4. DISCUSSION
The results of our study show that the two groups of patients had a significant difference in diabetes prevalence, NLR, CRP, and ALB. There was a positive correlation between diabetes, NLR, CRP and severe COVID-19 infection. However, ALB had a negative correlation with severe COVID-19 infection. Moreover, NLR was found to be an independent risk factor for severe COVID-19 infection.
Neutrophils are one of the human body’s vital immune cells. When pathogenic microorganisms invade the body, immune cells tend to rapidly chemotactically gather to the infection site and play the role of host defense and immune regulation.15 When the body’s neutrophils are significantly reduced, the body’s immunity is compromised, and thus the risk of infection is significantly increased.16 Lymphocytes are the main effector cells of the human immune response. The number of lymphocytes in the body is closely related to the body’s immunity and defense system against pathogenic microorganisms and is negatively correlated with the degree of inflammation.9 NLR encompasses two types of leukocyte subtypes, reflecting the balance of the body’s neutrophil and lymphocyte count levels and the degree of systemic inflammation. More accurately, it reflects the balance between the severity of the inflammation and the body’s immunity status,17 and is thus considered an important marker of systemic inflammatory response. Based on this, we speculated that heavy COVID-19 infection can have significant systemic inflammation and that NLR may have a role in predicting the infection’s severity.
The outbreak of COVID-19 is caused by the SARS-CoV-2 virus infection. The disease spectrum varies from no symptoms to severe disease and death. Clinical observation has found that some patients with mild disease progress to severe disease within a short period of time with a high risk of mortality. The specific pathological mechanism is unknown. Some believe that the sudden aggravation of the condition is due to the rapid emergence of ARDS, and subsequent multiple-organ dysfunction in the later period which may be related to the ”cytokine release storm”.18 The concept of an inflammatory factor storm was first proposed in 1993.19 In 2003, the SARS-CoV virus infection caused ARDS and multiple-organ failure, resulting in an exceedingly high rate of mortality – the underlying pathology of inflammatory factor storm that gradually attracted the attention of the medical community.20 The SARS-CoV-2 virus is extremely closely related to the SARS-CoV virus. In the virus spectrum, both belong to β-CoV coronavirus family,21in terms of genetic characteristics, both have 79.5% sequence similarity,22 and with regards to clinical manifestations, it is easy to progress to ARDS and multiple-organ dysfunction in infections caused by these viruses. Therefore, based on the close similarities between the two viruses, COVID-19 patients’ clinical condition changes from mild to critical, which may be related to the inflammatory factor storm. Li et al found in their study that the patients with COVID-19 pneumonia admitted to ICU had higher levels of inflammatory markers such as IL2, IL7, IL10, GSCF, IP10, MCP1, MIP1A, and TNFα in the plasma, reflecting severe inflammation.23 This is due to an apparent inflammatory response in the patient’s body, which is consistent with our findings.
In summary, our study conducted a prospective analysis of common clinical risk factors or parameters that can be easily obtained from the laboratory. Our study found that there was a significant difference in NLR between general and heavy group COVID-19 patients with heavy group patients tending to have significantly higher NLR. In addition to NLR being an independent risk factor for severe COVID-19 infection, the ROC curve calculation of AUC showed a high predictive value of NLR for severe COVID-19 infection. As per these results, we believe that increasing NLR can be used as a warning signal for rapidly deteriorating COVID-19 infection and can provide us with a certain objective basis for the early identification of severe COVID-19 pneumonia. This can further allow us to be prepared for the exploration of subsequent treatment mechanisms. However, this study had certain limitations, such as having a small sample size and being a single-center study. For more accurate and precise results, and wider generalizability of the findings, multicentred and larger sample size clinical studies are required to validate our results.