Discussion
The current study was performed to investigate whether clinical,
hematological, and biochemical variables had significant impacts on the
clinical course, therapeutic outcomes, and prognosis in adult COVID-19
patients. Our data yielded that advanced age, presence of at least 1
comorbid disease, increased length of hospitalization, elevated white
blood cell and neutrophil counts, increased serum levels of glucose,
blood urea nitrogen, AST, LDH, CRP, and D-dimer were associated with
increased mortality. On the other hand, decreased serum levels of
albumin, ALT, calcium, and platelet count were associated with higher
mortality. Remarkably, there was a positive and weak relationship
between serum D-dimer levels and length of hospitalization in adult
COVID-19 patients.
Some COVID-19 patients did not develop hypoxemia or respiratory stress,
suggesting that SARS-CoV-2 infection is a heterogeneous illness. One
accurate and practical biomarker is required to prognosticate the
COVID-19 pneumonia severity (9). The BCG vaccination has no effect on
the COVID-19 pneumonia severity. Low income and age are the primary
causes of COVID-19 pneumonia severe (10).
Mousavi et al. looked at the demographics, outcome, hematology-related,
and laboratory parameters of COVID-19 patients admitted to a tertiary
care hospital (11). They tried to figure out what hematologic factors
were linked to death in the 24 percent of our patients who died during
their stay. In prior investigations, it was discovered that being male
and older increased the risk of in-hospital mortality (12-14).
The average age of their hospitalized patients was 60 years old, with
non-survivors nearly ten years older than survivors. Around 67 percent
of non-survivors were over 60 years old. The deceased were mostly male
and elderly., according to Yang et al. (15). Despite the fact that male
patients were more likely to die, sex did not have a significant impact
on mortality (11). An immune response irregularity and a lack of
adaptive immunity cause severe inflammatory responses in patients with
COVID-19 (16). Thrombocytopenia and decreased nadir platelet counts have
been recorded in non-survivors (17).
Serum CRP levels were considerably greater in non-survivors compared to
discharged COVID-19 patients, according to Ruan et al. (17). Increased
CRP values were a common laboratory abnormality in individuals with
COVID-19 infection, according to Pan et al. Levi et al. discovered a
raised D-dimer concentration and
increased prothrombin time in
COVID-19 patients as typical signs of coagulopathy (18,19). Other
laboratory irregularities in COVID-19 that might be linked to thrombotic
microangiopathy and coagulopathy include ferritin concentrations and
high LDH (20).
In COVID-19, Yuan et al. found that a decrease in serum LDH could
indicate a good response to treatment (21). A minor increase in white
blood cell count was seen in patients with acute illness, but a
clinically significant increase was seen in individuals who died. As a
result, a considerable increase in WBCs in patients with severe disease
could indicate clinical deterioration and a higher risk of poor
outcomes. Although an increase in neutrophils may cause WBCs to
increase, lymphocytes, monocytes, and eosinophils may decrease.
Lymphocytes are thought to be essential for the elimination of virally
infected cells in the SARS virüs, and survival may be related to the
capacity of reviving lymphocytes destroyed by the virüs (22,23).
Both substantial and catastrophic outcomes are possible. Patients with a
positive test of COVID-19 had significant levels of cardiac and muscle
injury biomarkers. Non-survived patients showed a significant level of
high cardiac troponin at the time of admission, indicating a risk of
cardiac injury caused by multiple organ failure progression, viral
myocarditis, and secondary cardiac caused by organ-targeted diseases. A
significant increase in liver enzymes (ALT and AST) and renal indicators
(blood urea nitrogen) reveals a picture of multiple organ failure (24).
Plasma CRP levels were associated with the COVID-19 pneumonia severity.
As a result, it could help distinguish between patients with mild
COVID-19 pneumonia and those with moderate to severe COVID-19 pneumonia.
These findings could help clinicians better stratify patients for
transfer to an intensive care unit by serving as an early warning sign
of serious disease (25).
The clinical sequence of patients with severe COVID-19 from admission to
discharge was reported in this study, with various outcomes. Lymphocyte,
CRP, and LDH dynamic monitoring could be useful in predicting the severe
patients’ prognosis. Furthermore, the fatal aspect of COVID-19 was
primarily related to significant systemic inflammation with caused
cardiac failure (26). Comorbidities, age, secondary infection, and
higher indicators in inflammation were predictors of a fatal result in
COVID-19 cases. COVID-19 death could possibly be related to
virus-activated ”cytokine storm syndrome” or fulminant myocarditis,
according to the findings (17).
It is important to note the limitations of our study. Our findings may
be influenced by the retrospective design and possibly socioeconomic
factors. Given the pandemic’s rapid spread, these findings are
clinically significant and may aid clinicians in identifying and
treating persons with a higher risk of acquiring the severe disease.
Therefore, our findings should be regarded as preliminary and
exploratory. Because participants who are more likely to die exhibit
significant variations in some of these co-variates, the correlations we
observe should not be assumed to represent cause and effect.