Amyloid A fibril degrading activity in serum in liver disease--relation to serum acute phase and other protein levels.

Human serum contains amyloid A degrading activity. This activity is decreased in patients with reactive systemic amyloidosis. To study the specificity of this finding, we evaluated the effect of liver disease per se on the amyloid degrading activity in serum as well as its relation to serum amyloid A (SAA), the putative precursor of amyloid A fibrils, and other serum protein levels in alcoholic and non-alcoholic non-malignant liver diseases without signs of amyloidosis. The amyloid A-degrading activity was significantly decreased in liver cirrhosis. The lowest activity was seen in patients with advanced cirrhosis. There was a positive correlation between the degradative activity and indices of hepato-cellular synthetic function (serum albumin, r = 0.77; serum prealbumin, r = 0.65). Most of the patients with liver disease had a detectable SAA level; 77% had a level higher than 5 mg/l (compared to 12% among blood donors). However, the SAA increase was generally only slight, e.g. in alcoholic liver cirrhosis the median SAA level was 15 mg/l. The results show that liver dysfunction per se decreases amyloid A-degrading activity in serum. A reduced activity cannot therefore be regarded as specific for reactive amyloidosis. Since reactive amyloidosis is extremely rare in liver cirrhosis, it seems obvious that a reduced amyloid degrading activity alone, in the absence of a markedly elevated SAA level, does not predispose, at least in patients with liver disease, to amyloidosis.