Background: Studies on a new coronavirus disease (COVID-19) show the elevation of liver enzymes and liver fibrosis index (FIB-4) independently on pre-existing liver diseases. It points to increased liver fibrogenesis during acute COVID-19 with possible long-term consequences. This study aimed to assess liver fibrosis in COVID-19 patients by serum hyaluronic acid (HA) and FIB-4. Methods: The study included the acute COVID-19 group (66 patients, 50% females, mean age 58.3 ± 14.6), the post-COVID group (58 patients in 3–6 months after the recovery, 47% females, mean age 41.2 ± 13.4), and a control group (17 people, 47% females, mean age 42.8 ± 11.0). Ultrasound elastography was performed in the post-COVID and control groups. Results: Sixty-five percent of the acute COVID-19 group had increased FIB-4 (> 1.45), and 38% of patients had FIB-4 ≥ 3.25. After matching by demographics, 52% of acute COVID-19 and 5% of the post-COVID group had FIB-4 > 1.45, and 29% and 2% of patients had FIB-4 ≥ 3.25, respectively. Increased serum HA (≥ 75 ng/ml) was observed in 54% of the acute COVID-19 and 15% of the post-COVID group. In the acute COVID-19 group, HA positively correlated with FIB-4, AST, ALT, LDH, IL-6, and ferritin and negatively with blood oxygen saturation. In the post-COVID group, HA did not correlate with FIB-4, but it was positively associated with higher liver stiffness and ALT. Conclusion: More than half of acute COVID-19 patients had increased serum HA and FIB-4 related to liver function tests, inflammatory markers, and blood oxygen saturation. It provides evidence for the induction of liver fibrosis by multiple factors during acute COVID-19. Findings also indicate possible liver fibrosis in about 5% of the post-COVID group.

Objectives: This study aimed to define patterns of liver injury after severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection using multiparametric ultrasound (mpUS) in a variable patient population with differing severities of COVID‐19.Methods: Ninety patients were enrolled into the study: 56 had SARS‐CoV‐2 3–9 months prior to enrolment; 34 served as a clinically healthy control group. All patients underwent an mpUS evaluation of the liver (elastography, dispersion and attenuation imaging). Seventy‐six patients had abdominal magnetic resonance (MR) and noncontrast enhanced thoracic computed tomography (CT) scans performed at the same day. All patients were screened for biochemical markers of liver injury.Results: Liver elasticity, viscosity, and steatosis values were significantly altered in patients after COVID‐19, with particularly higher fibrosis scores compared to the control group (P < .001). Increased biochemical markers of liver injury correlated with changes in mpUS (P < .05), but not with findings on CT or MR findings. Seventeen of 34 hospitalized patients had a moderate or severe course of the disease course with more pronounced changes in mpUS. Increased body mass index was found to influence liver injury and correlated with more severe forms of COVID‐19 (P < .001).Conclusions: COVID‐19 can cause liver injury observable using mpUS. More severe forms of COVID‐19 and patient obesity are related to increased values of liver damage observed. In comparison to MRI and CT, mpUS appears to be more sensitive to involvement of liver parenchyma. Further research is warranted to establish this promising method for evaluating post‐COVID‐19 liver involvement in the aftermath of the pandemic.

Introduction: Pathogenic mechanisms and long-term consequences of COVID-19 require attention in studies on SARS-CoV-2. The association of the severity of COVID-19 with genetic factors, such as human leukocyte antigen (HLA) genes, remains underexplored. Our study assessed the relationships between HLA class II alleles and COVID-19 severity and blood-based indicators of systemic inflammation and organ damage, serum markers of epithelial cell apoptosis such as caspase-cleaved CK18 fragment M30 (CK18-M30) and the extracellular matrix product hyaluronic acid (HA). Material and methods: The study included 101 hospitalized COVID-19 patients (mean age 60 ±14 years). Clinical tests were performed at admission to the hospital. The levels of CK18-M30 and HA were detected in serum by enzyme-linked immunosorbent assay (ELISA). HLA typing was performed in HLA-DRB1, -DQA1, and -DQB1 loci by the polymerase chain reaction with low-resolution sequence-specific primers. Results: Sixty-one patients had a non-severe and 40 had a severe or critical disease course (following the WHO definition). The severity was associated with older age, male gender, higher HA, CK18-M30, and some indicators of inflammation. Despite the lack of direct association between HLA alleles and the severity of COVID-19, the presence of HLA-DRB1*04 and 12 alleles in the genotype was associated with lowered or elevated HA, respectively. The HLA-DQB1*03:01 allele was associated with lowered CK18-M30, aspartate aminotransferase, and ferritin. In addition, HLA-DQB1*06:01 was associated with elevated alanine aminotransferase. Conclusions: Associations of HLA class II alleles with markers of epithelial cell apoptosis and extracellular matrix production indirectly support the influence of HLA genes on acute COVID-19 severity.

Background: Liver damage in COVID-19 is multifaceted, including liver steatosis and inflammation. Multiparametric ultrasound (mpUS) is an imaging modality that has the capacity to evaluate various facets of overall liver health and is relatively accessible and thus is an excellent choice to determine parenchymal changes. Methods: A longitudinal prospective study was designed to evaluate long-term hepatic damage following COVID-19 using mpUS. Patients were assessed within a 3–6-month period after the initial episode of COVID-19 and subsequently had a follow-up after 3 years compared to a control group. Liver stiffness (2D-SWE), attenuation (ATI), and shear wave dispersion (SWD) were measured to quantify liver stiffness, steatosis, and tissue viscosity. Results: A total of 129 patients were scanned at the baseline assessment, 90 patients in research group (58 patients had a follow-up) and 39 as a clinically healthy control group, and all were included in the follow-up for evaluation after 3 years. The mpUS evaluation in research group revealed a median SWE decrease from 5.04 ± 1.74 kPa to 4.59 ± 0.81 kPa and SWD decrease from 11.88 ± 1.73 m/s/kHz to 10.83 ± 1.49 m/s/kHz (p > 0.05); in contrast, median ATI values showed slight increase over time—0.56 ± 0.09 dB/cm/MHz to 0.60 ± 0.09 dB/cm/MHz (p > 0.05). Control group was stratified according to subsequent COVID-19 status. In both the COVID-negative and -positive subgroups SWE slightly increased from initial 4.55 ± 0.78 kPa to 4.8 ± 0.88 kPa and 4.7 ± 1.29 kPa, median SWD had a slight decrease from initial 10.80 ± 1.73 m/s/kHz to 10.15 ± 1.87 m/s/kHz and 10.6 ± 1.82 m/s/kHz (p > 0.05), and ATI increased significantly from initial 0.57 ± 0.08 dB/cm/MHz to 0.62 ± 0.09 dB/cm/MHz and 0.65 ± 0.07 dB/cm/MHz (p < 0.05), respectively. Conclusions: The study found that initially COVID-19-affected patients showed stable ATI and BMI values, no hepatic steatosis, normal SWE, and reduced dispersion which suggests resolving inflammation without fibrosis. Controls showed increased ATI and mild steatosis, likely linked to BMI and metabolic changes rather than direct viral liver injury.

The COVID-19 pandemic caused more than seven million deaths, mostly via acute respiratory distress syndrome with microvascular thrombosis. Compared to the amount of information about pulmonary pathology, information about COVID-19-induced liver lesions is scarce, especially with regard to the long-term consequences. The aim of our study was to evaluate inflammatory, vascular and fibrotic changes in hepatobiliary tissues of patients with a history of COVID-19 (post-COVID-19 patients). Based on the Knodell score, moderate portal inflammation was observed in 41.2% of post-COVID-19 patients, contrasting with 14.3% of control cases (p = 0.06). Moderate periportal inflammation was present in 26.5% and 7.1% of patients, respectively (p = 0.08). Post-COVID-19 patients showed higher counts of CD3+ lymphocytes (p = 0.02) and lower counts of CD68+ macrophages (p = 0.04), as well as more frequent and extensive regenerative changes in hepatocytes and the biliary epithelium (p = 0.0007). We did not find significant fibrosis or pathological changes in blood vessels, and only mild steatosis was observed in both groups.

Data include following variables: Demographics, epidemiological history, comorbidities, diagnosis, complications, and symptoms on admission to the hospital. Also, body’s temperature and SpO2. Blood cells: white cells count (WBC), neutrophils (Neu), lymphocytes (Ly), eosinophils (Eo) and monocytes (Mo), percentages of segmented and banded neutrophils, erythrocytes (RBC), platelet count (PLT), hemoglobin (Hb), and hematocrit (HCT); Inflammatory indicators: erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP); Tissue damage indicators: alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and troponin T (TnT); Electrolytes: potassium and sodium concentration; Renal function indicators: creatinine and glomerular filtration rate (GFR); Coagulation tests: D-dimer, prothrombin time, and prothrombin index on admission to the hospital.