Biochemical and laboratory evaluations
We assessed blood group types of participants. The distribution of the
ABO blood groups system in COVID-19 suspicious outpatients tested for
SARS-CoV2 RT-PCR is presented in Table 1. We did not find any
significant difference in terms of blood group type between negative and
positive PCR groups (P =0.4).
In contrast with our results, some recent studies identified
associations between ABO blood groups and COVID-19. In one previous
study, 397 patients with confirmed diagnoses of COVID-19 were admitted
to Imam Khomeini Hospital Complex, Tehran, Iran. Also, 500 individuals
were selected to form the control group, all of whom had been disclosed
to the same medical center in June 2019, before the onset of the
outbreak. The results demonstrated ABO histo-blood phenotypes are
correlated with patients’ susceptibility to the infection. Specifically,
a higher rate of infection was observed among patients with the AB
histo-blood group, while patients with the O histo-blood group had shown
a lower rate of infection(18).
Also, a study on COVID-19 patients in Wuhan and Shenzhen, China,
discovered associations between ABO blood types and infection. They
found that the odds of having COVID-19 were higher among the A blood
group and lower among the O blood group relative to the general
populations of Wuhan and Shenzhen(19).
Previous work has identified similar associations between ABO blood
groups and different infections or disease severity following
infections, including SARS-CoV1(20), P. falciparum(21) , H.
pylori(22) , Norwalk virus(23), hepatitis B virus(24), and N.
gonorrhoeae(25). The difference between our observations and the results
obtained in the mentioned studies may be due to differences in the
population (especially in terms of race and ethnicity) or in the
severity and stage of the disease.
On the other hand, there are studies whose results are in line with the
results of our study. For instance, one study found insufficient
evidence to conclude that the blood group distribution among all
individuals tested for SARS-CoV2 is different from the general
population at NYP/CUIMC (ABO: P =0.64, Rh: P =0.36)(26).
Therefore, the results obtained regarding the possible relationship
between blood group type and the incidence and severity of COVID-19, as
well as the type of possible relationship, are still contradictory.
The results of the between-group analysis of serum levels of cortisol
are shown in Table 1. Serum levels
of cortisol did not show any significant differences between the two
groups (P =0.4). We also categorized serum levels of cortisol as
hypocortisolism (<5 μg/dL), norm cortisol (5-25 μg/dL), and
hypercortisolism (˃25 μg/dL).
Cortisol serum level categories are also shown in Table 1. Our results
revealed that 3.8%, 92.5%, and
3.8% of the negative PCR group presented hypo, norm, and
hypercortisolism, respectively. In the positive PCR group, 7.5%,
88.7%, and 3.8% were hypo, norm, and hypercortisolism, respectively.
Immune system response plays a crucial role in controlling and resolving
viral infection. Therefore, cortisol is linked to the immune system and
viral infection as part of the neuroendocrine stress axis. Exogenous or
endogenous glucocorticoid excess is characterized by increased
susceptibility to infections due to impairments of the innate and
adaptive immune systems. Thus, patients with chronic glucocorticoid
excess may be at high risk of developing COVID-19 with a severe clinical
course(27).
In line with our results, a descriptive and analytical cross-sectional
study was conducted in a population of patients infected with 2019-nCoV
in Cameroon. The researchers found no statistically significant
association between serum cortisol and disease severity. Like us, they
concluded that the absence of a marked rise of cortisol during COVID-19
suggests the possible involvement of the hypothalamic-pituitary-adrenal
axis in this infection. However, their study did not have a non-COVID
control group(28).
Another study compared baseline cortisol concentrations between COVID-19
patients and controls. Contrary to our results, they found that patients
with COVID-19 presented a marked and appropriate acute cortisol stress
response and that this response is significantly higher in this patient
cohort than in individuals without COVID-19(29).
The observed differences, as well as individual differences in stress
responses, might have arisen because COVID patients were not the same in
the two studies. Specifically, they were at different stages of the
disease—our study was conducted on asymptomatic/mild and moderate
outpatients of COVID-19. Serum levels of aldosterone also did not show
any significant differences between the two groups (P =0.2).
Table 1 shows the results of a comparison between the mean serum
aldosterone levels of negative and positive PCR groups. COVID-19 and the
RAAS are closely linked both in infection and in possible post-infection
inflammatory cascades(7). Campana et al. reported that increased levels
of aldosterone might be associated with severe forms of COVID‐19(30).
This report can confirm the result obtained in our study because lower
grades of the disease (mild and moderate) were evaluated in our study.
The results of a study by Henry et al., which included 30 COVID-19
patients and controls, align with our findings. They compared plasma
concentrations of aldosterone between patients and controls using the
Mann-Whitney U test and reported that aldosterone concentrations were
comparable between patients with and without COVID-19 (8.9
(IQR:5.8-16.2) vs. 9.0 (IQR:7.4-12.2) ng/dL, P =0.865)(31).