Secondary amyloidosis is associated with

Ref Robbins 8/e p252-253,9/e p257 The AA (amyloid-associated) fibril is a unique nonim- munoglobulin protein derived from a larger (12-kDa)serum precursor called SAA (serum amyloid-associated) protein that is synthesized in the liver. SAA is synthesized by liver cells under the influence of cytokines such as IL-6 and IL-1 that are produced during inflammation; thus, long-standing inflammation leads to elevated SAA levels, and ultimately the AA form of amyloid deposits. However, increased production of SAA by itself is not sufficient for the deposition of amyloid. Elevation of serum SAA levels is common to inflammatory states but in most instances does not lead to amyloidosis. There are two possible explanations for this. According to one view, SAA nor- mally is degraded to soluble end products by the action of monocyte-derived enzymes. Conceivably, people who develop amyloidosis have an enzyme defect that results in incomplete breakdown of SAA, thus generating insoluble AA molecules. Alternatively, a genetically determined structural abnormality in the SAA molecule itself renders it resistant to degradation by macrophages