Multiple Myeloma

Plasma cell malignancies or multiple myeloma usually develop later in life than solitary plasmacytoma. However, approximately 50% of patients with plasmacytoma progress to multiple myeloma. Presentation is generally preceded by serological abnormalities and progression may be slow, prognostic factors vary with immunoglobulin type. In IgG myeloma, the serum calcium and serum creatinine are most significant, whereas in IgA myeloma, hemoglobin, serum calcium and M component are the best predictors for outcome. In Bence Jones proteinuria, micromolecular M component (/c or X), creatinine, calcium, presence of B-J protein, diffuse osteolytic lesions and bone marrow plasma cells greater than 30% were best predictors [20], Controversy exists as to the precursor cell in multiple myeloma. Pre-B cells, memory B cells and pre-switched somatically mutated B cells have been proposed [21]. In another described germline neoplasm, lymphocytoplasmacytic cells occurred at different stages of terminal differentiation within a single neoplastic clone that was manifest by the evolution of one monoclonal protein (IgM-^r) to three monoclonal proteins (IgG-/c, IgA-a: and IgM-x:) [22],

A disproportionate number of patients with an IgA gammopathy type of multiple myeloma progress to an aggressive or anaplastic disease phase. The cell type resembles a high-grade anaplastic lymphoma and the natural history is short, characterized by rapidly enlarging soft tissue masses or bonemarrow replacement that is refractory to therapy. Studies support a clonal evolution of the original malignant cell line that is analogous to the terminal transformation associated with other lymphoproliferative disorders [23]. Simultaneous development of MM and nonlymphoblastic leukemia or myelodysplastic syndromes is unusual and likely represents the transformation of a single progenitor cell. The development of a myelopathy during treatment of MM is quite common [24],

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