Table 1 Host-oriented risk factors demonstrated in classes, types, and prognostic values, as well as the possible mechanisms and outcomes that may contribute to SIH in patients with COVID-19
From: Liver injury in COVID-19: an insight into pathobiology and roles of risk factors
Risk factors | Prognostic value | Possible mechanisms & outcomes | Reference | ||
|---|---|---|---|---|---|
Category | Class | Type | |||
Host factors | Demographic features | Age | > 65 years | - Immunopathogenesis - Comorbidity - Decrease of stem cells - Higher expression of ACE-2 & TMPRSS-2 | 1, 47–51 |
Gender | Male sex | - Sex hormones - Higher expression of ACE-2 - Sex-specific features of immune system | 47, 52, 53 | ||
Pre-existing diseases | ALD | Â | - Alcohol-related steatohepatitis - Liver fibrosis & cirrhosis - Increase of inflammatory cytokines | 54 | |
NAFLD / NASH | Â | - Chronic inflammation - Hypercoagulability - Oxidative stress - Liver fibrosis - Liver cirrhosis - Hepatonecrosis - Longer clearance time of viruses | 40, 56, 63 | ||
Liver cirrhosis |  | - Ischemic/hypoxic liver injury - Hepatic encephalopathy - HCC | 7, 16, 40, 54, 57–59 | ||
Liver transplantation | Â | - Higher chances of critical COVID-19 as a result of immunosuppression therapy | 55 | ||
Diabetes | Â | - Higher expression of ACE-2 & FURIN - Lymphocytopenia - Elevation of IL-6 | 60 | ||
Liver markers | ALT & AST | >3-fold of the upper limit | Â | 21, 22 | |
GGT | >2-fold of the upper limit | Â | |||
ALP & TBIL | >2-fold of the upper limit | Â | |||
Hypoalbuminemia | <34Â g/L | Â | 25 | ||