By S. Sarantseva

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013, log-rank test). , Baba, S. & Shono, M. (2006). 3 allele genotype in Japanese patients with amyloidosis secondary to rheumatoid arthritis. Rheumatology (Oxford), Vol. 45, No. 1, (January 2006), pp. ] Amyloidotic cardiac involvement has been revealed to trend to be a poor prognostic factor. Heart failure is likely to be directly responsible for death in only a minority of patients, however, patients with heart failure may be complicated by multiple organ failures in later phase of the RA disease course.

2 Inhibition of AA amyloid fibril deposits Eprodisate, a small sulfonated molecule with structural similarity to heparan sulfate, which can cause regression of amyloidosis by destabilizing the glycoasaminoglycan backbone of amyloid deposits, delayed progression of renal disease associated with AA amyloidosis. In a trial for AA amyloidosis, eprodisate had a beneficial effect on the rate of deterioration of renal function but no effect on urinary protein excretion . That eprodisate did not affect SAA levels and preserved kidney function but had no effect on proteinuria raises the interesting possibility that it is the precursors of mature amyloid fibrils are responsible for proteinuria in amyloidosis.

These cytokines induce a markedly increased synthesis of the acute-phase protein SAA by hepatocytes, the concentration of which can be 100 to 1000-fold higher than normal. The progressive nature of AA amyloidosis largely reflects the persistent nature of the activity of the underlying conditions and, due to fluctuations of disease activity, not all patients show evidence of an acute-phase response at the very time of diagnosis. Although it is still unknown exactly how the pathophysiological functions of SAA are associated with the pathogenesis of AA amyloidosis, there appears a certain subset of patients, who are prone to process SAA into AA amyloid fibrils under different factors, such as proteases, proteoglycans, serum amyloid P component (SAP).

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