Terminal complement complexes and anaphylatoxins in septic and ischemic patients

Arch Surg. 1988 Feb;123(2):188-92. doi: 10.1001/archsurg.1988.01400260068008.


Terminal complement complex (TCC) and anaphylatoxin formation in 18 patients with sepsis and 20 patients with acute limb ischemia were studied before the start of treatment and seven days later. The septic or ischemic patients had elevated levels of plasma TCC before start of therapy. In successfully treated patients these concentrations were within the normal range one week later. Similarly, the plasma anaphylatoxin level was increased before therapy and returned to the normal range within seven days. Escherichia coli incubated in vitro in fresh human serum at body temperature started formation of TCC in a dose-related manner. As complement will induce cellular lysis via TCC and edema via anaphylatoxins, anemia and impaired respiration in these patients may be influenced by increased concentrations of terminal complement complexes and of C3a and C5a.

MeSH terms

  • Aged
  • Anaphylatoxins / immunology*
  • Bacterial Infections / immunology*
  • Chemotactic Factors / metabolism
  • Complement C3 / analogs & derivatives
  • Complement C3 / metabolism
  • Complement C3a
  • Complement C5 / analogs & derivatives
  • Complement C5 / metabolism
  • Complement C5a
  • Complement C5a, des-Arginine
  • Complement Membrane Attack Complex
  • Complement System Proteins / immunology*
  • Escherichia coli / immunology
  • Humans
  • Ischemia / immunology*
  • Leg / blood supply
  • Peptides / immunology*
  • Respiratory Distress Syndrome / immunology


  • Anaphylatoxins
  • Chemotactic Factors
  • Complement C3
  • Complement C5
  • Complement C5a, des-Arginine
  • Complement Membrane Attack Complex
  • Peptides
  • complement C3a, des-Arg-(77)-
  • Complement C3a
  • Complement C5a
  • Complement System Proteins