The outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which later led to the 2019 coronavirus disease (COVID-19) pandemic, has claimed more than 6. 5 million lives worldwide.
Although SARS-CoV-2 is a breathing virus, liver disorders have been reported in only about 50% of inflamed patients. The manifestation of chronic liver disease (CLD) is not unusual in severely inflamed patients with COVID-19 who require hospitalization. .
A higher mortality rate has been linked to patients with severe cirrhosis from COVID-19. A recent report from Northern Gastroenterology Clinics summarizes the clinical outcomes of COVID-19 patients with CLD.
High levels of liver enzymes were observed in approximately 83% of COVID-19 patients who required hospitalization. Among all liver enzymes, maximal accumulation of aspartate transaminase (AST) was observed in this group of patients.
Elevated levels of bilirubin, glutamyl transferase (GGT), and alkaline phosphatase (ALP) have been reported in 3-23%, 13-54%, and 1-22% of COVID-19 patients, respectively. It should be noted that one of the main markers of COVID-19 severity is hypoalbuminemia.
The trend of liver damage similar to SARS-CoV-2 infection was mainly hepatocellular than cholestatic. In the early phase of infection, a slight elevation of AST and ALT was observed. In peak cases, AST grades were higher than ALT grades, with those grades expanding particularly with disease severity.
In most cases, liver biochemical abnormalities returned to general degrees within two to three weeks without the need for prompt treatment. COVID-19 patients with high AST and ALT levels were associated with increased mortality.
Pregnant women with COVID-19 had high AST and ALT levels, demonstrating the importance of tracking this organization for liver injury. People who had a history of complex liver disease, cirrhosis, had an increased risk of mortality after SARS-CoV-2 infection.
Several mechanisms related to liver injury have been reported in patients with COVID-19. Liver histology at autopsy reported microvesicular steatosis/macrovesicular steatosis, focal necrosis, lobular necroinflammation, portal inflammation, and portovenous/sinusoidal microthrombosis.
SARS-CoV-2 infects the mobile host by binding to angiotensin-converting enzyme 2 (ACE2) receptors. These receptors are found on hepatocytes and cholangiocytes, making the liver a target for infection.
In addition, SARS-CoV-2 attacks liver cells and damages epithelial cells in bile ducts. Autopsy samples also indicated hepatic tropism of SARS-CoV-2.
In severely inflamed COVID-19 patients, the host immune formula releases an excessive amount of inflammatory mediators, such as interleukin 6 (IL-6), IL-10, IL-2, and interferon γ (IFN γ), leading to cytokine storms, which can lead to severe liver dysfunction. Significant upregulation of type I and II IFN responses has also been observed in severely inflamed COVID-19 patients.
Some of the healing agents used to treat SARS-CoV-2 infection, such as immunomodulators, corticosteroids, antibiotics, and antiviral agents, can cause liver damage to varying degrees. For example, lopinavir/ritonavir increases liver damage fourfold.
In addition, remdesivir, which is a viral ribonucleic acid (RNA) polymerase analogue inhibitor, increased liver biochemical levels by 23%. COVID-19 patients treated with tocilizumab also experienced elevated transaminase levels.
Several large multicenter cohort studies have found that CLD is associated with increased mortality, specifically in patients with cirrhosis. Retrospective cohort studies discovered in Hong Kong and China found that hepatitis B virus (HBV) infection is not related to COVID-19 mortality.
Autoimmune hepatitis (HAI) is a rare end result after COVID-19. Data from several studies have shown that patients with IAI have an increased threat of adverse clinical outcomes after SARS-CoV-2 infection. Similarly, alcohol-related liver disease (ALD) has been reported to be an independent threat to mortality in CLD patients with COVID-19.
Liver transplant patients have the highest risk of contracting COVID-19; However, its mortality rate decreases particularly and is consistent with the effects of the general population.
Adult patients with CLD, especially those with cirrhosis and liver transplant recipients, have been strongly advised to get vaccinated against COVID-19. Compared with unvaccinated CLD patients, vaccinated patients were associated with a 64. 8% reduction in the risk of SARS-CoV-2 infection Patients vaccinated with CLD also opposed serious infections.
Some patients with cirrhosis have experienced an advance of COVID-19 infection after complete or partial vaccination. However, these infections were associated with reduced mortality in unvaccinated patients with CLD.
Most CLD patients and liver transplant recipients have favorable clinical outcomes after COVID-19 vaccination. A weaker serological reaction to vaccination was observed in older patients and those taking antimetabolite drugs and mobile B-depletion therapies.
Written By
Priyom holds a PhD in Plant Biology and Biotechnology from the University of Madras, India. She is an active and experienced science writer. Priyom also co-authored several original articles that have been published in reputable peer-reviewed journals. He is also an avid reader and amateur photographer.
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