[Inflammatory syndrome and changes in plasma proteins].

Inflammation can be considered as a reactional process towards an injury of any etiology. It is clinically characterized by the four major points described by Celse. The symptoms are usually associated with fever and with a biological syndrome including an increased sedimentation rate related to an elevation of inflammatory plasma proteins. The Acute Phase Reactant Proteins (orosomucoid, alpha 1-antitrypsin, alpha 1-antichymotrypsin, haptoglobin, ceruloplasmin, C reactive protein and fibrinogen) are released by the hepatocytes. The complement components C3 and C4, transferrin and alpha 2-macroglobulin can also be generated by the macrophages. At inflammation sites, the activated host phagocytes release a Leukocytic Endogenous Mediator (LEM) or Interleukin I. A circulating cleavage product of Interleukin I, called "Proteolysis Inducing Factor" induces an increased muscle proteolysis and hepatic amino acids uptake for inflammatory proteins synthesis, principaly in the form of Acute Phase Reactant Proteins. Furthermore, this monokin stimulates the T4 helpers lympocytes production of a lymphokin: Interleukin II. There is no "inflammation protein" characterized by the 5 criteria of the Clinical Biology French Society. Therefore the association of a high turn over protein (CRP) and a low turn over one (orosomucoid and/or haptoglobin) is usefull for the detection of an inflammatory process and to evaluate a therapeutic efficiency. These proteins are usually selected for early diagnosis of neonatal bacterial infections and for the diagnosis of myocardial infarction. In the present time, numerous studies using statistical methods try to separate inflammatory processes according to their etiology.