On March 20, The Lancet Gastroenterology & Hepatology published a newsletter (Correspondence) online that explored the link between new coronavirus pneumonia (COVID-19) and liver damage in patients.
The authors stated that COVID-19-induced liver injury is closely related to the innate immune dysfunction caused by the virus, which may cause clinical treatment disturbances, and more in-depth related research is urgently needed.
The article is titled "COVID-19 and the liver: little cause for concern". The authors of the article are from the liver intensive care unit of the National Health Service Foundation Trust of the University Hospital of the United Kingdom, respectively Mansoor N Bangash of the University of Birmingham's liver failure research group Jaimin Patel and Dhruv Parekh of the Birmingham Emergency Research Team.
To date, studies of COVID-19 have shown that the incidence of elevated aminotransferases and bilirubin in critically ill patients is at least twice that of others.
Although clinically significant liver dysfunction cannot be quantified by researchers, this and other studies have led some scientists to suggest that this phenomenon may pose clinical challenges.
The authors analyzed the existing data and found that patients with severe COVID-19 are more likely to have abnormal transaminase levels, but in fact, even if the data of the most severely ill patients are selected, clinically significant liver damage is less common.
In addition, according to published literature, the distribution of aminotransferase levels in patients with COVID-19 does not support hypoxic hepatitis as a common condition.
Although during the course of treatment, a high level of positive end expiratory pressure (PEEP), that is, artificial end of expiratory pressure during the breathing cycle, applying a pressure higher than atmospheric pressure in the airways and alveoli, can Preventing the occurrence of alveolar occlusion) can cause liver congestion due to increased right atrium pressure and impeded venous return.
However, data indicate that many hospitalized COVID-19 patients have abnormal liver blood tests without mechanical ventilation.
Drug-induced liver injury may be a possible cause of liver blood abnormalities after the patient begins treatment, which clinicians should consider.
However, for many COVID-19 patients, there is a mild liver test before their baseline use of the drug (the period during which the patient has been screened for the clinical study but has not started treatment). abnormal.
The authors have statistics on liver function-related indicators and mortality in previous studies
Several previous studies have reported that elevated levels of creatinine kinase and lactate dehydrogenase or myoglobin are associated with COVID-19 severity.
Earlier on February 20, "Chinese Journal of Hepatology" published a paper entitled "New Coronary Virus Pneumonia-related Liver Injury: Etiological Analysis and Treatment Strategies" by the corresponding author Yang Ling, Department of Gastroenterology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology.
The paper analyzes that there are four major causes of liver damage caused by new coronavirus pneumonia, which are immune damage, drug factors, systemic inflammation, and ischemic hypoxia-reperfusion injury.
In fact, the top medical journal "The Lancet" has paid attention to liver damage in 99 cases of new coronavirus pneumonia cases published on January 30, Beijing time.
The paper mentions that patients with new-type coronavirus pneumonia are very rare with liver damage as the first occurrence, and secondary liver damage is more common.
In the newsletter, the authors also pointed out that patients with elevated aminotransferases are not necessarily caused solely by the liver, and that COVID-19 infection may induce patients with myositis similar to severe influenza infections.
The authors believe that the cause of liver damage in patients with COVID-19 may not be directly caused by viral hepatitis:
First, the patient's abnormal liver function was clearly mild.
Second, when liver function tests are performed on patients with symptoms at different stages, there is no evidence that patients will develop more severe liver dysfunction over time.
The only liver biopsy report from a COVID-19 patient showed that the patient had only symptoms of vesicular steatosis in the liver, which is a common manifestation of sepsis.
Most importantly, other respiratory viruses produce similar elevations in liver function biomarkers, which are thought to be immune to implicated liver cytotoxic T cells and Kupffer cells (phagocytic cells on the inner surface of the liver sinus). Interactions are related to liver damage.
This phenomenon changes with changes in respiratory viral diseases and has nothing to do with liver virus replication, which may explain why 42 patients with chronic liver disease COVID-19 did not present poor clinical outcomes in the previous analysis.
Hepatic insufficiency in patients with severe COVID-19 is accompanied by more activation of the coagulation and hemolytic fiber pathways. At the same time, the platelet count is low, the neutrophil count and the neutrophil to lymphocyte ratio will increase, and ferritin levels Rise.
The authors say that although these markers are considered non-specific markers of inflammation, they can represent the severity of the disease and are consistent with functional failure of innate immune regulation.
This imbalanced immunity is conducive to NETosis (neutrophil extracellular trapping process), which refers to a new type of death of neutrophils different from apoptosis and necrosis. It uses DNA in the nucleus or mitochondria as the backbone. Loaded with antimicrobial peptides and hydrolytic enzymes to form a network structure, encapsulating and killing invading pathogens.
However, neutrophils will die after releasing the DNA in the nucleus), easily activate blood coagulation, and may also change the body's 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 coagulation and hemolytic fiber pathways.
The authors suggest that for patients with chronic liver disease and cirrhosis, clinicians cannot underestimate their risk of developing COVID-19.
Because these patients have poorer immune function than other severely ill patients, acute respiratory distress syndrome (ARDS) can lead to worse outcomes.
At the same time, the authors believe that the additional damage to the liver caused by virus-induced cytotoxic T cells and the innate immune response 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 stated that COVID-19-induced liver injury will, in most cases, cause clinical interference to doctors.
The authors advocate that clinicians and the scientific community focus on virus control and regulation of innate immune dysfunction brought about by COVID-19.
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