Humans ; Liver Cirrhosis, Biliary ; etiology

Humans ; Liver Cirrhosis ; diagnosis ; etiology

Ascites ; etiology ; Humans ; Liver Cirrhosis ; complications

Humans ; Liver Cirrhosis ; diagnosis ; etiology ; therapy

Humans ; Liver Cirrhosis, Biliary ; diagnosis ; etiology ; therapy

Fatigue ; etiology ; Humans ; Liver Cirrhosis, Biliary ; complications ; Pruritus ; etiology

The emergence of non-alcoholic fatty liver disease (NAFLD) as the leading chronic liver disease worldwide raises some concerns. In particular, NAFLD is closely tied to sedentary lifestyle habits and associated with other metabolic diseases, such as obesity and diabetes. At the end of the disease spectrum, non-alcoholic steatohepatitis (NASH) may progress to cirrhosis and hepatocellular carcinoma (HCC), representing a serious health problem to modern society. Recently, an increasing number of HCC cases originating from this progressive disease spectrum have been identified, with different levels of severity and complications. Updating the current guidelines by placing a bigger focus on this emerging cause and highlighting some of its unique features is necessary. Since, the drivers of the disease are complex and multifactorial, in order to improve future outcomes, having a better understanding of NASH progression into HCC may be helpful. The risks that can promote disease progression and currently available management strategies employed to monitor and treat NASH-related HCC make up the bulk of this review.
Carcinoma, Hepatocellular/etiology* ; Humans ; Liver Cirrhosis ; Liver Neoplasms/etiology* ; Non-alcoholic Fatty Liver Disease ; Obesity

Most patients with liver cirrhosis have hyperdynamic circulatory alterations with increased cardiac output, and decreased systemic vascular resistance and arterial pressure. But, in spite of the increased resting cardiac output, ventricular contractile response to stressful stimuli is attenuated in cirrhotic patients which is termed as cirrhotic cardiomyopathy. The prevalence of cirrhotic cardiomyopathy remains unknown at present. Clinical features include structural, histological, electrophysiological, systolic and diastolic dysfunction. Multiple factors are considered as responsible, including impaired beta-adrenergic receptor signal transduction, abnormal membrane biophysical characteristics, and increased activity of cardiodepressant systems mediated by cGMP. Generally, cirrhotic cardiomyopathy with overt severe heart failure is rare. However, major stresses on the cardiovascular system such as liver transplantation, infections and insertion of transjugular intrahepatic portosystemic shunts (TIPS) can unmask the presence of cirrhotic cardiomyopathy and thereby convert latent to overt heart failure. Cirrhotic cardiomyopathy may also contribute to the pathogenesis of hepatorenal syndrome and circulatory failure in liver cirrhosis. Because of the marked paucity of treatment studies, current recommendations for management are empirical, nonspecific measures. Further studies for pathogenesis and new therapeutic strategies in this area are required.
Cardiomyopathies/*diagnosis/*etiology/therapy ; Humans ; Liver Cirrhosis/*complications ; Prognosis

Adult ; Ascites ; etiology ; Ascitic Fluid ; Female ; Humans ; Liver Cirrhosis ; complications

Humans ; Ascites/etiology* ; Liver Cirrhosis/complications* ; Cholecystectomy/adverse effects*