Metabolic and nutritional triggers associated with increased risk of liver complications in SARS-CoV-2

Abstract

Obesity, diabetes, cardiovascular and respiratory diseases, cancer and smoking are risk factors for negative outcomes in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which can quickly induce severe respiratory failure in 5% of cases. Coronavirus disease-associated liver injury may occur during progression of SARS-CoV-2 in patients with or without pre-existing liver disease, and damage to the liver parenchyma can be caused by infection of hepatocytes. Cirrhosis patients may be particularly vulnerable to SARS-CoV-2 if suffering with cirrhosis-associated immune dysfunction. Furthermore, pharmacotherapies including macrolide or quinolone antibiotics and steroids can also induce liver damage. In this review we addressed nutritional status and nutritional interventions in severe SARS-CoV-2 liver patients. As guidelines for SARS-CoV-2 in intensive care (IC) specifically are not yet available, strategies for management of sepsis and SARS are suggested in SARS-CoV-2. Early enteral nutrition (EN) should be started soon after IC admission, preferably employing iso-osmolar polymeric formula with initial protein content at 0.8 g/kg per day progressively increasing up to 1.3 g/kg per day and enriched with fish oil at 0.1 g/kg per day to 0.2 g/kg per day. Monitoring is necessary to identify signs of intolerance, hemodynamic instability and metabolic disorders, and transition to parenteral nutrition should not be delayed when energy and protein targets cannot be met via EN. Nutrients including vitamins A, C, D, E, B6, B12, folic acid, zinc, selenium and ω-3 fatty acids have in isolation or in combination shown beneficial effects upon immune function and inflammation modulation. Cautious and monitored supplementation up to upper limits may be beneficial in management strategies for SARS-CoV-2 liver patients.

The Host Response to Influenza A Virus Interferes with SARS-CoV-2 Replication during Coinfection

“…More severe cases of COVID-19 involve the development of acute respiratory distress syndrome and lung injury, often leading to death. Several risk factors for disease severity have been identified, including sex, age, immunodeficiency, diabetes, and obesity ( 9 – 11 ). In addition, SARS-CoV-2 infection suppresses key components of the innate immune response.…”

COVID-19, Possible Hepatic Pathways and Alcohol Abuse—What Do We Know up to 2023?

“…Figure 2 shows mechanisms related to ethanol that participate in the presentation of COVID-19. Malnutrition and metabolic syndrome constitute other underlying issues [240,241]. The development of leaky gut and microbiota dysbiosis can be perceived as cofactors [242,243].…”

“…Ethanol induces the release of reactive oxygen species and promotes the secretion of various proinflammatory chemokines, simultaneously inhibiting the production of anti-inflammatory particles. Finally, the integrity of the epithelium becomes disrupted, leading to alveolar epithelial dysfunction and decreased concentration of pulmonary an- Malnutrition and metabolic syndrome constitute other underlying issues [240,241]. The development of leaky gut and microbiota dysbiosis can be perceived as cofactors [242,243].…”