Background and Aims Cholestasis is associated with disease severity and worse outcome in COVID‐19. Cases of secondary sclerosing cholangitis (SSC) after severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection have been described. Approach and Results Hospitalized patients with COVID‐19 between 03/2020 and 07/2021 were included. Patients were stratified as having (i) no chronic liver disease (CLD), (ii) non‐advanced CLD (non‐ACLD), or (iii) advanced CLD (ACLD). Patients with CLD and non–COVID‐19 pneumonia were matched to patients with CLD and COVID‐19 as a control cohort. Liver chemistries before (Pre) and at first, second, and third blood withdrawal after SARS‐CoV‐2 infection (T1–T3) and at last available time point (last) were recorded. A total of 496 patients were included. In total, 13.1% ( n = 65) had CLD (non‐ACLD: 70.8%; ACLD: 29.2%); the predominant etiology was NAFLD/NASH (60.0%). COVID‐19–related liver injury was more common among patients with CLD (24.6% vs. 10.6%; p = 0.001). After SARS‐CoV‐2 infection, patients with CLD exhibited progressive cholestasis with persistently increasing levels of alkaline phosphatase (Pre: 91.0 vs. T1: 121.0 vs. last: 175.0 U/L; p < 0.001) and gamma‐glutamyl transferase (Pre: 95.0 vs. T1: 135.0 vs. last: 202.0 U/L; p = 0.001). A total of 23.1% of patients with CLD ( n = 15/65) developed cholestatic liver failure (cholestasis plus bilirubin ≥6 mg/dl) during COVID‐19, and 15.4% of patients ( n = 10/65) developed SSC. SSC was significantly more frequent among patients with CLD and COVID‐19 than in patients with CLD and non–COVID‐19 pneumonia ( p = 0.040). COVID‐19–associated SSC occurred predominantly in patients with NAFLD/NASH and metabolic risk factors. A total of 26.3% ( n = 5/19) of patients with ACLD experienced hepatic decompensation after SARS‐CoV‐2 infection. Conclusions About 20% of patients with CLD develop progressive cholestasis after SARS‐CoV‐2 infection. Patients with NAFLD/NASH and metabolic risk factors are at particular risk for developing cholestatic liver failure and/or SSC after COVID‐19.

Background and Aims The coronavirus disease of 2019 (COVID‐19) causes considerable mortality worldwide. We aimed to investigate the frequency and predictive role of abnormal liver chemistries in different age groups. Methods Patients with positive severe acute respiratory distress syndrome‐coronavirus‐2 (SARS‐CoV‐2) polymerase chain reaction (PCR) test between 03/2020‐07/2021 at the Vienna General Hospital were included. Patients were stratified for age: 18–39 vs. 40–69 vs. ≥70 years (y). Aspartate aminotransferase (AST), alanine‐aminotransferase (ALT), alkaline phosphatase (ALP), gamma‐glutamyl transferase (GGT) and total bilirubin (BIL) were recorded. Results 900 patients (18–39 years: 32.2%, 40–69 years: 39.7%, ≥70 years: 28.1%) were included. Number of comorbidities, median D‐dimer and C‐reactive protein increased with age. During COVID‐19, AST/ALT and ALP/GGT levels significantly increased. Elevated hepatocellular transaminases (AST/ALT) and cholestasis parameters (ALP/GGT/BIL) were observed in 40.3% ( n = 262/650) and 45.0% ( n = 287/638) of patients respectively. Liver‐related mortality was highest among patients with pre‐existing decompensated liver disease (28.6%, p < .001). 1.7% of patients without pre‐existing liver disease died of liver‐related causes, that is consequences of hepatic dysfunction or acute liver failure. Importantly, COVID‐19‐associated liver injury (16.0%, p < .001), abnormal liver chemistries and liver‐related mortality (6.5%, p < .001) were most frequent among 40–69 years old patients. Elevated AST and BIL after the first positive SARS‐CoV‐2 PCR independently predicted mortality in the overall cohort and in 40–69 years old patients. Conclusions Almost half of the COVID‐19 patients exhibit abnormal hepatocellular and cholestasis‐related liver chemistries with 40–69 years old patients being at particularly high risk for COVID‐19‐related liver injury and liver‐related mortality. Elevated AST and BIL after SARS‐CoV‐2 infection are independent predictors of mortality, especially in patients aged 40–69 years.

This study aimed to determine the specific cytokine profile in peripheral blood during the early onset of COVID-19 infection. This was a cross-sectional exploratory, single center study. A total of 55 plasma samples were studied. Serum samples of adults showing symptoms of COVID-19 infection who were tested positive for SARS-CoV-2 infection (CoV+, n=18) at the COVID-19 outpatient clinic of the Medical University of Vienna were screened for immune activation markers by Luminex technology. Additionally, age and gender-matched serum samples of patients displaying COVID-19 associated symptoms, but tested negative for SARS-CoV-2 (CoV-, n=16) as well as healthy controls (HC, n=21) were analyzed. COVID-19 positive (CoV+) patients showed a specific upregulation of BLC (141; 74-189 pg/mL), SCD30 (273; 207-576 pg/mL), MCP-2 (18; 12-30 pg/mL) and IP-10 (37; 23-96 pg/mL), compared to patients with COVID19-like symptoms but negative PCR test (CoV-), BLC (61; 22-100 pg/mL), sCD30L (161; 120-210 pg/mL), MCP-2 (8; 5-12 pg/mL) and IP-10 (9; 6-12 pg/mL) and healthy controls (HC) (BLC 22; 11-36 pg/mL, sCD30 74; 39-108 pg/mL, MCP-2 6; 3-9. pg/mL, IP-10 = 8; 5-13). The markers APRIL, sIL-2R, IL7, MIF, MIP-1b, SCF, SDF-1a, sTNF-RII were elevated in both CoV+ and CoV- patient groups compared to healthy controls. HGF, MDC and VEGF-A were elevated in CoV- but not CoV+ compared to healthy controls. BLC, sCD30, MCP-2 and IP-10 are specifically induced during early stages of COVID-19 infection and might constitute attractive targets for early diagnosis and treatment of this disease.

Background and Aims Despite vaccination recommendations, hepatitis B (HBV) and D (HDV) coinfections are common in HIV+individuals. Methods HBV immunization status (anti‐HBs) as well as HBV (HBsAg/HBV‐DNA) and HDV (anti‐HDV) coinfection rates were assessed in 1870 HIV+individuals at HIV diagnosis (baseline, BL) and last follow‐up (FU). Results Sixty‐eight (3.6%) HIV patients were never tested for HBV. At BL, 89/1802 (4.9%) HIV patients were HBV coinfected. Four hundred and fifteen (23.0%) showed virological HBV clearance [HBsAg(‐)/anti‐HBc(+)/anti‐HBs(+)] and 210 (11.7%) presented with anti‐HBc(+) only. Seven hundred and ten (39.4%) were HBV naïve [HBsAg(‐)/anti‐HBs(‐)/anti‐HBc(‐)/HBV‐DNA(‐)], but only 378 (21.0%) received vaccinations with detectable anti‐HBs(+) titres. Among the 89 HBV/HIV‐coinfected patients, only 52 (58.4%) were tested for HDV: 11/49 (22.4%) had anti‐HDV(+) and 3/12 (25.0%) showed HDV‐RNA viraemia. During a median FU of 6.5 (IQR 7.2) years, 44 (4.6%) of the 953 retested BL HBV‐negative patients acquired new HBV infection (including 15/304, 4.9% of vaccinated patients). Of the 89 patients, 22 (24.7%) patients cleared their HBsAg, resulting in 60/1625 (3.7%) HIV/HBV individuals at FU: 34 (56.7%) showed HBV‐DNA suppression and 15 (25.0%) were HBV viraemic, while 12/89 (13.5%) remained without a FU test. Vaccinations induced anti‐HBs(+) in 137 of the retested 649 (21.1%) BL HBV‐naïve patients. Conclusion HBV testing is well established among Viennese HIV+patients with HBV coinfection rates around 4%‐5%. HBV vaccinations are insufficiently implemented since anti‐HBs titres were detected in only 21.1% of HBV‐naive HIV(+) patients and new HBV infections occurred in previously vaccinated patients. HDV testing is not systematically performed despite up to 25% of HIV/HBV patients may show HDV coinfection.

Background: In chronic liver disease, current biomarkers demonstrate limited mid-to long-term predictive value for prognostic relevant endpoints including liver transplantation (LT) or liver-related death (LRD). Aim: To determine the predictive value of 13 C-methacetin breath test (MBT, BreathID ® ; Exalenz) for deterioration requiring LT or LRD in patients with chronic hepatic dysfunction due to HCV infection. Methods: One hundred thirty-two HCV patients without co-infection or other underlying liver diseases underwent MBT, 127 underwent liver biopsy with ISHAK scoring, 5 had clinically diagnosed cirrhosis. Patients were followed up for up to 7 years according to standard of care including anti-viral treatment in a subgroup. Primary analysis endpoints were LT or LRD. Results: MBT peak percentage dose rate (PDR-Peak), cutoff 20%/h, predicted LT