Posttransplant Lymphoproliferative Disease Medication

  • Author: Sandeep Mukherjee, MB, BCh, MPH, FRCPC; Chief Editor: Ron Shapiro, MD   more...
 
Updated: Aug 6, 2010
 

Medication Summary

Numerous treatment options for PTLD exist. The general consensus is that immunosuppression should be reduced, or withdrawn, in the first instance; however, no strict guidelines exist for this process. The issue of which drug to withdraw or which drug to dose reduce is still an individual decision for the clinician. The aim is to achieve balance—to improve immune function to gain remission from lymphoproliferation while at the same time preserving the allograft. Effective therapy should be instituted before advanced disease leads to multisystemic disease and reduced performance status.[29]

Many immunosuppressive drug combinations and permutations are used in practice, adding to the complexity. Reducing immunosuppression depends to a large degree on the allograft in question. In the case of renal transplantation, an option to cut the immunosuppression significantly or withdraw it altogether is available. If allograft rejection or failure ensues, an adequate form of replacement therapy is available. In the case of heart transplantation, serious allograft rejection and/or failure likely heralds patient demise.

Other treatment options already have been discussed (see Treatment section). The second line of treatment varies, and the dose/duration of treatment depends on patient weight, response, complications, tolerance of treatment, and so forth. Bearing in mind that PTLD is an umbrella term that encompasses a wide spectrum of lymphoproliferative diseases, management of PTLD has to be tailored to the needs of the individual patient. Details provided regarding the medications below are to be regarded as general information. Doses or treatment durations provided here are not necessarily those utilized in the management of PTLD. Much of the information provided pertains to treatment of disease entities remote from PTLD. Many of these drugs have been used experimentally for the purpose of treating lymphoproliferative disease, and reports of their efficacy largely are anecdotal.

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Immunosuppressive Agents

Class Summary

Inhibit key factors that mediate immune reactions, which in turn decrease inflammatory responses.

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Cyclosporine (Sandimmune, Neoral)

 

Cyclic polypeptide that suppresses some humoral immunity and, to a greater extent, cell-mediated immune reactions, such as delayed hypersensitivity, allograft rejection, experimental allergic encephalomyelitis, and graft versus host disease for a variety of organs.

For children and adults, base dosing on ideal body weight.

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Tacrolimus (Prograf)

 

Suppresses humoral immunity (T-lymphocyte) activity.

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Mycophenolate (CellCept)

 

Inhibits inosine monophosphate dehydrogenase (IMPDH) and suppresses de novo purine synthesis by lymphocytes, thereby inhibiting their proliferation. Inhibits antibody production.

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Prednisone (Deltasone, Orasone, Meticorten, Sterapred)

 

Used as an immunosuppressive, anti-inflammatory agent and also as a component of both CHOP and ProMACE-CytaBOM chemotherapeutic regimens, which have been used to treat PTLD.

May decrease inflammation by reversing increased capillary permeability and suppressing PMN activity. Stabilizes lysosomal membranes and also suppresses lymphocytes and antibody production.

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Antiviral Agents

Class Summary

Nucleoside analogs initially are phosphorylated by viral thymidine kinase to eventually form a nucleoside triphosphate. These molecules inhibit herpes simplex virus (HSV) polymerase with 30-50 times the potency of human alpha-DNA polymerase.

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Acyclovir (Zovirax)

 

Inhibits activity of both HSV-1 and HSV-2. Has affinity for viral thymidine kinase and, once phosphorylated, causes DNA chain termination when acted on by DNA polymerase.

Routinely used to treat infections with HSV, mainly HSV-1 and HSV-2. EBV also is a herpes virus, but its use as prophylaxis against and treatment for EBV-related illness posttransplantation is controversial. If used for these purposes, doses and duration of treatment are variable and are determined by the clinician.

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Ganciclovir (Cytovene)

 

Synthetic guanine derivative active against CMV. An acyclic nucleoside analog of 2'-deoxyguanosine that inhibits replication of herpes viruses both in vitro and in vivo.

Levels of ganciclovir-triphosphate are as much as 100-fold greater in CMV-infected cells than in uninfected cells, possibly due to preferential phosphorylation of ganciclovir in virus-infected cells.

For patients who experience progression of CMV retinitis while receiving a maintenance treatment with either dosage form of ganciclovir, the re-induction regimen should be administered.

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Immunomodulator Agents

Class Summary

Rituximab (anti-CD20 monoclonal antibody) has been used primarily in the treatment of lymphoma; however, it has been reported to have successfully treated PTLD in some patients. Other monoclonal antibodies, such as anti-CD21, CD24, and anti-CD3 (OKT3), also have been used successfully for treatment of PTLD. Interferon alfa also has been used in the treatment of PTLD.

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Rituximab (Rituxan)

 

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

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Immune globulin intravenous (Gamimune, Gammagard S/D, Sandoglobulin)

 

Neutralizes circulating myelin antibodies through anti-idiotypic antibodies. Down-regulates proinflammatory cytokines, including INF-gamma. Blocks Fc receptors on macrophages. Suppresses inducer T and B cells and augments suppressor T cells. Blocks complement cascade. Promotes remyelination. May increase CSF IgG (10%).

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Interferon alfa-2b (Intron A)

 

Protein product manufactured by recombinant DNA technology. Mechanism of antitumor activity is not understood clearly; however, direct antiproliferative effects against malignant cells and modulation of host immune response may play important roles.

Doses and duration of treatment are as determined by the involved clinicians.

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Antineoplastic Agents

Class Summary

Disrupt DNA replication or cell division, thereby inhibiting cell growth and proliferation.

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Cyclophosphamide (Cytoxan, Neosar)

 

Chemically related to nitrogen mustards. As an alkylating agent, the mechanism of action of the active metabolites may involve cross-linking of DNA, which may interfere with growth of normal and neoplastic cells.

Component of CHOP and ProMACE-CytaBOM chemotherapeutic regimens.

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Doxorubicin (Adriamycin, Rubex)

 

Inhibits topoisomerase II and produces free radicals, which may cause the destruction of DNA. The combination of these 2 events can, in turn, inhibit the growth of neoplastic cells.

Component of CHOP and ProMACE-CytaBOM chemotherapeutic regimens.

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Vincristine (Oncovin, Vincasar PFS)

 

Mechanism of action is uncertain. May involve a decrease in reticuloendothelial cell function or an increase in platelet production. However, neither of these mechanisms would fully explain the effect in TTP and HUS.

Component of CHOP and ProMACE-CytaBOM chemotherapeutic regimens.

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Etoposide (Toposar, VePesid)

 

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

Component of ProMACE-CytaBOM regimen.

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Bleomycin (Blenoxane)

 

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

Component of ProMACE-CytaBOM regimen.

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Methotrexate (Folex PFS, Rheumatrex)

 

Antimetabolite that inhibits dihydrofolate reductase, thereby hindering DNA synthesis and cell reproduction in malignant cells. Satisfactory response observed 3-6 wk following administration. Adjust dose gradually to attain satisfactory response.

Component of ProMACE-CytaBOM regimen.

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Contributor Information and Disclosures
Author

Sandeep Mukherjee, MB, BCh, MPH, FRCPC  Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Sandeep Mukherjee, MB, BCh, MPH, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Merck Honoraria Speaking and teaching; Ikaria Pharmaceuticals Honoraria Board membership

Coauthor(s)

Mary Prendergast, MD  Internal Medicine, University of Nebraska Medical Center

Mary Prendergast, MD is a member of the following medical societies: Royal College of Physicians

Disclosure: Nothing to disclose.

Vinay Ranga, MD  Assistant Professor, Department of Internal Medicine, Division of Nephrology, Hartford Hospital

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Marcel E Conrad, MD  Distinguished Professor of Medicine (Retired), University of South Alabama College of Medicine

Marcel E Conrad, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American Association of Blood Banks, American Chemical Society, American College of Physicians, American Physiological Society, American Society for Clinical Investigation, American Society of Hematology, Association of American Physicians, Association of Military Surgeons of the US, International Society of Hematology, Society for Experimental Biology and Medicine, and Southwest Oncology Group

Disclosure: No financial interests None None

Chief Editor

Ron Shapiro, MD  Professor of Surgery, Robert J Corry Chair in Transplantation Surgery, Director, Kidney, Pancreas, and Islet Transplantation, Thomas E Starzl Transplantation Institute, University of Pittsburgh Medical Center

Ron Shapiro, MD is a member of the following medical societies: American College of Surgeons, American Society of Transplant Surgeons, Association for Academic Surgery, Central Surgical Association, and Society of University Surgeons

Disclosure: Astellas Honoraria Speaking and teaching; Brystol Meyer Squibb StemCell Data Monitoring Committee Consulting fee Review panel membership; Wyeth Honoraria Speaking and teaching; Stem Cells, Inc Consulting fee Review panel membership; Up To Date contracted Author

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Biopsy of gingival tissue (400 X) with hematoxylin and eosin stain demonstrates polymorphous infiltrate of atypical lymphoid cells, which is consistent with posttransplant lymphoproliferative disease (PTLD).
Biopsy of gingival tissue (400 X). Epstein-Barr virus encoded RNA (EBER) study shows numerous positive cells, which is consistent with posttransplant lymphoproliferative disease (PTLD).
 
 
 
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