Infections ACLF Death Different clinical courses of acutely decompensated cirrhosis Pre-ACLF Unstable decompensated cirrhosis Stable decompensated cirrhosis 0 90 180 270 360 Days Highlights Patients with acutely decompensated cirrhosis without ACLF develop 3 different clinical courses. Patients with pre-ACLF develop ACLF within 90 days and have high systemic inflammation and mortality. Patients with unstable decompensated cirrhosis suffer from complications of severe portal hypertension. Patients with stable decompensated cirrhosis have less frequent complications and lower 1-year mortality risk.
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Hepatic encephalopathy (HE) is a common and serious neuropsychiatric complication of cirrhosis, acute liver failure, and porto-systemic shunting. HE largely contributes to the morbidity of patients with liver disease, severely affecting the quality of life of both patients and their relatives and being associated with poor prognosis. Its presentation is largely variable, manifesting with a broad spectrum of cognitive abnormalities ranging from subtle cognitive impairment to coma. The pathogenesis of HE is complex and has historically been linked with hyperammonemia. However, in the last years, it has become evident that the interplay of multiple actors, such as intestinal dysbiosis, gut hyperpermeability, and neuroinflammation, is of crucial importance in its genesis. Therefore, HE can be considered a result of a dysregulated gut-liver-brain axis function, where cognitive impairment can be reversed or prevented by the beneficial effects induced by “gut-centric” therapies, such as non-absorbable disaccharides, non-absorbable antibiotics, probiotics, prebiotics, and fecal microbiota transplantation. In this context dietary modifications, by modulating the intestinal milieu, can also provide significant benefit to cirrhotic patients with HE. This review will provide a comprehensive insight into the mechanisms responsible for gut-liver-brain axis dysregulation leading to HE in cirrhosis. Furthermore, it will explore the currently available therapies and the most promising future treatments for the management of patients with HE, with a special focus on the dietary approach.
Introduction: Limited information is available about outcomes of patients with malignant adenomas endoscopically resected at screening. The aim of the study was to evaluate diagnostic and therapeutic quality indicators and to correlate them with clinical and surgical outcomes. Materials and Methods: We reviewed endoscopic and histology characteristics of all pT1 tumours endoscopically removed at the time of colonoscopy assessment in subjects with a positive screening test result in the context of a population-based program. Results: 392 pT1 tumours were completely removed by endoscopy (en-bloc= 86.7%, piecemeal= 13.3%) and the histology report was considered complete in 83.2% of cases. Treatment was limited to endoscopic excision for 120 patients (30.7%, Group 1), 272 (69.3%, Group 2) underwent radicalisation surgery. In patients who had at least 1 lymph node examined, the rate of nodal involvement was 5.4% (13/239); no metastatic node was found in the 21 (27.6%) out of 76 patients with low-risk adenomas, who underwent surgery. Conclusion: Risk of nodal involvement in colorectal pT1 tumours is well predicted by known histologic features also in a screening setting, although it was lower than among patients from clinical series. Surgical overtreatment is still significantly present and there is ample room for improvement regarding diagnostic and therapeutic flow-chart.
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