The complement lectin pathway after cardiac arrest.
Simon Foged HaugaardAnni Nørgaard JeppesenAnne TroldborgHans KirkegaardSteffen ThielAnne-Mette HvasPublished in: Scandinavian journal of immunology (2018)
The lectin pathway (LP) of the complement system may initiate inflammatory reactions when body tissue is altered. We aimed to investigate levels of the LP proteins in out-of-hospital cardiac arrest patients, and to compare these with healthy individuals. Furthermore, we aimed to clarify whether duration of targeted temperature management influenced LP protein levels, and we further examined whether LP proteins were associated with 30-day mortality. We included 82 patients resuscitated from out-of-hospital cardiac arrest. The patients were randomly assigned to 24 or 48 hours of targeted temperature management at 33±1 °C. Blood samples were obtained 22, 46 and 70 hours after target temperature was reached. Levels of the LP proteins (mannan-binding lectin (MBL), M-ficolin, H-ficolin, collectin liver 1 (CL-L1), MBL-associated serine protease 1 (MASP-1), MASP-2, MASP-3 and MBL-associated protein of 44 kDa (MAp44)) were measured using time-resolved immunofluorometric assays. Data from 82 gender matched healthy individuals were used for comparison. Levels of CL-L1, MASP-1, MASP-2 and MAp44 were significantly higher, whereas M-ficolin levels were significantly lower in cardiac arrest patients compared with healthy individuals. MASP-2, MASP-3 and M-ficolin levels changed significantly when comparing 24 and 48 hours of targeted temperature management. The LP protein levels were not different between 30-day survivors and non-survivors after cardiac arrest. The differences in LP protein levels between patients and healthy individuals may indicate that cardiac arrest patients have an activated LP. Overall, the LP protein levels were not influenced by duration of targeted temperature management, and the levels were not associated with 30-day mortality. This article is protected by copyright. All rights reserved.