Extramedullary Disease-Achilles Heel in Myeloma?

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Abstract

[Indexed for MEDLINE] Conflict of interest statement: Shaji Kumar has received research support from AbbVie, Adaptive, Celgene, Johnson & Johnson, KITE, MedImmune/Astra Zeneca, and Takeda, and has been an advisory committee member for AbbVie, Adaptive, Celgene Johnson & Johnson, KITE, MedImmune/Astra Zeneca, Merck, Novartis, Oncopeptides, Roche, Sanofi, and Takeda. Joshua Richter has served in a consulting/advisory role for AbbVie, Bristol Myers Squibb, Genentech, Johnson & Johnson, Karyopharm, Pfizer, Regeneron, Sanofi, and Takeda, and has participated in speaker's bureaus for Adaptive Biotechnologies, Bristol Myers Squibb, Johnson & Johnson, and Sanofi. Saad Z. Usmani has served a consulting or advisory role for AbbVie, Amgen, Bristol Myers Squibb, Celgene, Genentech, Gilead Sciences, GSK, Janssen, Karyopharm Therapeutics, Merck, and Takeda, and received research funding from Amgen, Array BioPharma, Bristol Myers Squibb, Celgene, GSK, Janssen, Merck, Pharmacyclics, Sanofi, Seattle Genetics, and Skyline Diagnostics; Yael C. Cohen has served a consulting or advisory role for Amgen, Bristol Myers Squibb, GSK, Johnson & Johnson, Medison, Pfizer, Roche, Sanofi Aventis, and Takeda; has received research funding from Johnson & Johnson and Takeda; and participates in a speakers' bureau for GSK and Johnson & Johnson. Jing Christine Ye has served in a consulting/advisory role for and received honoraria from Bristol Myers Squibb and Johnson & Johnson and has received research funding from Celgene, Genmab, GSK, MingSight, Novartis, Pfizer, and Regeneron. María‐Victoria Mateos has received honoraria from AbbVie, Amgen, BMS/Celgene, GSK, Johnson & Johnson, Kite Pharma, Oncopeptides, Pfizer, Regeneron, Sanofi, and Stemline. Vania Hungria has received honoraria from AbbVie, Amgen, Bristol Myers Squibb, GSK, Johnson & Johnson, Pfizer, Regeneron, Sanofi, and Takeda. Elena Zamagni has served a consulting or advisory role for and received honoraria from Amgen, Bristol Myers Squibb, Johnson & Johnson, Menarini Stemline, Oncopeptides, and Pfizer. 11. Hematology Am Soc Hematol Educ Program. 2015;2015:272-8. doi: 10.1182/asheducation-2015.1.272. Evolving diagnostic criteria for multiple myeloma. Rajkumar SV(1). Author information: (1)Division of Hematology, Mayo Clinic, Rochester, MN. Multiple myeloma (MM) is a plasma cell malignancy historically defined by the presence of end-organ damage, specifically, hypercalcemia, renal failure, anemia, and bone lesions (CRAB features) that can be attributed to the neoplastic process. In 2014, the International Myeloma Working Group (IMWG) updated the diagnostic criteria for MM to add specific biomarkers that can be used to make the diagnosis of the disease in patients who did not have CRAB features. In addition, the update allows modern imaging methods including computed tomography (CT) and positron emission tomography-CT to diagnose MM bone disease. These changes enable early diagnosis, and allow the initiation of effective therapy to prevent the development of end-organ damage in patients who are at the highest risk. This article reviews these and several other clarifications and revisions that were made to the diagnostic criteria for MM and related disorders. The updated disease definition for MM also automatically resulted in a revision to the diagnostic criteria for the asymptomatic phase of the disease termed smoldering MM (SMM). Thus the current diagnosis and risk-stratification of SMM is also reviewed in this article. Using specific prognostic factors, it is possible to identify a subset of patients with SMM who have a risk of progression to MM of 25% per year (high-risk SMM). An approach to the management of patients with low- and high-risk SMM is discussed. © 2015 by The American Society of Hematology. All rights reserved. DOI: 10.1182/asheducation-2015.1.272