ABSTRACT
The history of serum amyloid A (SAA) protein, a major acute phase reactant, had its beginning in the isolation and characterization of a unique protein found in tissues obtained at autopsy from patients with amyloidosis secondary to chronic inflammatory diseases. The weight of evidence linking SAA to lipoproteins, high density lipoproteins in particular, favors a role in lipid transport and metabolism as the major function of SAA. Finally, from the foregoing it is clear that the SAA family of proteins must represent important ingredients in the acute phase response to various forms of tissue damage. The discovery of the dramatic increases in SAA levels following tissue injury generated clinical interest in possible correlations between circulating SAA levels and the extent of injury or severity of inflammation. The existence of several SAA isoforms probably contributes to the difficulties.
