Cold activation of complement i. presence of coagulation-related activator.
Determination of the complement titer in the serum and plasm of 120 patients with chronic liver diseases showed that in eight (7%) patients with cirrhosis of the liver, chronic active or chronic inactive hepatitis complement in the serum was less than half in the plasma. The dissociation of complement serum and plasma was due to cold activation of the classical pathway of complement in vitro since serum drawn from these patients at 37 degrees C lost hemolytic activity in 4 hours when transferred to a cold environment. Neither HB antigen nor cryoglobulin participated in this phenomenon. The activation of complement in the cold could be prevented by increasing the ionic strength, or by adding vitamin E or, to a lesser extent its vehicle HCO-60, while heparin, Trasylol, soybean trypsin inhibitor, or hirudin had no effect. Trans-AMCHA prevented activation in one case. It is speculated that a factor appearing as a result of blood clotting is able to activate the classical pathway of complement in the cold; it is probably not related to Hageman factor (factor XII), factor VII, thrombin, kallikrein.
D000991:Antithrombins; D001779:Blood Coagulation Factors; D003080:Cold Temperature; D003169:Complement Inactivator Proteins; D003165:Complement System Proteins / Q000032:analysis; D006461:Hemolysis; D006801:Humans; D008103:Liver Cirrhosis / Q000276:immunology; D011480:Protease Inhibitors; D000515:alpha 1-Antitrypsin; D000511:alpha-Macroglobulins
D000991:Antithrombins; D001779:Blood Coagulation Factors; D003169:Complement Inactivator Proteins; D011480:Protease Inhibitors; D000515:alpha 1-Antitrypsin; D000511:alpha-Macroglobulins; D003165:Complement System Proteins