Comparative 30-day overall mortality 9 Cirrhotics SARS-CoV-2+ vs. Cirrhotics with bacterial infection: 34% (95% CI 23-49) vs. 17% (95% CI 8-32) p = 0.03 9 Cirrhotics SARS-CoV-2+ vs. NON cirrhotics SARS-CoV-2+: 34% (95% CI 23-49) vs. 18% (95% CI 15-22) p = 0.035 patients with cirrhosis SARS-CoV-2 + 30-day mortality rate 34% (95% CI 23-49) Highlights 50 patients with cirrhosis and SARS-CoV-2 infection were studied, with an overall 30-day mortality rate of 34%. Mortality was higher in patients with respiratory failure and in those with worsening liver function at COVID-19 diagnosis. 30-day mortality rates were higher in patients with cirrhosis and COVID-19 than in those with bacterial infections. No major adverse events were related to the thromboprophylaxis with heparin (given to 80% of patients) or antiviral treatments.

invasive stratification of hepatocellular carcinoma risk in non-alcoholic fatty liver using polygenic risk scores,

Although annular fibrosis is the hallmark of cirrhosis, other microscopic changes that affect liver function such as sinusoid capillarization or loss of metabolic zonation are common. A sustained virological response (SVR) may halt fibrosis deposition in hepatitis C virus (HCV)-infected patients, but its impact on the other cirrhosis-associated lesions is unknown. The aim of this study was to assess the impact of an SVR on cirrhosis-related histopathological features. Paired pre-and posttreatment liver biopsies from 38 HCV patients with cirrhosis with an SVR were analyzed. Fibrosis was staged using the METAVIR scoring system, and the area of fibrosis was measured using morphometry. Ductular proliferation, metabolic zonation, sinusoid capillarization, and hepatic stellate cell activation were assessed by anti-cytokeratin-7, anti-glutamine synthetase (GS), anti-cytochrome P4502E1 (CYP2E1), anti-CD34, and anti a-smooth muscle actin (aSMA). After 61 months from an SVR, cirrhosis regression was observed in 61%, and the collagen content decreased in 89%. Although periportal and lobular necroinflammation vanished, portal inflammation persisted in 66%. Ductular proliferation decreased in 92%. Before treatment, metabolic zonation was lost, as shown by GS and CYP2E1, in 71% and 88%, respectively, with normalization in 79% and 73%, after an SVR. Conversely, no changes in sinusoidal capillarization were observed after treatment, as assessed by CD34 (P 5 0.41) and aSMA (P 5 0.95). Finally, no differences in all the immunohistochemical scores emerged whether or not cirrhosis persisted. Conclusion: Cirrhosis regression and decreased fibrosis are frequently observed among HCV patients with cirrhosis with an SVR. Despite ductular proliferation vanishing and lobular zonation restoration, portal inflammation and sinusoidal capillarization may not regress after viral eradication. (HEPATOLOGY 2012;56:532-543)