Results
The study included 47 (53.4%) female and 41 (46.6%) male COVID-19 patients. The control group comprised 12 (60%) women and 8 (40%) men. Mean age was 49.1 ± 21.1 years in the patient group and 35.2 ± 6.9 years in the control group. The groups did not differ statistically in age or sex distribution (p=0.196, p=0.34).
Of the patients involved in the study and developed MAS, 10 had hypertension, 8 had diabetes mellitus, 8 had chronic obstructive pulmonary disease, 1 had epilepsy, 1 had an infarct in the temporoparietal region, and 1 had chronic kidney failure. All patients with MAS had ARDS, and the other 15 patients had hypertension, 3 had asthma and 1 had chronic renal failure. Of the 63 patients who did not develop ARDS and MAS, 5 had diabetes mellitus and 2 had diabetes.
Comparative analysis of the patients’ laboratory parameters at admission and day 5 of treatment and the control subjects’ IL-6 and SP-D levels are presented in Table 1. MCP-1 and SP-A levels of the COVID-19 patients were significantly higher at admission than on day 5 of treatment (p=0.001, p=0.001). The patients had significantly higher MCP-1 and SP-A levels at admission when compared with the control group (p=0.001, p=0.001). These levels were still higher than controls at day 5 of treatment, but only the difference in MCP-1 level was statistically significant (p=0.03, p=0.4). Comparative analysis of admitting and day-5 laboratory values of COVID-19 patients who developed MAS (n=20) and those without MAS (n=68) is shown in Table 2. The patients with MAS had significantly higher MCP-1 and SP-A levels both at admission (p=0.001, p=0.001) and on day 5 of treatment (p=0.05, p=0.04) compared to those without (Figure 1). Comparative analysis of admitting and day-5 laboratory values of COVID-19 patients who developed ARDS (n=35) and those without ARDS (n=53) is presented in Table 3. Similarly, MCP-1 and SP-A levels were significantly higher in patients who developed ARDS compared to those who did not at both time points (p=0.001 for all) (Figure 1). A total of 7 patients died. MCP-1 and SP-A levels were 459.4 ± 180.1 pg/ml and 905.8 ± 467.5 pg/ml among nonsurvivors and 90.7 ± 142.7 pg/ml and 349.1 ± 333.4 ng/ml among survivors, respectively. The difference between survivors and nonsurvivors was statistically significant for both parameters (p=0.001, p=0.001).
Correlation analysis between MCP-1 level and admitting clinical and laboratory values revealed inverse correlations with lymphocyte count (r=-0.443, p=0.01) and PaO2/FiO2(r=-0.646, p=0.01) (Figure 2) and positive correlations with neutrophil-lymphocyte ratio (r=0.392, p=0.01), prothrombin time (r=0.512, p=0.01), and levels of lactate dehydrogenase (LDH) (r=0.558, p=0.01), creatine (r=0.301, p=0.01), C-reactive protein (CRP) (r=0.717, p=0.05), troponin-I (r=0.307, p=0.01), D-dimer (r=0.412 p=0.01), and SP-A (r=0.346, p= 0.01) (Figure 2).
Similarly, correlation analysis between SP-A level and admitting clinical and laboratory values demonstrated inverse correlations with lymphocyte count (r=-0.252, p=0.01) and PaO2/FiO2 (r=-0.364, p=0.01) (Figure 2) and positive correlations with prothrombin time (r=0.455, p=0.01) and levels of CRP (r=0.325, p=0.01), LDH (r=0.355, p=0.01), and D-dimer (r=0.31, p=0.01) (Figure 2).