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          Multiple Myeloma

          Updated: Jan 28, 2026
          • Author: Dhaval Shah, MD; Chief Editor: Emmanuel C Besa, MD more...
          Sections
          Overview

          Background

          Multiple myeloma (MM) is a plasma cell malignancy in which monoclonal plasma cells proliferate in bone marrow, resulting in an overabundance of monoclonal paraprotein (M protein), destruction of bone, and displacement of other hematopoietic cell lines. [1]MM is part of a spectrum of diseases ranging from monoclonal gammopathy of unknown significance (MGUS) to plasma cell leukemia. See the image below.

           

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          Pathophysiology

          The development of MM is commonly preceded by MGUS, a premalignant condition that results when plasma cells undergo mutations that restore their capacity for proliferation. In MGUS, these clonal plasma cells take up less than 10% of bone marrow. The serum protein value is less than 3 g/dL, and myeloma-related end-organ damage is absent. An intermediate disease stage between MGUS and MM, termed smoldering MM, is characterized by an M protein level of 3 g/dL or more and over 10% clonal plasma cells in bone marrow, but no symptoms of myeloma-related end-organ damage. [2]  .

          A variety of cytogenetic abnormalities are found in MGUS and MM. Almost half of cases are hyperdiploid, usually with extra copies of the odd-numbered chromosomes (exception of chromosomes 1, 13, and 21). Most of the remainder are nonhyperdiploid and are characterized by a primary translocation involving the immunoglobulin heavy-chain (IgH) gene at 14q32. [2] In addition, virtually all cases involve dysregulation of the cyclin D/retinoblastoma (cyclin D/RB) pathway. This genetic heterogeneity contributes to the rapid emergence of drug resistance in MM. [3]

          Increasing evidence suggests that the bone marrow microenvironment of tumor cells plays a pivotal role in the pathogenesis of myelomas. [4] This discovery has resulted in the expansion of treatment options.

          The role of cytokines in the pathogenesis of MM is an important area of research. Interleukin (IL)-6 is also an important factor promoting the in vitro growth of myeloma cells. Other cytokines are tumor necrosis factor and IL-1b.

          The pathophysiologic basis for the clinical sequelae of MM involves the skeletal, hematologic, renal, and nervous systems, as well as general processes (see below).

          Skeletal processes

          Plasma-cell proliferation causes extensive skeletal destruction with osteolytic lesions, anemia, andhypercalcemia. Mechanisms for hypercalcemia include bony involvement and, possibly, humoral mechanisms. Isolated plasmacytomas (which affect 2-10% of patients) lead to hypercalcemia through production of the osteoclast-activating factor.

          Destruction of bone and its replacement by tumor may lead to pain, spinal cord compression, and pathologic fracture. The mechanism of spinal cord compression symptoms may be the development of an epidural mass with compression, a compression fracture of a vertebral body destroyed by multiple myeloma, or, rarely, an extradural mass. With pathologic fracture, bony involvement is typically lytic in nature.

          Hematologic processes

          Bone marrow infiltration by plasma cells results in neutropenia, anemia, and thrombocytopenia. M components may interact specifically with clotting factors, leading to defective aggregation.

          Renal processes

          The most common mechanisms of kidney injury in MM are direct tubular injury, amyloidosis, or involvement by plasmacytoma. [5,6] Renal conditions that may be observed include the following:

          Neurologic processes

          The nervous system may be involved as a result of radiculopathy and/or cord compression due to nerve compression and skeletal destruction (amyloid infiltration of nerves).

          General processes

          General pathophysiologic processes includehyperviscosity syndrome. This syndrome is infrequent in MM and occurs with overproduction of IgG1, IgG3, or IgA. Sludging in the capillaries can result in purpura, retinal hemorrhage, papilledema, coronary ischemia, or central nervous system (CNS) symptoms (eg, confusion, vertigo, seizure).Cryoglobulinemia causesRaynaud phenomenon, thrombosis, and gangrene in the extremities.

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          Etiology

          The precise etiology of MM has not yet been established. Roles have been suggested for a variety of factors, including genetic causes, environmental or occupational causes, MGUS, radiation, chronic inflammation, and infection.

          Genetic causes

          MM has been reported in two or more first-degree relatives and in identical twins, although no evidence suggests a hereditary basis for the disease. A study by the Mayo Clinic found MM in eight siblings from a group of 440 patients; these eight siblings had different heavy chains but the same light chains.

          Some studies have shown that abnormalities of certain oncogenes, such asc-myc, are associated with development early in the course of plasma cell tumors and that abnormalities of oncogenes such asN-ras andK-ras are associated with development after bone marrow relapse. Abnormalities of tumor suppressor genes, such asTP53, have been shown to be associated with spread to other organs. [7]

          Ongoing research is investigating whether human leukocyte antigen (HLA)-Cw5 or HLA-Cw2 may play a role in the pathogenesis of multiple myeloma.

          Environmental or occupational causes

          Case-controlled studies have suggested a significant risk of developing MM in individuals with significant occupational exposures in the agriculture, food, and petrochemical industries. An increased risk has been reported in farmers, especially in those who use herbicides and insecticides (eg, chlordane), and in people exposed to benzene and other organic solvents. There is conflicting evidence regarding long-term (> 20 y) exposure to hair dyes and possible increased risk of developing MM. [8]

          MGUS/Smoldering multiple myeloma (SMM)

          Monoclonal gammopathy of undetermined significance (MGUS) is defined by the presence of three criteria:

          • Serum monoclonal M protein (M-protein) concentration < 3 g/dL
          • Bone marrow plasma cell concentration < 10%
          • No evidence of end-organ damage

          MGUS is seen in 2-3% of the elderly White population. It is divided into the following three subtypes:

          • Non-IgM MGUS
          • IgM MGUS
          • Light-chain MGUS

          Patients with non-IgM MGUS have a risk of progression to MM at a rate of 1% per year. For these patients, risk factors for progression to MM are as follows:

          • M protein concentration > 1.5 g/dL
          • Non-IgG isotype
          • An abnormal free light chain (FLC)(kappa:lambda) ratio

          Patients with IgM MGUS have a risk of progression to Waldenström macroglobulinemia and less frequently lymphoma or amyloid light chain (AL) amyloidosis. IgM MGUS rarely progresses to MM. Light-chain MGUS has a tendency to progress to light-chain MM, AL amyloidosis, or light-chain deposition disease.

          A study by Wadhera et al examined secondary MGUS that developed in patients with MM. Of 1942 patients with MM, 128 (6.6%) developed a secondary MGUS at a median of 12 months from the diagnosis of MM. Overall survival was superior in patients with MM who developed secondary MGUS compared with the rest of the cohort. [9]

          Smoldering MM is present when the serum M protein concentration is > 3 g/dL or the bone marrow plasma cell concentration is > 10% but there is no evidence of end-organ damage. Risk factors for progression of SMM to MM include any of the following:

          • M protein concentration > 3 g/dL
          • Abnormal FLC ratio
          • Bone marrow plasma cell concentration >10%

          The time to progression decreases with increasing numbers of risk factors, as follows:

          • One factor: 10 years
          • Two factors: 5.1 years
          • Three factors: 1.9 years

          Radiation

          Radiation may play a role in some patients. An increased risk has been reported in atomic-bomb survivors exposed to more than 50 Gy: In 109,000 survivors of the atomic bombing of Nagasaki during World War II, 29 died from MM between 1950 and 1976. Some more recent studies, however, do not confirm that these survivors have an increased risk of developing MM.

          A study of workers at the Oak Ridge Diffusion Plant in eastern Tennessee showed only a weak correlation of risk of MM to uranium exposure. [10]

          Chronic inflammation

          A relationship between MM and preexisting chronic inflammatory diseases has been suggested, but studies of a possible relationship between autoimmune diseases and MM risk have reported contradictory results. A Mendelian randomization study concluded that genetic susceptibility to primary sclerosing cholangitis might be causally related to a modestly increased risk of MM, but found no evidence of increased risk related to type 1 diabetes mellitus, rheumatoid arthritis, systemic lupus erythematosus, psoriasis, multiple sclerosis, primary biliary cirrhosis, or juvenile idiopathic arthritis. [11]

          Infection

          Human herpesvirus 8 (HH8) infection of bone marrow dendritic cells has been found in patients with MM and in some patients with MGUS.

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          Epidemiology

          MM accounts for 10% of all hematologic cancers. [12,13] The American Cancer Society estimates that in the United States, approximately 36,000 new cases of MM (20,150 in men and 15,850 in women) will be diagnosed in 2026. [14] The lifetime risk of getting MM is approximately 1 in 108 for men and 1 in 133 for women (overall, 0.8%). [14,15] Approximately 10,850 deaths from MM (5780 in men and 5070 in women) are expected to occur in the US in 2026. [14] Rates for new MM cases rose slightly over the last decade, from 7.0 per 100,000 persons in 2011 to 7.1 per 100,000 persons in 2021, while death rates declined slightly, from 3.4 to 2.8 per 100,000 from 2012 to 2022. [15]

          In the US, the annual incidence of MM per 100,000 persons is 8.1 cases in White men, 5.1 cases in White women, 17.1 cases in Black men, and 13.0 cases in Black women. For Hispanics, the rates are 7.9 in men and 5.8 in women. Rates are lowest for Asians/Pacific Islanders, at 5.1 in men and 3.3 in women. [15] According to a study of the ethnic disparities among patients with MM, Hispanics had the youngest median age at diagnosis (65 years) and Whites had the oldest (71 years). Asians had the best overall survival rates, while Hispanics had the worst. [16]

          The median age at diagnosis of MM is 69 years. Less than 14% of patients are younger than 55 years, and only about 3% are younger than 45 years. [15]

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          Prognosis

          MM is a heterogeneous disease, with survival ranging from 1 year to more than 10 years. Median survival in unselected patients with MM is 3 years. The 5-year relative survival rate is 61.1%. [15] Survival is higher in younger people and lower in the elderly. [7,17]

          The tumor burden and the proliferation rate are the two key indicators for the prognosis in patients with MM. Many schemas have been published to aid in determining the prognosis. One schema uses C-reactive protein (CRP) and beta-2 microglobulin (which is an expression of tumor burden) to predict survival, as follows [18]:

          • If levels of both proteins are less than 6 mg/L, the median survival is 54 months.
          • If the level of only one component is less than 6 mg/L, the median survival is 27 months.
          • If levels of both protein values are greater than 6 mg/L, the median survival is 6 months.

          Poor prognostic factors include the following:

          • Tumor mass
          • Hypercalcemia
          • Bence Jones proteinemia
          • Kidney impairment (ie, stage B disease or creatinine level > 2 mg/dL at diagnosis)

          The prognosis by treatment is as follows:

          • Conventional therapy: Overall survival is approximately 3 years, and event-free survival is less than 2 years.
          • High-dose chemotherapy with stem-cell transplantation: The overall survival rate is greater than 50% at 5 years.

          Infections are an important cause of early death in MM. In a United Kingdom study, 10% of patients died within 60 days after diagnosis of MM, and 45% of those deaths were due to infection. [19] In a Swedish study, 22% of patients died of infection within the first year after diagnosis. The risk of both bacterial infections (eg, meningitis, septicemia, pneumonia) and viral infections (eg, herpes zoster, influenza) was seven times higher in patients with MM than in matched controls. The Swedish investigators also found that the risk of infections has increased in recent decades, and they argue that the use of more intensive treatment measures for MM (ie, newer drugs and high-dose chemotherapy with transplantation) has contributed to the increased risk. [20]

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          Patient Education

          Patient education is very important in the management of MM. The International Myeloma Foundation (IMF) offers educational resources, a quarterly newsletter, and conferences. Patients or physicians can contact the IMF by phone at (800) 452-CURE (800-452-2873) in the United States and Canada or on the internet atInternational Myeloma Foundation.

          Patient education should address, at a minimum, the following questions:

          • What is MM, and how does it affect the body?
          • What are the causes of MM?
          • What is the treatment for MM?
          • What are the adverse effects of treatment? (As an example, patients should be informed of the risk of osteonecrosis of the jaw, which has been associated with bisphosphonate therapy in MM.)
          • What are some of the complications of MM?
          • Where can additional information be found?
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          References

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          Contributor Information and Disclosures
          Author

          Dhaval Shah, MD Helen F Graham Cancer Center and Research Institute

          Dhaval Shah, MD is a member of the following medical societies:American Society of Clinical Oncology,American Society of Hematology

          Disclosure: Nothing to disclose.

          Coauthor(s)

          Karen Seiter, MD Professor, Department of Internal Medicine, Division of Oncology/Hematology, New York Medical College

          Karen Seiter, MD is a member of the following medical societies:American Association for Cancer Research,American College of Physicians,American Society of Hematology

          Disclosure: Received honoraria from Novartis for speaking and teaching; Received consulting fee from Novartis for speaking and teaching; Received honoraria from Celgene for speaking and teaching.

          Pharmacy Editor

          Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

          Disclosure: Received salary from Medscape for employment.

          Chief Editor

          Emmanuel C Besa, MD Professor Emeritus, Department of Medicine, Division of Hematologic Malignancies and Hematopoietic Stem Cell Transplantation, Kimmel Cancer Center, Jefferson Medical College of Thomas Jefferson University

          Emmanuel C Besa, MD is a member of the following medical societies:American Association for Cancer Education,American Society of Clinical Oncology,American College of Clinical Pharmacology,American Federation for Medical Research,American Society of Hematology,New York Academy of Sciences

          Disclosure: Nothing to disclose.

          Additional Contributors

          Lesley Elizabeth Fox, MD Pathologist, ReitPath Pathology, Austin, Texas

          Lesley Elizabeth Fox, MD is a member of the following medical societies:Alpha Omega Alpha,American Society for Clinical Pathology,American Society of Hematology,College of American Pathologists,Texas Medical Association,United States and Canadian Academy of Pathology

          Disclosure: Nothing to disclose.

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