric oxide (NO) dysregulation as central, interacting pathophysiological mechanisms in cirrhosis progression. Intestinal barrier dysfunction facilitates bacterial translocation and thereby exposes the liver to lipopolysaccharides and pathogen-associated molecular patterns that trigger hepatic inflammation via Toll-like receptor signalling, a phenomenon aggravated by dysbiosis. This immune activation stimulates inducible NO synthase in Kupffer cells and systemic endothelium, generating excess NO that drives splanchnic vasodilation and worsens portal hypertension. Paradoxically, intrahepatic endothelial NO synthase activity becomes impaired, reducing sinusoidal NO availability and increasing intrahepatic vascular resistance. These interconnected disturbances perpetuate inflammation and fibrogenesis, contributing to cirrhosis decompensation and spontaneous bacterial peritonitis. Despite substantial mechanistic insight into these pathways, therapeutic translation remains limited. Statins show promise by restoring intrahepatic eNOS function and reducing portal pressure, while microbiota-targeted interventions (antibiotics, probiotics, fecal transplantation) address gut-derived inflammation. This review synthesizes our current understanding of the gut-liver-NO axis in cirrhosis, highlighting how dysbiosis and aberrant NO signalling reinforce each other through inflammatory feedback loops, and identifies critical gaps between mechanistic knowledge and clinical application that warrant further investigation.

Cirrhosis and hepatocellular carcinoma (HCC) are interconnected outcomes of chronic liver disease, with portal hypertension playing a key part in cirrhosis decompensation, and influencing HCC prognosis and treatment. Despite their overlap, current guidelines address portal hypertension and HCC separately, leading to suboptimal risk stratification and treatment selection. This Review proposes a stage-based, integrated approach to HCC management that incorporates the prognostic stages of cirrhosis and emphasizes clinically significant portal hypertension (CSPH) as a key stratifying factor in compensated cirrhosis. CSPH is associated with an increased risk of cirrhosis decompensation, and its presence often limits the feasibility of curative treatments such as surgical resection. Although CSPH is strictly defined as hepatic venous pressure gradient (HVPG) of ≥10 mmHg, non-invasive tools (liver stiffness and platelet count) have largely replaced HVPG in cirrhosis; in patients with HCC, emerging data suggest that these non-invasive tests are poised to replace HVPG and its traditional surrogates, imaging and endoscopy. We explore the management of both cirrhosis and HCC across all cirrhosis stages - compensated (with or without CSPH), decompensated, and further decompensated - in relation to all HCC stages (very early, early, intermediate and advanced). Future research should validate non-invasive CSPH assessment in HCC and support outcome trials stratified by cirrhosis and HCC stage to guide personalized therapy and improve outcomes.

Spontaneous bacterial peritonitis is a severe complication in patients with cirrhosis and remains a major cause of hospitalization and mortality. Early diagnosis is essential and relies on ascitic fluid analysis showing a polymorphonuclear neutrophil count greater than 250/mm[3]. Prompt initiation of antibiotic therapy combined with albumin infusion has markedly improved patient outcomes, leading to a significant reduction in mortality since the condition was first described. The aim of this review is to provide an updated synthesis of best practices in the diagnosis, treatment, and prevention of spontaneous bacterial peritonitis, considering recent changes in bacterial epidemiology.

Gastrointestinal (GI) disease complicates anticoagulation by simultaneously increasing bleeding risk and maintaining high thromboembolic vulnerability. Mucosal injury, portal hypertension, malignancy, inflammatory bowel disease, and vascular lesions predispose to hemorrhage, whereas interruption of therapy increases the risk of stroke, venous thromboembolism, and stent thrombosis. Contemporary management follows an indication-first, risk-balanced approach that integrates thrombotic urgency, GI disease phenotype, and patient-specific bleeding-risk factors. Direct oral anticoagulants demonstrate heterogeneous GI bleeding profiles, with higher risk observed with dabigatran and rivaroxaban, while apixaban is comparatively safer in high-risk populations. Periprocedural management is guided by procedural bleeding risk, renal function, and drug pharmacokinetics, with strategies emphasizing appropriate interruption and minimal use of bridging. In acute GI bleeding, management prioritizes hemodynamic stabilization, restrictive transfusion strategies, and early endoscopic or interventional radiology-guided source control, with selective use of reversal agents in severe cases. Adjunctive measures, including proton pump inhibitor therapy and Helicobacter pylori eradication, reduce recurrent bleeding risk. Resumption of anticoagulation is generally associated with improved survival and reduced thromboembolic events when timed appropriately. Key knowledge gaps remain regarding optimal reversal strategies, lesion-specific restart timing, and management in cirrhotic populations.

Pancreatic arteriovenous malformation is exceptionally rare with fewer than 200 cases reported in the literature. It is usually asymptomatic, although patients can present with abdominal pain, gastrointestinal bleeding, or portal hypertension. Their radiological features can closely mimic those of other hypervascular pancreatic lesions, particularly pancreatic neuroendocrine tumours, making accurate diagnosis challenging. We report the case of a 77-year-old patient with incidentally detected hypervascular pancreatic nodules and the importance of a multimodal approach in establishing the diagnosis of pancreatic arteriovenous malformation.