# The Interaction of Complement and Intrinsic Coagulation System: A Comparative Study between COVID-19 and Bacterial Sepsis Patients

## TL;DR

This study compares how the immune system's complement and coagulation systems are activated in patients with COVID-19 and bacterial sepsis.

## Contribution

The study provides a comparative analysis of complement and coagulation activation in two critical illnesses using longitudinal patient samples.

## Key findings

- Coagulation factors XI and XII were elevated in both groups, with no significant differences between them.
- Complement factors C3a and C5a were significantly higher in COVID-19 patients compared to bacterial sepsis patients.
- The findings suggest additional pathways for complement activation in SARS-CoV-2 infection.

## Abstract

Background/Objectives: Through the past several years, a constant interaction has been implicated between complement and coagulation cascades. SARS-CoV-2 infection and bacterial sepsis are potent activators of both cascades. This study aims to compare the extent of complement and intrinsic coagulation pathway activation (and the interplay between them) among patients with COVID-19 and bacterial sepsis. Methods: Serum and plasma samples were collected from 25 ICU patients (11 patients with COVID-19 and 14 patients with bacterial sepsis) at two time points (on admission and either on improvement or deterioration). The activities of coagulation factors XI and XII and complement factors C3a and C5a were measured at both time points. Results: The activities of factors XI and XII were increased in both groups of patients and at both time points. However, there were no statistically significant differences between SARS-CoV-2 and bacterial sepsis patients. On the other hand, both C3a and C5a were significantly higher in the COVID-19 group on admission. This correlation was preserved on reassessment. Conclusions: Complement activation seems to be more enhanced in COVID-19 than bacterial sepsis. However, the lack of statistical significance in factors XI and XII indicates t the presence of additional pathways for complement activation in SARS-CoV-2 infection.