UNCOMMON CONDITIONS UNDERLYING AA AMYLOIDOSIS

摘要

Secondary or reactive (AA) amyloidosis represents a substantial proportion of systemic amyloidoses. its pathogenesis is multifactorial and involves many variables such as the primary structure of the precursor protein, the presence of non-fibriilar proteins (e.g. amyloid P component, apolipoprotein E, proteoglycans and basement membrane proteins), receptors, lipid metabolism and proteases. The persistent and substantial elevation of the serum concentration of the amyloidogenic precursor, serum amyloid A protein (SAA), is necessary, but not sufficient, for the development of AA amyloidosis (1). SAA is an apolipoprotein of high-density lipoprotein, and is synthesized by hepatocytes under the transcriptional control of a number of cytokines, principally IL-1, IL-6 and TNFa. The increased/deregulated production of cytokines can be caused by the conditions listed in Table 1.