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.