Endocrine Abstracts

Objectives: The excessive production of pro-inflammatory cytokines has been previously reported in the severe form of COVID-19. The cytokine storm is responsible for the induction of an inflammatory endothelial cell phenotype which is associated with the shedding of adhesion molecules. VCAM-1 is an endothelial adhesion protein that belongs to the immunoglobulin superfamily. Pro-inflammatory cytokines lead to the induction of VCAM-1 in the endothelium of blood vessels which is crucial for the recruitment, adhesion, and migration of leukocytes. The level of the soluble form of VCAM-1 (sVCAM-1) was shown to be increased in patients with severe COVID-19 and was associated with disease progression and mortality.

Aim: To assess VCAM-1 concentration in patients 6 months after the mild SARS-Cov2 infection (without hospitalization) in comparison to the control group as well as biochemical, hormonal, and anthropometric parameters, considering the influence of sex.

Material and Methods: The study group included 53 patients with a history of COVID-19 and 87 healthy subjects in the control group. Anthropometric parameters were measured. VCAM-1 concentration as well as hormonal (testosterone, insulin, morning cortisol) and biochemical parameters (glucose, alanine transferase, asparagine transferase, lipids) were measured.

Results: The statistically higher VCAM-1 concentrations were observed in the control group in comparison to the COVID-19 group (830, 342 ng/ml vs 772, 509 ng/ml, P=0.03). No statistically significant differences in C-reactive protein concentrations were observed between the groups. Significant positive correlations were observed between VCAM-1 and alanine and aspartate aminotransferases as well as with HDL-concertation in the COVID-19 group, although we did not observe significant differences in the concentration of aminotransferases and HDL cholesterol between both groups.

Conclusions: Based on the results of our study, it can be concluded that, at least 6 months after mild COVID-19 infection, there is no strong evidence of endothelial dysfunction in COVID-19 survivors. Surprisingly, we observed a significantly higher concentration of VCAM-1 in the apparently healthy control group.