Complement is part of the host’s natural defense mechanisms against pathogens. Its exploration is based in first intention on a quantitative evaluation of the C3 and C4 fractions by automated and standardized immunoassay techniques. Serum protein electrophoresis (SPEP) separates proteins into 6 fractions. The beta-2 globulin fraction contains complement C3-C4, the amplitude of which allows their quantification. In this context, we carried out a comparative study between the two assay techniques. We included all patients who had simultaneously received a weight determination of the C3 and C4 fractions by turbidimetry on a SPA Plus® automaton and an SPEP on a Capillarys Sebia® automaton over a period of one year. Our study demonstrated a positive correlation between these two methods with Pearson r=0.801, P-value<0.001. Studies have reported that SPEP can be used for the detection of hypocomplementemia by a decrease in the fraction of beta-2 globulins. In capillary electrophoresis (Capillarys Sebia®), beta-2 globulins contain almost exclusively complement. To date, our study is the first to seek the correlation between two electrophoretic and turbidimetric methods for the quantification of complement.
We report two cases of patients with COVID-19. Clinical and biological features of the two patients confirm severe form of COVID-19 associated with cytokine storm. High levels of IL-6 and IL-17 were found. Unfortunately the patients died because of the multi-organ failure secondary to the cytokine storm. Cytokine storm is a systemic inflammatory syndrome which leads to aberrant release of cytokines. IL-6 is the most frequently reported cytokine to be increased in COVID-19 patients. Naïve T CD4+ cells in the presence of TGF β and IL-6 will differentiate into T helper 17 cells responsible for secreting IL-17A and IL-17F, which target macrophages, dendritic cells, endothelial cells, and fibroblasts to increase the production of cytokines. IL-6 and IL-17 have been shown to play a role in increasing risk of airway disease. They synergistically promote viral persistence by protecting virus-infected cells from apoptosis. Immune hyperactivation in cytokine storm amplified levels of cytokines that will have systemic effects and cause collateral damage to vital organ systems. Immunotherapy can play a crucial role in COVID-19 managing. Tocilizumab an anti-IL6 receptor antibody was used with clinical improvement. The possibility of inhibiting IL17 as therapy for COVID-19 should be also considered.