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Editorials |

C-Reactive Protein in Pneumonia : Let Me Try Again

Carlos M. Luna
Author and Funding Information

Affiliations: Buenos Aires, Argentina
 ,  Dr. Luna is Associate Professor of Internal Medicine, University of Buenos Aires.

Correspondence to: Carlos M. Luna, MD, PhD, FCCP, Acevedo 1070, Banfield, 1828, Buenos Aires, Argentina; e-mail: cymluna@fmed.uba.ar



Chest. 2004;125(4):1192-1195. doi:10.1378/chest.125.4.1192
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The initial description of C-reactive protein (CRP) was based on patients with pneumonia. CRP was identified in 1930 and subsequently considered to be an early nonspecific but sensitive marker of inflammation, so called “acute-phase protein.”1 An acute-phase protein has been defined as one whose plasma concentration increases (positive acute-phase proteins) or decreases (negative acute-phase proteins) by at least 25% during inflammatory disorders.2 Other acute-phase proteins include proteinase inhibitors and coagulation, complement, and transport proteins; the other major acute-phase protein that displays sensitivity, response speed, and dynamic range comparable to those of CRP is serum amyloid A protein.34 Some acute-phase proteins initiate or sustain inflammation, while other acute-phase proteins may have anti-inflammatory actions. Like other acute-phase proteins, CRP is predominantly synthesized in the liver.

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