Host Defense against Opportunist Microorganisms Following Trauma.
Abstract
Reduction in C3 conversion in patients with severe thermal injury was shown to be caused by a deficiency of proteins required for alternative complement pathway activation, rather than to an inhibitor of C3 conversion. No correlation was demonstrated between this humoral abnormality and the occurrence, duration, or outcome of septicemia. Consumption of the classical complement pathway occurred preferentially prior to and during septicemia in thermally injured patients. Reduction in classical pathway activity was not demonstrated in non-septic burned patients, suggesting that this humoral abnormality was predictive of septic episodes. Alternative pathway consumption occurred infrequently during septicemia and appeared to result from generation of C3b via consumption of the classical pathway. Consumption of components of the alternative and/or classical complement pathway did not decrease the opsonic capacity of the patients' sera for their own infecting microorganisms. Multiple abnormalities of the classical and alternative complement pathways, immunoglobulins, and opsonins were shown to occur following abdominal trauma, some of which persisted after the first week post trauma. The humoral abnormalities in the trauma patients were not related to surgical procedures or to fluid imbalances. Patients who subsequently developed microbial infections were the only patients who had decreased classical pathway activity that appeared to result from consumption of components.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jun 01, 1978
- Accession Number
- ADA060569
Entities
People
- Ann B. Bjornson
- H. Stephen Bjornson
- William A. Altemeier
Organizations
- University of Cincinnati