Abstract
Systemic light-chain (AL) amyloidosis is both a protein deposition disorder and a monoclonal plasma cell dyscrasia. Effective treatment depends on reduction of the clonal plasma cells that produce the toxic light chains. Although high-dose melphalan with autologous stem cell transplant (MEL SCT) is effective for AL patients, the mobilization and collection of peripheral blood stem cells with G-CSF can be problematic despite their lack of prior chemotherapy and minimal marrow infiltration with plasma cells. In addition, unusual toxicities of G-CSF mobilization such as hypotension have been noted in AL patients. As new therapies show efficacy in AL, the role of stem cell mobilization and MEL SCT will likely be re-evaluated, increasing the importance of understanding the variability in stem cell mobilization. Recent work has shown that the mechanism of G-CSF mobilization likely involves the sympathetic nervous system (
Disclosure: No relevant conflicts of interest to declare.
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