Multiple Myeloma Medication

  • Author: Karen Seiter, MD; Chief Editor: Emmanuel C Besa, MD   more...
 
Updated: May 8, 2012
 

Medication Summary

Multiple myeloma (MM) is treated with several categories of medications. Chemotherapeutic agents are used to reduce the disease burden, and bisphosphonates are used to promote bone healing and to provide secondary prophylaxis against skeletal-related events (eg, hypercalcemia, bone fracture, spinal cord compression, need for radiation, and need for surgery). In addition, erythropoietin is used to treat anemia, either alone or in conjunction with chemotherapy.

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Chemotherapeutic Agents

Class Summary

The choice of chemotherapy depends on several factors, including the patient’s performance status, age, renal function, desire for inpatient or outpatient therapy, and likelihood of receiving future autologous stem cell transplantation.

In patients with renal failure or highly aggressive disease, therapy with vincristine, Adriamycin (doxorubicin), and dexamethasone (VAD) may be preferred. In elderly patients or patients in whom autologous transplantation is not possible in the future, melphalan and prednisone (MP) therapy is preferred because of its ease of administration and low toxicity.

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Melphalan (Alkeran)

 

The most widely used regimen is MP. Melphalan is an alkylating agent and a derivative of mechlorethamine that inhibits mitosis by cross-linking DNA strands. It is indicated for the palliative treatment of multiple myeloma.

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Doxorubicin (Adriamycin, Rubex)

 

Doxorubicin is part of VAD therapy. It inhibits topoisomerase II and produces free radicals, which may cause destruction of DNA; these 2 events, in turn, can inhibit growth of neoplastic cells.

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Vincristine (Oncovin)

 

Vincristine inhibits cellular mitosis by inhibition of intracellular tubulin function, binding to microtubules, and synthesis of spindle proteins in the S phase. Vincristine is part of VAD therapy. Its mechanism of action is complex and includes depolymerization of microtubules.

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Bortezomib (Velcade)

 

Bortezomib is the first drug approved in the group of anticancer agents known as proteasome inhibitors. The proteasome pathway is an enzyme complex existing in all cells, which degrades ubiquitinated proteins that control the cell cycle and cellular processes and maintains cellular homeostasis. Reversible proteasome inhibition disrupts pathways supporting cell growth, thus decreasing cancer cell survival. Bortezomib is indicated for patients with multiple myeloma. Development of peripheral neuropathy is a limiting factor. A decreased incidence of peripheral neuropathy has been observed with SC administration compared with the IV route.

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Doxorubicin liposomal (Doxil)

 

Doxorubicin liposomal is a pegylated formulation that protects the liposomes and, thereby, increases blood circulation time. The drug inhibits topoisomerase II and produces free radicals, which may cause destruction of DNA; these 2 events can, in turn, inhibit growth of neoplastic cells.

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Corticosteroids

Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body’s immune response to diverse stimuli.

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Prednisone (Deltasone, Orasone, Meticorten)

 

The most widely used regimen is MP. Prednisone stabilizes lysosomal membranes and suppresses lymphocyte and antibody production.

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Dexamethasone (Decadron)

 

Dexamethasone is part of VAD therapy. Many believe that the high-dose steroid component of VAD accounts for much of its efficacy. In some patients, high-dose dexamethasone alone may produce significant clinical responses. Dexamethasone stabilizes lysosomal membranes and suppresses lymphocyte and antibody production.

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Interferons

Class Summary

Interferons are naturally produced proteins with antiviral, antitumor, and immunomodulatory actions. Alfa-, beta-, and gamma-interferons may be administered topically, systemically, and intralesionally.

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Interferon alfa-2A (Roferon A)

 

Interferon alfa-2A is a protein product manufactured by recombinant DNA technology. The mechanism of the antitumor activity is not clearly understood; however, direct antiproliferative effects against malignant cells and modulation of the host immune response may play important roles.

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Interferon alfa-2B (Intron A)

 

Interferon alfa-2B is a protein product manufactured by recombinant DNA technology. The mechanism of antitumor activity is not clearly understood; however, direct antiproliferative effects against malignant cells and modulation of host immune response may play important roles.

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Bisphosphonates

Class Summary

Bisphosphonates inhibit bone resorption via action on osteoclasts or osteoclast precursors.

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Pamidronate (Aredia)

 

Pamidronate inhibits normal and abnormal bone resorption. It appears to inhibit bone resorption without inhibiting bone formation and mineralization. The optimal timing and duration of therapy are being studied. Pamidronate is administered intravenously (IV) over 2 hours. Newer drugs similar in structure and function are being studied and may have improved efficacy and greater convenience.

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Zoledronic acid (Zometa)

 

Zoledronic acid inhibits bone resorption, possibly by acting on osteoclasts or osteoclast precursors. It is effective in treating the hypercalcemia of malignancy.

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Colony-stimulating Factors

Class Summary

Colony-stimulating factors induce erythropoiesis.

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Epoetin alfa, erythropoietin (Epogen, Procrit)

 

Erythropoietin stimulates the division and differentiation of committed erythroid progenitor cells and induces the release of reticulocytes from bone marrow into the blood stream.

Erythropoietin is a naturally occurring hormone produced by the kidneys to stimulate bone marrow production of red blood cells. In patients with MM, administration of exogenous erythropoietin may correct anemia, leading to a significant improvement in performance status and quality of life.

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Immunosuppressant Agents

Class Summary

Immunosuppressant agents inhibit key factors in the immune system that are responsible for immune reactions.

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Thalidomide (Thalomid)

 

Thalidomide, when used in combination with dexamethasone, is indicated for the treatment of patients with newly diagnosed multiple myeloma. Thalidomide is an immunomodulatory agent that may suppress excessive production of tumor necrosis factor (TNF)-alpha and may down-regulate selected cell-surface adhesion molecules involved in leukocyte migration. Because of concerns regarding teratogenicity, thalidomide can only be prescribed by registered physicians and is dispensed by registered pharmacists. Patients must participate in ongoing surveys to receive therapy, and only a 28-d supply can be prescribed at a time.

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Lenalidomide (Revlimid)

 

Lenalidomide in combination with dexamethasone is indicated for multiple myeloma in patients treated with at least 1 year of prior therapy. It is structurally similar to thalidomide. Lenalidomide elicits immunomodulatory and antiangiogenic properties. It inhibits proinflammatory cytokine secretion and increases anti-inflammatory cytokines from peripheral blood mononuclear cells.

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Antineoplastic Agents

Class Summary

Antineoplastic agents inhibit cell growth and proliferation.

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Cyclophosphamide (Cytoxan, Neosar)

 

Cyclophosphamide is chemically related to nitrogen mustards. It is an alkylating agent, and its mechanism of action of active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells.

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Contributor Information and Disclosures
Author

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, and American Society of Hematology

Disclosure: Novartis Honoraria Speaking and teaching; Novartis Consulting fee Speaking and teaching; Eisai Honoraria Speaking and teaching; Celgene Honoraria Speaking and teaching

Coauthor(s)

Dhaval Shah, MD  Fellow, Department of Hematology/Oncology, Baylor College of Medicine

Disclosure: Nothing to disclose.

Sara J Grethlein, MD  Senior Attending Physician, Cancer Treatment Center, Bassett Healthcare Network

Sara J Grethlein, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Society of Clinical Oncology, and American Society of Hematology

Disclosure: Nothing to disclose.

Seema S Rizvi, MD  Associate Medical Director, Lutheran Care Center

Seema S Rizvi, MD is a member of the following medical societies: American Academy of Family Physicians and American Medical Association

Disclosure: Nothing to disclose.

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, American Society of Clinical Oncology, and American Society of Hematology

Disclosure: Nothing to disclose.

Specialty Editor Board

Koyamangalath Krishnan, MD, FRCP, FACP  Paul Dishner Endowed Chair of Excellence in Medicine, Professor of Medicine and Chief of Hematology-Oncology, 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.

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

Disclosure: Medscape Salary Employment

Harris Gellman, MD  Consulting Surgeon, Broward Hand Center; Voluntary Clinical Professor of Orthopedic Surgery and Plastic Surgery, Departments of Orthopedic Surgery and Surgery, University of Miami, Leonard M Miller School of Medicine

Harris Gellman, MD is a member of the following medical societies: American Academy of Medical Acupuncture, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Society for Surgery of the Hand, and Arkansas Medical Society

Disclosure: Nothing to disclose.

Chief Editor

Emmanuel C Besa, MD  Professor, Department of Medicine, Division of Hematologic Malignancies, 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 College of Clinical Pharmacology, American Federation for Medical Research, American Society of Clinical Oncology, American Society of Hematology, and New York Academy of Sciences

Disclosure: Nothing to disclose.

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Amyloidosis infiltrating the tongue in multiple myeloma. All images and text are (c) 2002 by the American Society of Hematology. All rights reserved.
Radiograph of the skull demonstrating a typical lytic lesion in multiple myeloma. All images and text are (c) 2002 by the American Society of Hematology. All rights reserved.
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 malignant plasma cells in multiple myeloma. All images and text are (c) 2002 by the American Society of Hematology. All rights reserved.
 
 
 
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