Terminal Complement Complex C 5b-9

$6 TERMINAL C O M P L E M E N T COMPLEX C 5b-9 : Role in the early diagnosis of infection in critically ill patients. A. Donati, L. Cola, R. Danieli, D. Achilli, E. Kalagy, G. Pomponio ~ M. Fratini~ A. Gabrielli~ P. Pietropaoli. INSTITUTE OF MEDICAL AND SURGICAL EMERGENCIES ~ INSTITUTE OF INTERNAL MEDICINE UNIVERSITY OF ANCONA, ITALY INRODUCTION The Terminal Complement Complex (TCC) C5b-9 is a macromolecolar complex deriving from activation of the Complement system's terminal pathway. This Complex plays an important role in inflammatory process following acute and chronic flogosis or tissue necrosis. The observation of a significant elevation of plasmatic TCC levels in animal models treated with large amount of endotoxin suggests its possible involvement in the pathogenesis of septic shock. A previous prospectical study on 19 patients affected by hematological malignancies who received chemotherapy and underwent to severe neutropenia, showed a good correlation between the early elevation of TCC plasmatic levels and the initial bacteriemia following the infective episode. Our target is to detect the utility of monitoring the TCC plasmatic levels as an early parameter of infection in patients admitted in Intensive Care Unit. PATIENTS and METHODS We have prospectively studied 6 consecutive patients (mean age 49.5 + 16.6) all male for a period of 21.5 + 14.3 days, admitted in Intensive Care Unit whit a diagnosis of politrauma, head injury or stroke. Plasma-EDTA and serum samples were collected every day to measure TCC, CRP, IL-6, IL-8 and other immunologic parameters. Two times a week patients were submitted to surveillance coltures (bronchial, tracheal rectal, oral swab, urinocolture); in the case of cutaneous fever up to 38~ blood coltures were collected. Twent~ plasma samples from normal donors were tested as control. Plasma samples were tested for SC5b-9 by using a double-sandwich ELISA method and the monoclonal antibody MCaE11 (Diatec). RESULTS Four of the six patients showed at least one febrile episode with nine episodes in total: one happened during massive cerebral necrosis and was considered as a failure of thermoregulation; three episodes were related to positive biological coltures. We observed three episodes of sepsis (one of them severe) and one death due to complication following severe head injury. TCC plasrna levels had a mean value of 30.8 +_U/L significatively higher than the range of the normal donors plasma (mean 2.7 _+ 2.9 U/L) with p<0.00Ol. In 7 (87.5%) febrile episodes there was a significant increase of TCC levels (delta= 344 + 241%) observed 1.7 _+ 1.6 days before the rise of cutaneous temperature. High increase in the plasmatic TCC concentrations (delta = 326 _+ 333) were observed during the two necrotic events. TCC plasma levels were related to CRP, I1-6, I1-8 levels. CONCLUSIONS Our results seems to confirm data collected in previous studies on animal models and hematological patients. TCC plasmatic concentration appears a sensitive test to "predict" a possible septic event developing in selected patient of an Intensive Care Unit. We postulate that TCC can be involved in the early phases of the inflammatory response to the infection. On the clinical ground monitoring TCC plasma levels could be useful as precocious marker of infection in susceptible patients.