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Cold activation of complement i. presence of coagulation-related activator
Insights
Complement levels in chronic liver disease patients showed lower serum than plasma levels due to cold activation. This immune response was preventable with vitamin E or increased ionic strength.
Area of Science:
- Immunology
- Hepatology
Background:
- Complement system plays a crucial role in immune response.
- Chronic liver diseases can impact various physiological processes, including immune function.
Purpose of the Study:
- To investigate complement titers in serum and plasma of patients with chronic liver diseases.
- To determine the cause of observed discrepancies in complement levels between serum and plasma.
Main Methods:
- Collected serum and plasma samples from 120 patients with chronic liver diseases.
- Assessed complement hemolytic activity at different temperatures (37°C and cold).
- Tested various substances (vitamin E, HCO-60, heparin, etc.) for their effect on cold activation.
Main Results:
- Eight patients (7%) exhibited significantly lower serum complement than plasma complement.
- This dissociation was attributed to in vitro cold activation of the classical complement pathway.
- Activation was inhibited by increasing ionic strength or adding vitamin E; heparin and other inhibitors were ineffective.
Conclusions:
- Cold activation of the complement system occurs in specific chronic liver disease patients.
- A factor related to blood clotting, not Hageman factor or thrombin, may initiate this cold activation.
- Vitamin E shows potential in preventing cold-induced complement activation in these patients.
Abstract:
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.