Discussion
Coronavirus disease 2019 (COVID-19) is the seventh known human
coronavirus[2]. It
is a new coronavirus caused by SARS-COV-2 coronavirus. The new virus has
an envelope[3],
consisting of a single strand of RNA.Sars-cov-2 is thought to have
originated in bats, with 89% to 96% of its nucleic acid sequence
identical to that of the virus carried by
bats[4]. SARS-CoV-2
is believed to have originated in bats, similar to many other
coronaviruses, because it shares 89% to 96% nucleotide identity with
bat coronaviruses. Sars-cov-2 mainly transmitted through droplets, but
can also be transmitted by aerosols. The median incubation period of the
virus is 4-5 days, and 97.5% of patients develop symptoms at 11.5 days
after infection. At the start of the pandemic, The median period from
clinical symptoms onset to progression to death is about 14
days[5]. Morbidity
and mortality varied from time to time and region to region, for reasons
that may be related to virus variation in addition to regional
differences.
For its infectiousness, the number of cases increases exponentially
without control measures. The hyperinflammatory response triggered by
SARS-CoV-2 is the principal causes of death in infected
patients[6].The most
common symptoms are fever and tussiculation, some patients appear runny
nose, sneezing, a small number of patients develop nausea, vomiting or
diarrhea. Part of the population can have no symptoms, or tends to
improve after the infection, some people can appear rapid progression
such as respiratory failure even to
death[7]. The
mortality increased significantly in patients with cardiovascular
diseases, diabetes, COPD and hypertension[8].
Fatality increases with the progression of the severity of disease. We
analyzed some relevant indicators and outcomes of patients diagnosed
with COVID-19 in a hospital in wuhan in order to provide guidance for
the treatment and prognosis of patients with coronavirus pneumonia.
The study included 239 patients with confirmed COVID-19. All patients
were assessed until disease outcome( improve or dead). The study
showed that 140 patients were discharged with a better health condition
and 99 patients died. There was a statistically significant difference
in age between the two groups, suggesting that old age is a risk factor
for the disease, which is usually accompanied by a variety of
complications, resulting in complicated conditions.
Data from the Chinese Center for Disease Control and Prevention showed
that 80% patients experienced mild disease or even non-symptom and 20%
developed severe symptoms such as respiratory failure and
multiple organ failure. Previous observational studies reported patients
with old age and comorbidities were more likely to deteriorate. It was
later found that previously healthy patients also developed severe
hypoxemia and respiratory failure, which were caused by
inflammatory cascades[6,
9]. Pathological examination showed
lesions involved multiple organs in severe
patients[10].
Studies have shown that inflammatory markers C-reactive protein and
neutrophil-to-lymphocyte ratio are risk factors in COVID
patients[11-13]. Excessive
inflammatory responses, including high levels of cytokines,
lymphocytosis, and mononuclear macrophage infiltration, are considered
important reasons for the rapid progression of the
disease[6]. Our
study found significant differences in white blood cell counts,
neutrophil counts and lymphocyte counts between the improvement group
and the death group, CRP was also associated with the risk of death,
suggesting that excessive inflammation is a risk factor for patients and
should be controlled clinically. Given the consideration of the
importance of white blood cell and neutrophil counts for the COVID-19,
we also plot the two factors in the survival curve.
In our study, survival analysis suggests that renal function factor such
as blood urea nitrogenis was associated with a risk
of death in patients. The differences of urea nitrogen and creatinine
between the improvement group and the death group were statistically
significant. Data from complete autopsy including histopathologic and
virologic analysis in 12 patients who died from COVID-19 showed that
high viral RNA titers were detected in
kidney[14]. A
study[15] involving
701 patients with COVID-19 found that 5.1% patients experienced acute
kidney injury. The mechanism involved acute tubular injury may be
associated with infiltration of lymphocytes and monocytes in renal
tissue. In addition, cytokine injury and organ interference may
also play a role in some biological processes. Patients with renal
dysfunction who are infected with SARS-CoV-2 coronavirus will face an
increased risk of death, suggesting that effective renal function
control should be paid attention into the clinical treatment. Serum
albumin levels partially reflect body’s immune state. Patients
with bad nutritional status are more likely to experience lower serum
albumin levels, which is harmful to the antibody production and virus
clearance, and should be given high attention.
Recent study suggest [9]showed that poor nutritional status was significant risk factors for
severe COVID-19 infection. Severe anorexia, and malnutrition may
increase risks for respiratory failure and even required noninvasive
ventilation[16].
Assessment of the risk factors of the disease is helpful for clinicians
to timely understand the risk of disease progression, so as to carry out
appropriate and multifaceted intervention earlier to achieve the best
therapeutic purpose. There were a few limitations in our study. Our data
sources were single-center and the sample size was not large enough to
represent all infected people. Highly subjective outcomes such as pain
may bias the accessment results. Patients without access to treatment
were not included. Some patients were complicated with uremia, resulting
in a large degree of dispersion of creatinine values in samples.