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.