eMedicine Specialties > Hematology > Plasma Cell Disorders

Multiple Myeloma

Author: Sara J Grethlein, MD, Associate Dean for Graduate Medical Education, Associate Professor, Department of Internal Medicine, Division of Hematology and Oncology, State University of New York Upstate Medical University
Coauthor(s): Lilian M Thomas, MD, Fellow, Department of Hematology/Oncology, State University of New York Upstate Medical University
Contributor Information and Disclosures

Updated: Aug 12, 2009

Introduction

Background

Multiple myeloma is a debilitating malignancy that is part of a spectrum of diseases ranging from monoclonal gammopathy of unknown significance (MGUS) to plasma cell leukemia. First described in 1848, multiple myeloma is a disease characterized by a proliferation of malignant plasma cells and a subsequent overabundance of monoclonal paraprotein. An intriguing feature of multiple myeloma is that the antibody-forming cells (ie, plasma cells) are malignant and, therefore, may cause unusual manifestations.


Bone marrow aspirate demonstrating plasma cells o...

Bone marrow aspirate demonstrating plasma cells of multiple myeloma. Note the blue cytoplasm, eccentric nucleus, and perinuclear pale zone (or halo). All images and text are (c) 2002 by the American Society of Hematology. All rights reserved.

Bone marrow aspirate demonstrating plasma cells o...

Bone marrow aspirate demonstrating plasma cells of multiple myeloma. Note the blue cytoplasm, eccentric nucleus, and perinuclear pale zone (or halo). All images and text are (c) 2002 by the American Society of Hematology. All rights reserved.


Bone marrow biopsy demonstrating sheets of malign...

Bone marrow biopsy demonstrating sheets of malignant plasma cells in multiple myeloma. All images and text are (c) 2002 by the American Society of Hematology. All rights reserved.

Bone marrow biopsy demonstrating sheets of malign...

Bone marrow biopsy demonstrating sheets of malignant plasma cells in multiple myeloma. All images and text are (c) 2002 by the American Society of Hematology. All rights reserved.


The presentation of multiple myeloma can range from asymptomatic to severely symptomatic with complications requiring emergent treatment. Systemic ailments include bleeding, infection and renal failure; local catastrophes include pathologic fractures and spinal cord compression. Although patients benefit from treatment (ie, longer life, less pain, fewer complications), currently no cure exists. Recent advances in therapy have helped to lessen the occurrence and severity of adverse effects of multiple myeloma.

For excellent patient education resources, visit eMedicine's Blood and Lymphatic System Center. Also, see eMedicine's patient education article Myeloma.

Pathophysiology

Multiple myeloma can cause a wide variety of problems. The proliferation of plasma cells may interfere with the normal production of blood cells, resulting in leukopenia, anemia, and thrombocytopenia. The cells may cause soft-tissue masses (plasmacytomas) or lytic lesions in the skeleton. Feared complications of multiple myeloma are bone pain, hypercalcemia, renal failure, and spinal cord compression. The aberrant antibodies that are produced lead to impaired humoral immunity, and patients have a high prevalence of infection, especially with encapsulated organisms such as Pneumococcus. The overproduction of these antibodies may lead to hyperviscosity, amyloidosis, and renal failure.

Frequency

United States

The age-adjusted annual incidence of multiple myeloma is 4.3 cases per 100,000 white men, 3 cases per 100,000 white women, 9.6 cases per 100,000 black men, and 6.7 cases per 100,000 black women.

Mortality/Morbidity

  • Multiple myeloma affects the kidneys in several ways. The most common mechanisms of renal injury are direct tubular injury, amyloidosis, or involvement by plasmacytoma.1,2 Physicians manage the acute clinical condition with plasmapheresis to rapidly lower circulating abnormal proteins. Data about this approach are limited, but a small randomized study showed a survival advantage with the use of apheresis.2 Conventional therapy may take weeks to months to show a benefit. Renal impairment resulting from multiple myeloma is associated with a very poor prognosis. A recent case series demonstrated that patients with renal failure from myeloma may benefit from autologous stem cell transplants, and as many as one third may demonstrate improvement in their renal function with this approach.3
  • Spinal cord compression is one of the most severe adverse effects of multiple myeloma. Reports indicate that as many as 20% of patients develop spinal cord compression at some point during the course of their disease. Symptoms typically include back pain, weakness or paralysis in the legs, numbness, or dysesthesias in the lower extremities. However, depending on the level of involvement, patients may present with upper extremity symptoms. The mechanism of these 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. The dysfunction may be reversible, depending on the duration of the cord compression; however, once established, the dysfunction is only rarely fully reversed.
  • A frequent complication of multiple myeloma is pathologic fractures. Bony involvement is typically lytic in nature. Physicians should orthopedically stabilize (ie, typically pin) and irradiate these lesions. Careful attention to a patient's bony symptoms, intermittent radiographic surveys, and the use of bisphosphonates may be useful to prevent fractures.4,5,6
  • Patients with multiple myeloma commonly develop hypercalcemia. The mechanisms include bony involvement and, possibly, humoral mechanisms. Treatment for myeloma-induced hypercalcemia is the same as that for other malignancy-associated hypercalcemia; however, the dismal outcome observed with hypercalcemia in solid tumors is not observed in multiple myeloma.

Race

Multiple myeloma accounts for 1.1% of the malignancies in white US residents and 2.1% of the malignancies in black residents.

Sex

The male-to-female ratio of multiple myeloma is 3:2.

Age

The median age of patients with multiple myeloma is 68 years for men and 70 years for women.

Clinical

History

Presenting symptoms of multiple myeloma include bone pain, pathologic fractures, weakness, anemia, infection (often pneumococcal), hypercalcemia, spinal cord compression, or renal failure. Increasingly, physicians are identifying asymptomatic patients through routine blood screening. Typically, a large gap between the total protein and the albumin levels observed on an automated chemistry panel suggests a problem (ie, protein minus albumin equals globulin).

  • Bone pain
    • This is the most common presenting symptom in multiple myeloma. Most case series report that 70% of patients have bone pain at presentation.
    • The lumbar spine is one of the most common sites of pain.
  • Pathologic fractures and bone lesions
    • Pathologic fractures are very common in multiple myeloma; 93% of patients have more than one site of bony involvement.
    • A severe bony event is a common presenting issue.
  • Spinal cord compression
    • This complication occurs in approximately 10-20% of patients with multiple myeloma at some time during the course of disease.
    • The symptoms that should alert physicians to consider spinal cord compression are back pain, weakness, numbness, or dysesthesias in the extremities.
    • It is common for spinal cord compressions in multiple myeloma to occur at multiple levels, so comprehensive evaluation of the spine is warranted.
    • Patients who are ambulatory at the start of therapy have the best likelihood of preserving function and avoiding paralysis.
  • Bleeding
    • Occasionally, a patient may come to medical attention for bleeding resulting from thrombocytopenia.
    • Rarely, monoclonal protein may absorb clotting factors and lead to bleeding.
  • Hypercalcemia
    • Confusion, somnolence, bone pain, constipation, nausea, and thirst are the presenting symptoms of hypercalcemia.
    • This complication may be present in as many as 30% of patients with multiple myeloma at presentation. In most solid malignancies, hypercalcemia carries an ominous prognosis, but in multiple myeloma, its occurrence does not adversely affect survival.
  • Infection
    • Abnormal humoral immunity and leukopenia may lead to infection.
    • Pneumococcal organisms are commonly involved, but shingles (ie, herpes zoster) and Haemophilus infections are also more common among patients with multiple myeloma.
  • Hyperviscosity
    • Epistaxis may be a presenting symptom of multiple myeloma with a high tumor volume. Occasionally, patients may have such a high volume of monoclonal protein that their blood viscosity increases, resulting in complications such as stroke, myocardial ischemia, or infarction.
    • Patients may report headaches and somnolence, and they may bruise easily and have hazy vision. Patients with multiple myeloma typically experience these symptoms when their serum viscosity is greater than 4 times that of normal serum.
  • Neurologic symptoms
    • Carpal tunnel syndrome is a common complication of myeloma.
    • Meningitis (especially that resulting from pneumococcal or meningococcal infection) is more common in patients with multiple myeloma.
    • Some peripheral neuropathies have been attributed to multiple myeloma.
  • Anemia
    • Anemia, which may be quite severe, is the most common cause of weakness in patients with multiple myeloma.

Physical

  • Pallor from anemia may be present.
  • Ecchymoses or purpura from thrombocytopenia may be evident.
  • Bony tenderness is not uncommon in multiple myeloma, resulting from focal lytic destructive bone lesions or pathologic fracture. Pain without tenderness is typical.
  • Neurologic findings may include a sensory level change (ie, loss of sensation below a dermatome corresponding to a spinal cord compression), weakness, or carpal tunnel syndrome.
  • Extramedullary plasmacytomas, which consist of soft-tissue masses of plasma cells, are not uncommon. Plasmacytomas have been described in almost every site in the body. Although the aerodigestive tract is the most common location, reports also describe orbital, ear canal, cutaneous, gastric, rectal, prostatic, and retroperitoneal lesions.
  • Amyloidosis may develop in some patients with multiple myeloma. The characteristic physical examination findings that suggest amyloidosis include the following:
    • The shoulder pad sign is defined by bilateral swelling of the shoulder joints secondary to amyloid deposition. Physicians describe the swelling as hard and rubbery. Amyloidosis may also be associated with carpal tunnel syndrome and subcutaneous nodules.
    • Macroglossia is a common finding in patients with amyloidosis (see Image 1 or below).
      Amyloidosis infiltrating the tongue in multiple m...

      Amyloidosis infiltrating the tongue in multiple myeloma. All images and text are (c) 2002 by the American Society of Hematology. All rights reserved.

      Amyloidosis infiltrating the tongue in multiple m...

      Amyloidosis infiltrating the tongue in multiple myeloma. All images and text are (c) 2002 by the American Society of Hematology. All rights reserved.

    • Skin lesions that have been described as waxy papules or nodules may occur on the torso, ears, or lips.
    • Postprotoscopic peripalpebral purpura strongly suggests amyloidosis. Patients may develop raccoonlike dark circles around their eyes following any procedure that parallels a prolonged Valsalva maneuver. The capillary fragility associated with amyloidosis may account for this observation. In the past, this correlation was observed when patients underwent rectal biopsies to make the diagnosis.
  • The most widely accepted schema for the diagnosis of multiple myeloma uses particular combinations of laboratory, imaging, and procedure findings as diagnostic criteria. The findings are as follows:
    • I = Plasmacytoma on tissue biopsy
    • II = Bone marrow with greater than 30% plasma cells
    • III = Monoclonal globulin spike on serum protein electrophoresis, with an immunoglobulin (Ig) G peak of greater than 3.5 g/dL or an IgA peak of greater than 2 g/dL, or urine protein electrophoresis (in the presence of amyloidosis) result of greater than 1 g/24 h
    • a = Bone marrow with 10-30% plasma cells
    • b = Monoclonal globulin spike present but less than category III
    • c = Lytic bone lesions
    • d = Residual IgM level less than 50 mg/dL, IgA level less than 100 mg/dL, or IgG level less than 600 mg/dL
  • The following combinations of findings are used to make the diagnosis of multiple myeloma:
    • I plus b, c, or d
    • II plus b, c, or d
    • III plus a, c, or d
    • a plus b plus c
    • a plus b plus d

Causes

  • Genetic causes
    • A study by the Mayo clinic found multiple myeloma in 8 siblings from a group of 440 patients; these 8 siblings had different heavy chains but the same light chains.
    • 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 multiple myeloma in individuals with significant exposures in the agriculture, food, and petrochemical industries. Long-term (>20 y) exposure to hair dyes has been tied to an excessive risk of developing multiple myeloma.
  • MGUS: Approximately 19% of patients with MGUS develop multiple myeloma within 2-19 years.
  • Radiation
    • Radiation has been linked to the development of multiple myeloma.
    • In 109,000 survivors of the atomic bombing of Nagasaki during World War II, 29 died from multiple myeloma between 1950 and 1976; however, some more recent studies do not confirm that these survivors have an increased risk of developing multiple myeloma.
    • A recent study of workers at the Oak Ridge Diffusion Plant in eastern Tennessee showed only a weak correlation of risk of multiple myeloma to uranium exposure.7

More on Multiple Myeloma

Overview: Multiple Myeloma
Differential Diagnoses & Workup: Multiple Myeloma
Treatment & Medication: Multiple Myeloma
Follow-up: Multiple Myeloma
Multimedia: Multiple Myeloma
References
Further Reading

References

  1. Ludwig H, Drach J, Graf H, Lang A, Meran JG. Reversal of acute renal failure by bortezomib-based chemotherapy in patients with multiple myeloma. Haematologica. Oct 2007;92(10):1411-4. [Medline][Full Text].

  2. Zucchelli P, Pasquali S, Cagnoli L, Ferrari G. Controlled plasma exchange trial in acute renal failure due to multiple myeloma. Kidney Int. Jun 1988;33(6):1175-80. [Medline].

  3. Parikh GC, Amjad AI, Saliba RM, Kazmi SM, Khan ZU, Lahoti A, et al. Autologous hematopoietic stem cell transplantation may reverse renal failure in patients with multiple myeloma. Biol Blood Marrow Transplant. Jul 2009;15(7):812-6. [Medline].

  4. Kyle RA, Yee GC, Somerfield MR, et al. American Society of Clinical Oncology 2007 clinical practice guideline update on the role of bisphosphonates in multiple myeloma. J Clin Oncol. Jun 10 2007;25(17):2464-72. [Medline][Full Text].

  5. Djulbegovic B, Wheatley K, Ross J, et al. Bisphosphonates in multiple myeloma. Cochrane Database Syst Rev. 2001;CD003188. [Medline].

  6. Bloomfield DJ. Should bisphosphonates be part of the standard therapy of patients with multiple myeloma or bone metastases from other cancers? An evidence-based review. J Clin Oncol. Mar 1998;16(3):1218-25. [Medline].

  7. Yiin JH, Anderson JL, Daniels RD, Seel EA, Fleming DA, Waters KM, et al. A nested case-control study of multiple myeloma risk and uranium exposure among workers at the Oak Ridge Gaseous Diffusion Plant. Radiat Res. Jun 2009;171(6):637-45. [Medline].

  8. Bataille R, Boccadoro M, Klein B, Durie B, Pileri A. C-reactive protein and beta-2 microglobulin produce a simple and powerful myeloma staging system. Blood. Aug 1 1992;80(3):733-7. [Medline][Full Text].

  9. Dimopoulos M, Terpos E, Comenzo RL, et al, for the International Myeloma Working Group. International Myeloma Working Group consensus statement and guidelines regarding the current role of imaging techniques in the diagnosis and monitoring of multiple myeloma. Leukemia. May 7 2009;epub ahead of print. [Medline].

  10. Hung GU, Tsai CC, Tsai SC, Lin WY. Comparison of Tc-99m sestamibi and F-18 FDG-PET in the assessment of multiple myeloma. Anticancer Res. Nov-Dec 2005;25(6C):4737-41. [Medline].

  11. Shortt CP, Gleeson TG, Breen KA, McHugh J, O'Connell MJ, O'Gorman PJ, et al. Whole-Body MRI versus PET in assessment of multiple myeloma disease activity. AJR Am J Roentgenol. Apr 2009;192(4):980-6. [Medline].

  12. Durie BG, Salmon SE. A clinical staging system for multiple myeloma. Correlation of measured myeloma cell mass with presenting clinical features, response to treatment, and survival. Cancer. Sep 1975;36(3):842-54. [Medline].

  13. Greipp PR, San Miguel J, Durie BG, et al, for the International Myeloma Working Group. International staging system for multiple myeloma. J Clin Oncol. May 20 2005;23(15):3412-20. [Medline][Full Text].

  14. Dimopoulos MA, Moulopoulos A, Smith T, Delasalle KB, Alexanian R. Risk of disease progression in asymptomatic multiple myeloma. Am J Med. Jan 1993;94(1):57-61. [Medline].

  15. He Y, Wheatley K, Clark O, et al. Early versus deferred treatment for early stage multiple myeloma. Cochrane Database Syst Rev. 2003;CD004023. [Medline].

  16. Ludwig H, Fritz E, Kotzmann H, et al. Erythropoietin treatment of anemia associated with multiple myeloma. N Engl J Med. Jun 14 1990;322(24):1693-9. [Medline].

  17. Wilson J, Yao GL, Raftery J, Bohlius J, Brunskill S, Sandercock J, et al. A systematic review and economic evaluation of epoetin alpha, epoetin beta and darbepoetin alpha in anaemia associated with cancer, especially that attributable to cancer treatment. Health Technol Assess. Apr 2007;11(13):1-202, iii-iv. [Medline].

  18. Lokhorst HM, Sonneveld P, Cornelissen JJ, et al. Induction therapy with vincristine, adriamycin, dexamethasone (VAD) and intermediate-dose melphalan (IDM) followed by autologous or allogeneic stem cell transplantation in newly diagnosed multiple myeloma. Bone Marrow Transplant. Feb 1999;23(4):317-22. [Medline][Full Text].

  19. Moreau P, Hullin C, Garban F, et al. Tandem autologous stem cell transplantation in high-risk de novo multiple myeloma: final results of the prospective and randomized IFM 99-04 protocol. Blood. Jan 1 2006;107(1):397-403. [Medline][Full Text].

  20. Cavo M, Tosi P, Zamagni E, et al. Prospective, randomized study of single compared with double autologous stem-cell transplantation for multiple myeloma: Bologna 96 clinical study. J Clin Oncol. Jun 10 2007;25(17):2434-41. [Medline].

  21. Attal M, Harousseau JL, Stoppa AM, et al. A prospective, randomized trial of autologous bone marrow transplantation and chemotherapy in multiple myeloma. Intergroupe Français du Myélome. N Engl J Med. Jul 11 1996;335(2):91-7. [Medline][Full Text].

  22. Gerull S, Goerner M, Benner A, et al. Long-term outcome of nonmyeloablative allogeneic transplantation in patients with high-risk multiple myeloma. Bone Marrow Transplant. Dec 2005;36(11):963-9. [Medline].

  23. Vesole DH, Zhang L, Flomenberg N, Greipp PR, Lazarus HM. A Phase II trial of autologous stem cell transplantation followed by mini-allogeneic stem cell transplantation for the treatment of multiple myeloma: an analysis of Eastern Cooperative Oncology Group ECOG E4A98 and E1A97. Biol Blood Marrow Transplant. Jan 2009;15(1):83-91. [Medline].

  24. Zonder JA, Crowley J, Hussein MA, et al. Superiority of lenalidomide (Len) plus high-dose dexamethasone (HD) compared to HD alone as treatment of newly-diagnosed multiple myeloma (NDMM): results of the randomized, double-blinded, placebo-controlled SWOG trial S0232 [abstract 77]. Blood. 110;2007:32a. [Full Text].

  25. Zervas K, Mihou D, Katodritou E, et al. VAD-doxil versus VAD-doxil plus thalidomide as initial treatment for multiple myeloma: results of a multicenter randomized trial of the Greek Myeloma Study Group. Ann Oncol. Aug 2007;18(8):1369-75. [Medline][Full Text].

  26. Richardson PG, Barlogie B, Berenson J, et al. A phase 2 study of bortezomib in relapsed, refractory myeloma. N Engl J Med. Jun 26 2003;348(26):2609-17. [Medline][Full Text].

  27. Harousseau JL, Mathiot C, Attal M, et al. VELCADE/dexamethasone (Vel/D) versus VAD as induction treatment prior to autologous stem cell transplantation (ASCT) in newly diagnosed multiple myeloma (MM): updated results of the IFM 2005/01 trial [abstract 450]. Blood. 2007;110:139a. [Full Text].

  28. Cavo M, Patriarca F, Tacchetti P, et al. Bortezomib (Velcade[R])-thalidomide-dexamethasone (VTD) vs thalidomide-dexamethasone (TD) in preparation for autologous stem-cell (SC) transplantation (ASCT) in newly diagnosed multiple myeloma (MM) [abstract 73]. Blood. 2007;110:30a. [Full Text].

  29. Vickrey E, Allen S, Mehta J, Singhal S. Acyclovir to prevent reactivation of varicella zoster virus (herpes zoster) in multiple myeloma patients receiving bortezomib therapy. Cancer. Jan 1 2009;115(1):229-32. [Medline].

  30. Rajkumar SV, Jacobus S, Callander N, et al. A randomized trial of lenalidomide plus high-dose dexamethasone (RD) versus lenalidomide plus low-dose dexamethasone (Rd) in newly diagnosed multiple myeloma (E4A03): a trial coordinated by the Eastern Cooperative Oncology Group [abstract 74]. Blood. 2007;110:31a. [Full Text].

  31. Jagannath S, Richardson PG, Sonneveld P, et al. Bortezomib appears to overcome the poor prognosis conferred by chromosome 13 deletion in phase 2 and 3 trials. Leukemia. Jan 2007;21(1):151-7. [Medline].

  32. Sagaster V, Ludwig H, Kaufmann H, et al. Bortezomib in relapsed multiple myeloma: response rates and duration of response are independent of a chromosome 13q-deletion. Leukemia. Jan 2007;21(1):164-8. [Medline].

  33. Myeloma Trialists' Collaborative Group. Combination chemotherapy versus melphalan plus prednisone as treatment for multiple myeloma: an overview of 6,633 patients from 27 randomized trials. J Clin Oncol. Dec 1998;16(12):3832-42. [Medline].

  34. [Best Evidence] Facon T, Mary JY, Hulin C, et al. Melphalan and prednisone plus thalidomide versus melphalan and prednisone alone or reduced-intensity autologous stem cell transplantation in elderly patients with multiple myeloma (IFM 99-06): a randomised trial. Lancet. Oct 6 2007;370(9594):1209-18. [Medline].

  35. Palumbo A, Falco P, Falcone A, Benevolo G, Canepa L, Gay F, et al. Melphalan, Prednisone, and Lenalidomide for Newly Diagnosed Myeloma: Kinetics of Neutropenia and Thrombocytopenia and Time-to-Event Results. Clin Lymphoma Myeloma. Apr 2009;9(2):145-50. [Medline].

  36. Cooper MR, Dear K, McIntyre OR, et al. A randomized clinical trial comparing melphalan/prednisone with or without interferon alfa-2b in newly diagnosed patients with multiple myeloma: a Cancer and Leukemia Group B study. J Clin Oncol. Jan 1993;11(1):155-60. [Medline].

  37. Berenson JR, Lichtenstein A, Porter L, et al. Efficacy of pamidronate in reducing skeletal events in patients with advanced multiple myeloma. Myeloma Aredia Study Group. N Engl J Med. Feb 22 1996;334(8):488-93. [Medline][Full Text].

  38. Wang EP, Kaban LB, Strewler GJ, Raje N, Troulis MJ. Incidence of osteonecrosis of the jaw in patients with multiple myeloma and breast or prostate cancer on intravenous bisphosphonate therapy. J Oral Maxillofac Surg. Jul 2007;65(7):1328-31. [Medline].

  39. American Society of Clinical Oncology 2007 clinical practice guideline update on the role of bisphosphonates in multiple myeloma. National Guideline Clearinghouse. Available at http://www.guideline.gov/summary/summary.aspx?doc_id=10857&nbr=005670. Accessed May 1, 2009.

  40. Niesvizky R, Jayabalan DS, Christos PJ, et al. BiRD (Biaxin [clarithromycin]/Revlimid [lenalidomide]/dexamethasone) combination therapy results in high complete- and overall-response rates in treatment-naive symptomatic multiple myeloma. Blood. Feb 1 2008;111(3):1101-9. [Medline][Full Text].

  41. Alexanian R, Dimopoulos MA, Delasalle K, Barlogie B. Primary dexamethasone treatment of multiple myeloma. Blood. Aug 15 1992;80(4):887-90. [Medline][Full Text].

  42. Alyea EP, Anderson KC. Allogeneic bone marrow transplantation in the treatment of multiple myeloma. PPO Updates. 2000;14:1-10.

  43. Barlogie B, Smith L, Alexanian R. Effective treatment of advanced multiple myeloma refractory to alkylating agents. N Engl J Med. May 24 1984;310(21):1353-6. [Medline].

  44. Barosi G, Boccadoro M, Cavo M, et al. Management of multiple myeloma and related-disorders: guidelines from the Italian Society of Hematology (SIE), Italian Society of Experimental Hematology (SIES) and Italian Group for Bone Marrow Transplantation (GITMO). Haematologica. Jun 2004;89(6):717-41. [Medline][Full Text].

  45. Boccadoro M, Marmont F, Tribalto M, et al. Multiple myeloma: VMCP/VBAP alternating combination chemotherapy is not superior to melphalan and prednisone even in high-risk patients. J Clin Oncol. Mar 1991;9(3):444-8. [Medline].

  46. Evans AJ, Jensen ME, Kip KE, et al. Vertebral compression fractures: pain reduction and improvement in functional mobility after percutaneous polymethylmethacrylate vertebroplasty retrospective report of 245 cases. Radiology. Feb 2003;226(2):366-72. [Medline][Full Text].

  47. Gahrton G, Svensson H, Björkstrand B, et al. Syngeneic transplantation in multiple myeloma - a case-matched comparison with autologous and allogeneic transplantation. European Group for Blood and Marrow Transplantation. Bone Marrow Transplant. Oct 1999;24(7):741-5. [Medline][Full Text].

  48. Hjorth M, Westin J, Dahl IMS, et al, for the The Nordic Myeloma Study Group. Interferon-alpha 2b added to melphalan-prednisone for initial and maintenance therapy in multiple myeloma. A randomized, controlled trial. Ann Intern Med. Jan 15 1996;124(2):212-22. [Medline][Full Text].

  49. Kumar A, Loughran T, Alsina M, Durie BG, Djulbegovic B. Management of multiple myeloma: a systematic review and critical appraisal of published studies. Lancet Oncol. May 2003;4(5):293-304. [Medline].

  50. Kyle RA, Greipp PA. Plasma cell dyscrasias: current status. Crit Rev Oncol Hematol. 1988;8(2):93-152. [Medline].

  51. Samson D, Gaminara E, Newland A, et al. Infusion of vincristine and doxorubicin with oral dexamethasone as first-line therapy for multiple myeloma. Lancet. Oct 14 1989;2(8668):882-5. [Medline].

  52. Singhal S, Mehta J, Desikan R, et al. Antitumor activity of thalidomide in refractory multiple myeloma. N Engl J Med. Nov 18 1999;341(21):1565-71. [Medline][Full Text].

  53. Varterasian ML. Biologic and clinical advances in multiple myeloma. Oncology (Williston Park). May 1995;9(5):417-24; discussion 429-30. [Medline].

  54. Weber DM, Chen C, Niesvizky R, et al. Lenalidomide plus dexamethasone for relapsed multiple myeloma in North America. N Engl J Med. Nov 22 2007;357(21):2133-42. [Medline][Full Text].

Further Reading

Additional resources on asthma are available at Medscape’s Multiple Myelome Resource Center and Medscape’s Multiple Myeloma Resource Center CME.

Keywords

multiple myeloma, myeloma, bone marrow malignancy, bone marrow cancer, myeloma multiple, plasma cell myeloma, Kahler's disease, Kahler disease, plasma cell dyscrasia, plasma cell leukemia, leukopenia, anemia, thrombocytopenia, bone pain, hypercalcemia, spinal cord compression, hyperviscosity, amyloidosis, renal failure, monoclonal gammopathy of unknown significance, MGUS,

M and P chemotherapy, leukemia, plasma cell leukemia, VAD chemotherapy, plasmacytoma, renal impairment, compression fracture of vertebral body, shingles, herpes zoster, Haemophilus infections, epistaxis, stroke, myocardial ischemia, myocardial infarction, carpal tunnel syndrome, meningitis, peripheral neuropathies, ecchymoses, purpura, macroglossia

Contributor Information and Disclosures

Author

Sara J Grethlein, MD, Associate Dean for Graduate Medical Education, Associate Professor, Department of Internal Medicine, Division of Hematology and Oncology, State University of New York Upstate Medical University
Sara J Grethlein, MD is a member of the following medical societies: American Society of Hematology
Disclosure: Nothing to disclose.

Coauthor(s)

Lilian M Thomas, MD, Fellow, Department of Hematology/Oncology, State University of New York Upstate Medical University
Lilian M Thomas, MD is a member of the following medical societies: American College of Physicians and American Society of Clinical Oncology
Disclosure: Nothing to disclose.

Medical Editor

Koyamangalath Krishnan, MD, FRCP, FACP, Paul Dishner Endowed Chair of Excellence in Medicine, Professor of Medicine and Chief of Hematology-Oncology, Program Director, Hematology-Oncology Fellowship, James H Quillen College of Medicine at East Tennessee State University
Koyamangalath Krishnan, MD, FRCP, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, American Society of Hematology, and Royal College of Physicians
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Troy H Guthrie, Jr, MD, Director of Cancer Institute, Baptist Medical Center
Troy H Guthrie, Jr, MD is a member of the following medical societies: American Federation for Medical Research, American Medical Association, American Society of Hematology, Florida Medical Association, Medical Association of Georgia, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

Rajalaxmi McKenna, MD, FACP, Southwest Medical Consultants, SC, Department of Medicine, Good Samaritan Hospital, Advocate Health Systems
Rajalaxmi McKenna, MD, FACP is a member of the following medical societies: American Society of Clinical Oncology, American Society of Hematology, and International Society on Thrombosis and Haemostasis
Disclosure: Nothing to disclose.

Chief Editor

Emmanuel C Besa, MD, Professor, Department of Medicine, Division of Hematologic Malignancies, Kimmel Cancer Center, Thomas Jefferson University
Emmanuel C Besa, MD is a member of the following medical societies: American Association for Cancer Education, American College of Clinical Pharmacology, American Federation for Medical Research, American Society of Hematology, and New York Academy of Sciences
Disclosure: Nothing to disclose.

 
 
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