Management of monoclonal gammopathy of undetermined significance (MGUS) and smoldering multiple myeloma (SMM)

Division of Hematology, Mayo Clinic, Rochester, Minnesota 55905, USA.
Oncology (Williston Park, N.Y.) (Impact Factor: 2.32). 06/2011; 25(7):578-86.
Source: PubMed


Monoclonal gammopathy of undetermined significance (MGUS) is defined as a serum M protein level of less than 3 g/dL, less than 10% clonal plasma cells in the bone marrow, and the absence of end-organ damage. The prevalence of MGUS is 3.2% in the white population but is approximately twice that high in the black population. MGUS may progress to multiple myeloma, AL amyloidosis, Waldenström macroglobulinemia, or lymphoma. The risk of progression is approximately 1% per year, but the risk continues even after more than 25 years of observation. Risk factors for progression include the size of the serum M protein, the type of serum M protein, the number of plasma cells in the bone marrow, and the serum free light chain ratio. Smoldering (asymptomatic) multiple myeloma (SMM) is characterized by the presence of an M protein level of 3 g/dL or higher and/or 10% or more monoclonal plasma cells in the bone marrow but no evidence of end-organ damage. The overall risk of progression to a malignant condition is 10% per year for the first 5 years, approximately 3% per year for the next 5 years, and 1% to 2% per year for the following 10 years. Patients with both MGUS and SMM must be followed up for their lifetime.

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    • "An abnormal serum-free light chain ratio, non-IgG MGUS, and a high serum M protein level (> 1.5) are the three risks identified that may predict progression to multiple myeloma. However, an abnormal light chain ratio increases the risk regardless of the type of M protein involved (Kyle et al., 2011; Wadhera & Rajkumar, 2010). "
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    ABSTRACT: Oncology nurses working in ambulatory care often encounter patients with nonmalignant hematologic disorders because the specialties of hematology and oncology are closely entwined. A variety of nonmalignant hematologic disorders can evolve into blood malignancies; therefore, close surveillance of nonmalignant hematologic disorders in an oncology/hematology clinic is important for early detection of malignancy. Monoclonal gammopathy of undetermined significance (MGUS) is one nonmalignant, hematologic disorder that is usually aproblematic; however, it can evolve into a blood malignancy such as multiple myeloma or be associated with other chronic conditions. This article provides an overview of MGUS with a focus on implications for the oncology nurse and patient education.
    Clinical Journal of Oncology Nursing 12/2013; 17(6):614-9. DOI:10.1188/13.CJON.614-619 · 0.91 Impact Factor
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    • "This diminishes gradually thereafter. SMM is a more advanced pre-malignant condition than monoclonal gammopathy of undetermined significance (MGUS).The cornerstone of managing SMM is a " watch and wait " strategy [1] . Although it is currently not possible to predict the clinical course of SMM, features predicting patients at highest risk include the size and type of M-protein, with IgA having a higher risk compared to IgG paraprotein, % plasma cell dyscrasia, and an abnormal serum-free light chain ratio. "

    02/2013; 3(1):1-6. DOI:10.5430/jhm.v3n1p18
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    ABSTRACT: Monoclonal gammopathy of undetermined significance (MGUS) is a common plasma cell dyscrasia, comprising the most indolent form of monoclonal gammopathy. However, approximately 25% of MGUS cases ultimately progress to plasma cell myeloma (PCM) or related diseases. It is difficult to predict which subset of patients will transform. In this study, we examined the immunophenotypic differences of plasma cells in MGUS and PCM. Bone marrow specimens from 32 MGUS patients and 32 PCM patients were analyzed by 4-color flow cytometry, using cluster analysis of ungated data, for the expression of several markers, including CD10, CD19, CD20, CD38, CD45, CD56 and surface and intracellular immunoglobulin light chains. All MGUS patients had two subpopulations of plasma cells, one with a "normal" phenotype [CD19(+), CD56(-), CD38(bright +)] and one with an aberrant phenotype [either CD19(-)/CD56(+) or CD19(-)/CD56(-)]. The normal subpopulation ranged from 4.4 to 86% (mean 27%) of total plasma cells. Only 20 of 32 PCM cases showed an identifiable normal subpopulation at significantly lower frequency [range 0-32%, mean 3.3%, p < 0.001]. The plasma cells in PCM were significantly less likely to express CD19 [1/32 (3.1%) vs. 13/29 (45%), p < 0.001] and more likely to express surface immunoglobulin [21/32 (66%) vs. 3/28 (11%), p < 0.001], compared to MGUS. Those expressing CD19 did so at a significantly lower level than in MGUS, with no overlap in mean fluorescence intensities [174 +/- 25 vs. 430 +/- 34, p < 0.001]. There were no significant differences in CD56 expression [23/32 (72%) vs. 18/29 (62%), p = 0.29], CD45 expression [15/32 (47%) vs. 20/30 (67%), p = 0.10] or CD38 mean fluorescence intensities [6552 +/- 451 vs. 6365 +/- 420, p = 0.38]. Two of the six MGUS cases (33%) with >90% CD19(-) plasma cells showed progression of disease, whereas none of the cases with >10% CD19(+) plasma cells evolved to PCM. MGUS cases with potential for disease progression appeared to lack CD19 expression on >90% of their plasma cells, displaying an immunophenotypic profile similar to PCM plasma cells. A higher relative proportion of CD19(+) plasma cells in MGUS may be associated with a lower potential for disease progression.
    BMC Clinical Pathology 12/2008; 8(1):13. DOI:10.1186/1472-6890-8-13
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