Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2018 Apr;6(7):115.
doi: 10.21037/atm.2018.01.30.

No association between systemic complement activation and intensive care unit-acquired weakness

Affiliations

No association between systemic complement activation and intensive care unit-acquired weakness

Esther Witteveen et al. Ann Transl Med. 2018 Apr.

Abstract

Background: The main risk factors for intensive care unit-acquired weakness (ICU-AW) are sepsis, the systemic inflammatory response syndrome (SIRS) and multiple organ dysfunction. These risk factors are associated with systemic complement activation. We hypothesized that critically ill patients who develop ICU-AW have increased systemic complement activation compared to critically ill patients who do not develop ICU-AW.

Methods: Complement activation products C3b/c, C4b/c and C5a were measured in plasma of ICU patients with mechanical ventilation for ≥48 hours. Samples were collected at admission to the ICU and for 6 consecutive days. ICU-AW was defined by a mean Medical Research Council (MRC) score <4. We compared the level of complement activation products between patients who did and who did not develop ICU-AW.

Results: Muscle strength measurements and complement assays were available in 27 ICU patients, of whom 13 patients developed ICU-AW. Increased levels of C4b/c were seen in all patients. Neither admission levels, nor maximum, minimum and mean levels of complement activation products were different between patients who did and did not develop ICU-AW.

Conclusions: Complement activation is seen in critically ill patients, but is not different between patients who did and who did not develop ICU-AW.

Keywords: Complement activation; critical illness myopathy; critical illness polyneuropathy; intensive care unit-acquired weakness (ICU-AW); systemic inflammation.

PubMed Disclaimer

Conflict of interest statement

Conflicts of Interest: Prof. IN van Schaik received departmental honoraria for serving on scientific advisory boards and a steering committee for CSL-Behring. The other authors have no conflicts of interest to declare.

Figures

Figure 1
Figure 1
Levels of C3b/c, C4b/c and C5a in patients who developed and did not develop ICU-AW. Levels of C3b/c (A), C4b/c (B) and C5a (C) at admission (day 0) and 6 consecutive ICU days in patients who developed and who did not develop ICU-AW. Data are presented as median with interquartile range for each time point and numbers below the lines represent the number of samples of patients with ICU-AW (upper) and without ICU-AW (lower). Dotted lines (in A and B) represent the reference values. ICU, intensive care unit; ICU-AW, intensive care unit-acquired weakness.

References

    1. Latronico N, Bolton CF. Critical illness polyneuropathy and myopathy: a major cause of muscle weakness and paralysis. Lancet Neurol 2011;10:931-41. 10.1016/S1474-4422(11)70178-8 - DOI - PubMed
    1. Rittirsch D, Flierl MA, Ward PA. Harmful molecular mechanisms in sepsis. Nat Rev Immunol 2008;8:776-87. 10.1038/nri2402 - DOI - PMC - PubMed
    1. Hack CE, Nuijens JH, Felt-Bersma RJ, et al. Elevated plasma levels of the anaphylatoxins C3a and C4a are associated with a fatal outcome in sepsis. Am J Med 1989;86:20-6. 10.1016/0002-9343(89)90224-6 - DOI - PubMed
    1. Stöve S, Welte T, Wagner TO, et al. Circulating complement proteins in patients with sepsis or systemic inflammatory response syndrome. Clin Diagn Lab Immunol 1996;3:175-83. - PMC - PubMed
    1. Ramaglia V, Tannemaat MR, de Kok M, et al. Complement inhibition accelerates regeneration in a model of peripheral nerve injury. Mol Immunol 2009;47:302-9. 10.1016/j.molimm.2009.09.019 - DOI - PubMed

LinkOut - more resources