In response to a variety of inflammatory lesions, there appears in the blood of humans a protein substance not normally present, which is identified by its capacity to form a precipitate with the somatic Cpolysaccharide of the pneumococcus.1 It has consequently been named C-reactive protein (CRP). Present knowledge points toward C-reactive protein being a β-globulin, probably bound to a lipid. Minute amounts of this protein may be demonstrated in human serum by a precipitin test employing a specific antiserum obtained from rabbits hyperimmunized by repeated injections of a purified C-reaction protein. In previous studies it has been demonstrated that the appearance of C-reactive protein in the blood is a nonspecific but extremely sensitive indicator of an inflammatory reaction due to infection. It has also been found in other disease processes of a noninfectious nature, such as malignancy and myocardial infarction. Kroop and Shackman 2 reported negative tests in
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