We determined the concentration of serum amyloid A protein (SAA) in plasma and each lipoprotein fraction from patients with inflammatory disease (n = 62) and healthy subjects (n = 35). The mean SAA concentration in the patients with inflammatory disease (396 mg/L) significantly exceeded that in healthy subjects (1.4 mg/L). In the patients with acute inflammatory disease SAA was distributed mainly in the high-density lipoprotein (HDL) fraction. HDL-cholesterol (HDL-C) showed an initial increase followed by an immediate decrease, and gradually returned to the baseline. Plasma concentrations of apoA-I and apoA-II (apolipoprotein, apo) were decreased, and gradually returned to normal along with HDL-C. In patients with rheumatic disease the concentration of HDL-C, apoA-1, or apoA-II was lower than in healthy subjects, and was inversely correlated with the concentration of plasma SAA (r = -0.409, r = -0.642, r = 0.545, respectively). These results are in keeping with the suggested mechanism of SAA displacing apoA-I and apoA-II, which may result in increased catabolism of HDL.