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C1INH is the most potent endogenous regulator of compliment as well as intrinsic coagulation pathways and the kallekrein-kinin system.
C1INH systemic activity was studied in patients who were enrolled within 48 hours after onset of sepsis (ACCP, 1992). The analysis of C1INH activity in quartiles (Q) was conducted in terms of RCT of human purified C1INH (Bicizar, Russia).
Sepsis patients (n = 40) responded with an increase of C1INH activity in comparison with healthy individuals (Figure (Figure1).1). Thirty percent of Q1 patients had ARDS and septic shock whereas in Q4 everyone showed only signs of sepsis. The CRP level was higher in Q1 patients (243.4 ± 39.9 mg/l) than in Q4 (144.0 ± 20.07 mg/l; P = 0.04), whereas the C4 subunit was lower in Q1 (0.19 ± 0.04 g/l) than in Q4 (0.32 ± 0.04 g/l; P = 0.05).
Inability to upregulate C1INH activity in sepsis was associated with enhanced systemic inflammation, higher number of ARDS and septic shock cases.