On March 20, local time, the international medical journal The Lancet Gastroenterology and Hepatology published an online newsletter. The relationship between the new coronavirus pneumonia (COVID-19) and liver damage in patients was discussed.
CoVID-19-induced liver damage is closely related to congenital immune dysfunction caused by the virus, which may lead to clinical interference and requires more in-depth research, the authors said.
The article, entitled “COVID-19 and the liver: little cause for concern”, was written by Mansoor N, a member of the National Health Service Foundation Trust’s liver unit at university hospitals, Birmingham Bangash, Jaimin Patel of the Birmingham Emergency Research Group and Dhruv Parekh.
So far, studies of COVID-19 have shown that the incidence of elevated aminotransferas and bilirubin in severely ill patients is at least twice that of others. Although clinically significant liver abnormalities cannot be quantified by researchers, this and other studies have led some scientists to suggest that this phenomenon may pose clinical challenges.
The authors counted available data and found that patients with severe COVID-19 were more likely to experience abnormal transaminase levels, but in fact, even if data from the most severely ill patients were selected, clinically apparent liver damage was less common. In addition, according to published literature, the distribution of amino metastase levels in COVID-19 patients does not support the prevalence of hypoxic hepatitis.
Although during treatment, a high level of end-of-exhalation positive pressure ventilation (positive end end pressure, PEEP, i.e. artificially at the end of the exhalation during the respiratory cycle, a pressure above atmospheric pressure in the airway and in the alveoli, is applied in the airways and in the alveoli, Preventing the occurrence of alveolar clots) can cause liver bruising due to increased right atrial pressure and obstruction of venous reflux, but the data show that many hospitalized COVID-19 patients have abnormal liver and blood tests without mechanical ventilation.
Drug-induced liver damage may be a possible cause of liver and blood abnormalities after a patient begins treatment, which clinicians should consider, but for many COVID-19 patients, they are in the baseline period prior to heavy use of the drug (i.e., in clinical studies, There are mild liver test abnormalities in patients who have been screened for study but have not yet begun medication.
The authors counted indicators and fatality rates related to liver function in previous studies
Several previous studies have reported that elevated levels of creatinine kinase and lactic acid dehydrogenase or myoglobin are associated with coVID-19 severity.
Prior to February 20, the Chinese Journal of Liver Disease published a paper by the author of the newsletter for Yang Ling of Digestive Medicine, Tongji Medical College affiliated with Huazhong University of Science and Technology: “New Coronary Virus Pneumonia-Related Liver Injury: Etiological Analysis and Treatment Strategy.”
The paper analyzed that there are four main causes of liver injury to new coronary pneumonia, namely, immune injury, drug factors, systemic inflammation, ischemic hypoxia re-injection damage.
In fact, the top medical journal, The Lancet, has focused on liver damage in 99 cases of new coronary pneumonia published on January 30, Beijing time. The paper mentions that it is very rare for patients with new coronary pneumonia to perform with liver injury as the first, while secondary liver injury is more common.
In the newsletter, the authors also point out that the increase in amino transfer asease in patients is not necessarily caused solely by the liver, and that COVID-19 infections may cause patients to develop myositis similar to severe flu infections.
The authors argue that liver damage in PATIENTS WITH COVID-19 may not be due to viral hepatitis as a direct result of:
First, the patient’s abnormal liver function was significantly mild.
Second, when patients with symptoms at different stages are examined for liver function, there is no evidence that more severe liver dysfunction occurs over time. The only liver biopsy from coVID-19 patients showed that the patient’s liver had only small bubbly fatty degeneration symptoms, a common manifestation of sepsis.
Most importantly, other respiratory viruses produce similar elevated liver function biomarkers, which are thought to be associated with liver damage caused by immune interactions involving cytotoxic T cells and Kupffer cells (copfercells located on the inner surface of the liver sinuses).
This phenomenon changes with changes in respiratory viral diseases and is not associated with liver virus replication, which may explain why 42 patients with chronic liver disease COVID-19 did not show poor clinical outcomes in previous analyses.
The liver function of patients with severe COVID-19 is not completely accompanied by more clotting and hemolytic fibrous pathway activation, while platelet count is lower, neutrophil count and neutrophil-to-lymphocytic ratio increases, and ferritin levels rise.
Although these markers are considered nonspecific markers of inflammation, they can represent the severity of the disease and are consistent with functional failures in innate immunomodulation, the authors said.
This unbalanced immunity is beneficial to NETosis (the neutlyte granulocytes extracellular networking process, which refers to a new type of death of neutrophils different from apoptosis and necrosis, with DNA in the nucleus or mitochondria as the skeleton, loaded with antimicrobial peptides and hydrolysises to form a mesh structure, enveloping and killing foreign invasion pathogens, But neutrophils die after releasing DNA from the nucleus, easily activate coagulation, and may alter body iron metabolism after causing macrophages to activate.
It is worth noting that this change in immune balance occurs more with age, so older patients are expected to get worse and become more dependent on the blood clotting and hemolytic fiber pathways.
The authors suggest that clinicians should not underestimate the risk of developing COVID-19 in patients with chronic liver disease and cirrhosis. Because these patients have poor immune function compared to other patients with severe illness, acute respiratory distress syndrome (ARDS) results in worse outcomes.
At the same time, the authors believe that the additional damage to the liver of virally induced cytotoxic T-cells and innate immune reflexes are more likely explanations for the association between abnormal liver markers and the severity of COVID-19 disease.
At the end of the article, the authors say that COVID-19-induced liver damage can in most cases cause clinical disruption to doctors. The authors argue that clinicians and the scientific community are focused on virus control and regulating congenital immune dysfunction caused by COVID-19.