Serum amyloid A and high density lipoproteins during the acute phase response

Abstract

Serum amyloid A and high density lipoprotein (HDL) interrelationships were evaluated in 11 normal men during an acute phase response induced by the inflammatory steroid etiocholanolone. Compared with baseline, HDL-cholesterol levels were significantly elevated at 30 h but not at 50 h (P < 0·05) after etiocholanolone. A-apoprotein concentrations were unchanged at 30 h but were reduced at 54 h (P < 0·01). Four subjects were sampled every 6–8 h for 5 days. Two men had peak SAA concentrations of 30 and 33 mg dl^-1. Their A-apoprotein levels declined as SAA rose and remained low even after SAA levels had returned to baseline. High density lipoprotein cholesterol levels did not fall, however, when SAA was increasing, and fell only after SAA levels declined. No changes in HDL-cholesterol or protein were observed in two subjects whose peak SAA concentrations were 10 and 12 mg dl^-1. These observations suggest that a threshold level of acute phase response is required before HDL reductions occur. Column chromatography of SAA-rich plasma did not demonstrate the presence of either SAA or A-apoproteins that were unassociated with lipoproteins. Serum amyloid A, moreover, demonstrated little capacity to displace A-proteins from HDL at SAA concentrations typically observed during the acute phase response. We infer from these studies that SAA may substitute for the A-apoproteins and temporarily maintain HDL-cholesterol levels; but that low HDL levels during the acute phase response are likely due to reduced A-protein synthesis rather than displacement by SAA.