| Abstrakt: |
Dialysis amyloidosis is a frequent complication encountered in patients receiving long-term hemodialysis. These amyloid deposits are composed mainly of an insoluble fibrillar material that consists of beta 2-microglobulin (beta 2-m). While this fibrillar protein is a major component of these deposits, numerous other substances have been identified in the amyloid deposits; e.g., amyloid P component, calcium, glycosaminoglycans, chondroitin sulfate, hyaluronic acid, collagen, protease inhibitors, k-chain protein, ubiquitin, apolipoprotein E and macrophages. Hypotheses on the pathogenesis of amyloidosis have suggested roles for each of these factors. The pathogenesis of beta 2-m-related amyloidosis is probably multifactorial, with the retention of beta 2-m presumed to be the basic requirement for its initiation. It has been demonstrated in vivo that radiolabeled beta 2-m accumulates at the site of amyloid deposits. Our autoradiographic study of synovial tissue demonstrated that the cells had taken up radiolabeled beta 2-m, indicating that circulating radiolabeled-beta 2-m could be detected as an accumulation because it is taken up by the cells around the amyloid deposits. At present it can not be said that any basic treatment for beta 2-m-related amyloidosis has been established. It has been reported that the administration of a low dose of a corticosteroid may be effective in treating beta 2-m amyloid-related arthropathy. The articular symptoms resolved in most patients with corticosteroid. However, it should be borne in mind that corticosteroid may induce some adverse effects. Corticosteroid should be used only in patients with severe articular symptoms. |
