Can serum amyloid a or macrophage colony stimulating factor serve as marker of amyloid formation process?

Amyloid formation depends on amyloid precursor production and is influenced by the activity of the underlying disorder and mediated by some proinflamm atory cytokines. In this pilot study we tried to find some specific markers that could establish the activity of the disease. We investigated 45 sampl es of sera and 38 samples of urine from patients (pts) with secondary amylo idosis (AA), primary amyloidosis (AL), systemic autoimmune diseases with re nal impairment (Vasc) and healthy controls (Co). Pts with AA had increased plasma levels of TNF alpha (9.97 +/- 4.22 vs. 2.63 +/- 1.34 pg/mL, p < 0.00 1) and SAA (43.14 +/- 16.0 vs. 3.42 +/- 0.7 ng/mL, p < 0.05) in comparison with Co. Plasma levels of M-CSF in the AA group were significantly increase d in comparison with Co (1077.34 +/- 238.6 vs. 137.71 +/- 19.6, pg/mL, p < 0.001) and also in comparison with Vase (482.24 +/- 86.7 pg/mL, p < 0.05). Urinary excretions of' TNF alpha (8.92 +/- 8.1 vs. 0.17 +/- 0.11 mu g/mol c reatinine, p < 0.01), sIL-6R (1.39 +/- 1.14 vs. 0.07 +/- 0.05 g/mol creatin ine, p < 0.01) and M-CSF (650.2 +/- 153.7 vs. 33.3 +/- 8.6 mu g/mol creatin ine, p < 0.01) in AA were significantly increased in comparison with Co. Pt s with AL had increased plasma levels of M-CSF (819.83 +/- 264.2 vs. 137.71 +/- 19.6 pg/mL, p < 0.05) and urinary excretion of M-CSF (865.0 +/- 188.4 vs. 33.3 +/- 8.6 mu g/mol creatinine, p < 0.01) in comparison with Co. SAA has a low specificity for amyloidosis but is a sensitive acute phase reacta nt. TNF alpha, a proinflammatory cytokine, may reflect the activity of the underlying diseases in secondary amyloidosis. M-CSF was increased both in p lasma and urine in amyloidosis groups and seems to be the most promising (p ossibly specific) marker of amyloidosis.