Mucosa-Associated Lymphoid Tissue Medication

  • Author: Sara J Grethlein, MD; Chief Editor: Emmanuel C Besa, MD   more...
 
Updated: Dec 6, 2011
 

Medication Summary

In patients with H. pylori infection in association with a MALToma, especially gastric MALToma, the first line of therapy is treatment for the H. pylori infection. In patients with low-grade MALTomas who are not infected with H. pylori or whose MALToma does not respond to H. pylori treatment, options in asymptomatic patients include observation versus active intervention.

If treatment is required, treatments similar to those used for other low-grade NHLs are used. Examples are single-agent therapy such as chlorambucil, cyclophosphamide, fludarabine, or rituximab. Combinations of chemotherapy agents with or without rituximab may also be used. Patients with large-cell MALTomas are treated with combination chemotherapy (usually the CHOP regimen), with or without rituximab.

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Antineoplastics

Class Summary

Antineoplastics interrupt proliferative activity and induce programmed cell death in proliferating B lymphocytes of MALTomas.

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Cyclophosphamide (Cytoxan)

 

Transformed primarily in the liver to active alkylating metabolites. Metabolites interfere with the growth of susceptible rapidly proliferating malignant cells. The mechanism of action is thought to involve cross-linking of tumor cell DNA.

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Doxorubicin (Adriamycin, Adriamycin PF)

 

Results in a conformational change of DNA and interferes with RNA polymerase, causing inhibition of protein synthesis.

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Vincristine (Oncovin)

 

Vinca alkaloid extracted from the plant Catharanthus rosea. Exerts therapeutic effects on cells by interfering with microtubules of mitotic spindle fibers, causing metaphasic cell cycle arrest.

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Biologic Response Modifiers

Class Summary

Biologic response modifiers suppress immune cells involved in MALTomas.

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Prednisone (Deltasone, Orasone, Meticorten)

 

Metabolized by liver to active metabolite prednisolone. Binds extensively to albumin and transcortin. Unbound portion crosses cell membranes and binds to specific cytoplasmic receptors, inducing a response by modifying transcription and, ultimately, protein synthesis.

Prednisolone is further metabolized to inactive compounds. Used as a component of the CHOP combination chemotherapy regimen.

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Fludarabine (Fludara)

 

Nucleotide analogue of vidarabine converted to 2-fluoro-ara-A that enters the cell and is phosphorylated to form the active metabolite 2-fluoro-ara-ATP, which inhibits DNA synthesis.

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Etoposide (Toposar, VePesid)

 

Inhibits topoisomerase II and causes DNA strand breakage, causing cell proliferation to arrest in the late S or early G2 portion of the cell cycle.

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Mitoxantrone (Novantrone)

 

Inhibits cell proliferation by intercalating DNA and inhibiting topoisomerase II.

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Bleomycin (Blenoxane)

 

Glycopeptide antibiotic that inhibits DNA synthesis. For palliative measure in the management of several neoplasms.

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Chlorambucil (Leukeran)

 

Alkylates and cross-links strands of DNA, inhibiting DNA replication and RNA transcription

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Monoclonal Antibodies

Class Summary

Monoclonal antibodies are genetically engineered chimeric murine/human monoclonal antibodies directed against proteins involved in cell cycle initiation.

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Rituximab (Rituxan)

 

Genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen that is found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1-kappa immunoglobulin containing murine light- and heavy-chain variable region sequences and human constant region sequences.

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Antibiotics

Class Summary

Antibiotics are the mainstay in the eradication of H. pylori, the major etiologic agent in gastric MALToma.

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Clarithromycin (Biaxin, Biaxin XL)

 

Inhibits bacterial growth, possibly by blocking the dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

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Metronidazole (Flagyl)

 

Imidazole ring-based antibiotic that is active against various anaerobic bacteria and protozoa. Used in combination with other antimicrobial agents (except for Clostridium difficile enterocolitis).

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Proton Pump Inhibitors

Class Summary

Proton pump inhibitors are used in combination with antibiotics for H. pylori eradication.

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Omeprazole (Prilosec)

 

Decreases gastric acid secretion by inhibiting parietal cell H+/K+ -ATP pump.

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Contributor Information and Disclosures
Author

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.

Coauthor(s)

Jose A Perez Jr, MD, MBA, MSEd  Consulting Staff, Department of Medicine, Methodist Hospital; Associate Professor of Clinical Medicine, Weill Cornell Medical College

Jose A Perez Jr, MD, MBA, MSEd is a member of the following medical societies: American College of Physician Executives, American College of Physicians, Society of General Internal Medicine, and Society of Hospital Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

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

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

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.

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, 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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