Abstract

Serum opsonic activity for E. coli 075, concentration of native C3 and C3 conversion by inulin were determined in the sera of five patients with burns involving 45% to 80% total body surface during 3 weeks postburn. In all patients, opsonic activity, C3 concentration, and C3 conversion were reduced during the first week following the injury. C3 was restored to normal or elevated levels by the end of the first week postburn and remained normal or elevated thereafter for the duration of the study. In two patients, opsonic activity and C3 conversion were markedly reduced during the entire 3-week postburn period. In the other three patients, opsonic activity was fully restored to normal within 1 week postburn and, in two of these patients, remained normal thereafter for the duration of the study. In the other patient, opsonic activity became reduced again during the third postburn week. C3 conversion in all five patients remained at a low normal or abnormal level during the entire period of study. Addition of normal human serum to the burn sera fully restored opsonic activity to normal but did not normalize C3 conversion. The results suggest that reduced opsonization is related to a deficiency of serum proteins, whereas reduced C3 conversion may be caused by a circulating inhibitor. Both abnormalities were shown to be associated with microbial infections in burned patients.

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