Serum amyloid A (SAA) proteins comprise a family of apolipoproteins co
ded for by at least three genes with allelic variation and a high degr
ee of homology between species. The synthesis of certain members of th
e family is greatly increased in inflammation. However, SAA is not oft
en used as an acute-phase marker despite being at least as sensitive a
s C-reactive protein. SAA proteins can be considered as apolipoprotein
s since they associate with plasma lipoproteins mainly within the high
density range, perhaps through amphipathic alpha-helical structure. I
t is not known why certain subjects expressing SAA develop secondary s
ystemic amyloidosis. There is still no specific function attributed to
SAA; however, a popular hypothesis suggests that SAA may modulate met
abolism of high density lipoproteins (HDL). This may impede the protec
tive function of HDL against the development of atherosclerosis. The p
otential significance of the association between SAA and lipoproteins
needs further evaluation.