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Posttransplant Lymphoproliferative Disease

  • Author: Phillip M Garfin, MD, PhD; Chief Editor: Ron Shapiro, MD  more...
Updated: Apr 09, 2015


Posttransplant lymphoproliferative disease (PTLD) is a well-recognized complication of both solid organ transplantation (SOT) and allogeneic hematopoietic stem cell transplantation (HSCT). It is one of the most common posttransplant malignancies. In most cases, PTLD is associated with Epstein-Barr virus (EBV) infection of B cells, either as a consequence of reactivation of the virus posttransplantation or from primary EBV infection. In cases of primary infection, EBV may be acquired from the donor graft or, less commonly, from environmental exposure. While T-cell lymphoproliferative disorders that are not typically associated with EBV infection also occur after SOT and HSCT, the vast majority are B-cell proliferations.

PTLD is identified by having a high index of suspicion in the appropriate clinical setting. The diagnosis is made by histopathological evidence of lymphoproliferation, commonly with the presence of EBV DNA, RNA, or protein detected in tissue. Most cases of PTLD occur within the first posttransplant year. The more intense the immunosuppression used, the greater the risk of PTLD and the earlier it tends to occur.

The cornerstone of initial management of PTLD is reduction or withdrawal of immunosuppression, which in some situations may reverse the lymphoproliferative process. This potential for reversibility with reduction of immunosuppression distinguishes PTLD from neoplastic lymphoproliferative disorders that occur in immunocompetent patients. Reduction of immunosuppression also carries the risk of inducing allograft dysfunction or loss and is not always feasible depending on the grafted organ or clinical situation. Other potential treatments include surgical excision of the lesion, localized radiation therapy, antiviral therapy, immunoglobulin therapy, combination chemotherapy, monoclonal antibodies, and the use of cytotoxic T lymphocytes.

The American Society for Transplantation has recommended that the term PTLD also be applied to posttransplantation infectious mononucleosis and plasma cell hyperplasia (reactive hyperplasias) in addition to neoplastic disease.[1] When the term PTLD is not qualified, it refers to neoplastic disease. The 2008 World Health Organization (WHO) classification system recognizes 4 major histopathologic subtypes of PTLD: (1) early hyperplastic lesions, (2) polymorphic lesions (which may be polyclonal or monoclonal), (3) monomorphic lesions, and (4) classic Hodgkin-type lymphomas.[2]

In recognition of the growing prevalence of PTLD and the challenges in diagnosing and classifying this disease, a multidisciplinary panel met in Seville, Spain in 2009 to review the current understanding of risk factors, disease classification, and strategies to reduce the risk of PTLD. This panel of experts developed a new classification scheme that incorporates the 2008 WHO histologic classification system as well as other important clinical and virologic features of PTLD.[3] The use of a more consistent and comprehensive system to classify the clinical and pathologic features of PTLD would facilitate better understanding of the diversity of this spectrum of disease and allow for clearer assessment of therapeutic options.

Medicolegal issues

Transplantation and the accompanying immunosuppression put patients at risk for potentially fatal infection and malignancy. Transplant candidates must be fully informed of these risks as part of the consent process pretransplantation.

PTLD can assume an astonishing number of guises. It can mimic relatively benign conditions in its presentation, so a high degree of clinical vigilance and an awareness of its highly variable presentation are required if the diagnosis is not to be missed.

Treatment of PTLD risks allograft dysfunction. Patients need to be made aware that PTLD is a serious consequence of transplantation and immunosuppression, that it requires treatment, and that this treatment may result in the loss of the allograft.

Failure to inform the patient of relevant risks and possible outcomes at every stage puts the physician at risk for medical litigation.

Treating physicians must consider the diagnosis of PTLD in immunosuppressed patients, even when clinical symptoms or signs are atypical, and should perform the appropriate diagnostic tests to exclude the diagnosis of PTLD.



The vast majority of cases of posttransplant lymphoproliferative disease (PTLD) are caused by EBV infection.[4, 5] EBV is a herpes virus that is thought to infect up to 95% of the adult population.[6] Primary infection with EBV in childhood usually results in mild, self-limiting illness.[6] In immunocompetent older children and adults, EBV infection causes infectious mononucleosis.[7] EBV was discovered in the 1960s by electron microscopy of cells cultured from a Burkitt lymphoma.[8] Since 1968, it has been known to cause infectious mononucleosis and has been associated with non-Hodgkin lymphoma and oral hairy leukoplakia in patients with HIV infection and with nasopharyngeal carcinoma, particularly in patients from Southeast Asia.[7, 9, 10]

Structurally, the EBV genome is enclosed in a nuclear capsid surrounded by a glycoprotein envelope. Once infected with EBV, the virus persists in a person for life, latently in B-cell lymphocytes and chronically replicating in the cells of the oropharynx.[11]

The EBV genome is a linear DNA molecule that encodes for approximately 100 viral proteins that are expressed during replication. The CD21 molecule on the surface of the B cell is the target receptor of the EBV glycoprotein envelope. Infection of B-cell lymphocytes with EBV results in either viral replication and B-cell lysis (ie, lytic replication) or a transformation of the cell with only partial EBV genome expression (ie, latency). Cell transformation is associated with B-cell activation and continuous proliferation. In patients who are immunocompetent, proliferation of transformed B cells usually is controlled by cytotoxic T cells. This is not the case, however, with patients who are immunosuppressed.[6]

During latency, the viral genome adopts an episomal configuration and expresses only 9 proteins. This change in gene expression creates increased difficulty for T-cell recognition, facilitating persistent EBV infection. Latency occurs in resting memory B cells. The 9 proteins expressed during latency are EBV latent membrane proteins, ie, LMP-1, LMP-2A, and LMP-2B and EBV nuclear antigens EBNA-1, EBNA-2, EBNA-3A, EBNA-3B, EBNA-3C, and EBNA-LP. LMP-1 is considered an oncogene. Its expression results in increased levels of CD23, which is a B-cell activation antigen. LMP-1 also induces expression of bcl-2, an inhibitor of apoptosis in infected cells. LMP-2 prevents EBV reactivation in latently infected cells. EBNA-1 maintains the episomal configuration of the latent virus. EBNA-2 up-regulates the expression of LMP-1 and LMP-2, which are necessary for transformation of the B cell.[6]

The lymphoproliferative tissue from most cases of PTLD has detectable EBV DNA and expression of 3 antigens in particular—EBNA-1, EBNA-2, and LMP-1. Two of these 3 proteins usually are not expressed in other EBV-related malignancies and so may be distinguishing features. Of note, the classic t(8;14) or t(8;22) chromosomal translocations observed in Burkitt lymphoma are often not detected in the tumors of patients with PTLD, even in cases of monomorphic/monoclonal B cell lymphoproliferations.[11, 12, 13]

EBV infection normally results in both a humoral and cellular immune response by the host. Cellular immunity—CD4 and CD8 T cells and natural killer cells—is thought to be more important in controlling proliferation of infected B lymphocytes. Antibodies produced to viral capsid and nuclear proteins facilitate the diagnosis of EBV infection. In individuals who are immunocompetent, these mechanisms prevent outgrowth of EBV-infected lymphocytes. The immunosuppression required to prevent graft rejection post transplantation impairs T-cell immunity, potentially allowing for uncontrolled proliferation of EBV-infected B-cells, which may result in a spectrum of B-cell proliferations that range from hyperplasia to true lymphoma.[14, 15, 16, 17]

In the initial stages of PTLD, proliferation is polyclonal. With mutation and selective growth, the lesion becomes oligoclonal and, later, monoclonal. Lymphocytes from patients treated with cyclosporin following transplantation do not exhibit an appropriate T-cell response to EBV-infected B cells in vitro. The activity of natural killer cells also is reduced for several months following transplantation, contributing to the impairment of the most important regulator of proliferation: cellular immune response.[5, 18, 19]

The mechanisms that cause EBV-negative PTLD are not well understood. It often presents with a later onset, monomorphic histology, and a more aggressive course than EBV-positive PTLD, suggesting that it may have a different pathophysiology.[20, 21]





The frequency of posttransplant lymphoproliferative disease (PTLD) depends largely on the type of transplant received and the immunosuppression that the particular transplant requires. Primary EBV infection, such as may develop in an EBV-seronegative recipient who receives an allograft from an EBV-seropositive donor, is recognized as probably the most significant risk factor for developing PTLD. It is therefore not surprising that in general, PTLD rates are reported to be higher in pediatric transplant recipients than in adult transplant recipients.[22, 23, 1, 24]

The incidence of PTLD varies with the type of transplanted allograft. Reported rates are higher in heart, heart-lung, and small bowel transplants compared with kidney and liver transplants. This presumably reflects in part the need for more intense immunosuppression to maintain certain types of allografts. In terms of lymphoproliferative disease occurring within the allograft itself, this also depends on the type of graft. The lungs are frequently a site of involvement in patients undergoing heart-lung or heart-alone transplantation. Similarly, in small bowel transplants, the grafted bowel is commonly a site of PTLD. In cardiac transplants, the heart itself seldom is involved.

Kidney transplantation

A French kidney transplant registry consisting of data from adult patients who were enrolled prospectively from 1998 through 2007 was evaluated for PTLD. This study, reported by Caillard et al, found a 1% incidence of PTLD after 5 years, which increased to 2.1% by 10 years post transplantation. The more recently the transplant was performed, however, the less likely was the recipient to develop PTLD. Additionally, a report from the Organ Procurement and Transplantation Network (OPTN) of the United States reported a range of PTLD incidence following kidney transplantation from 0.6-1.5%. Risk factors identified by this study found an association between Medicare status, white race, and receipt of T-cell–depleting antibodies with the development of PTLD. A November 2012 report from the US OPTN published an incidence rate of 1.58 cases of PTLD per 1000 patient years post transplantation.[25]

In pediatric kidney transplant recipients, reports range from 4.4-6.9% PTLD incidence, with a wide range of times until onset—from less than 6 months to greater than 3 years.[26, 27] The majority of cases reported were B-cell proliferations. Both age younger than 5 years at the time of transplantation and EBV-positive allograft donor to an EBV-seronegative recipient significantly increased the risk ratio for developing PTLD. Many of the cases occurred while patients were still receiving steroids for immunosuppression.

Heart transplantation

In adults, heart transplantation is associated with approximately a 5% cumulative incidence of PTLD. Some reports have suggested that it may be as high as 8.9%.[28] Many reports of PTLD in heart transplant patients are single-institution studies and thus there may be greater variation seen in these reports compared with registry or cooperative studies. The US OPTN reports a rate of 2.24 cases of PTLD per 1000 patient years post heart transplantation.[25]

In children, the rate of PTLD following heart transplantation is even higher. Manlhiot et al found a 13% rate of PTLD at 4 years following pediatric heart transplantation at the Hospital for Sick Children at the University of Toronto. In this study, higher EBV load and longer induction of immunosuppression were associated with greater risk for PTLD.

Liver transplantation

An analysis of the Scientific Registry of Transplant Recipients of the United States reported PTLD rates of approximately 1% following liver transplantation in adult and pediatric recipients. The US OPTN reports a rate of 2.44 cases of PTLD per 1000 patient years post liver transplantation. A retrospective analysis from the Mayo Clinic of 1206 orthotopic liver transplants (OLT) reported a cumulative incidence of PTLD of 1.1% at 18 months and 4.7% at 15 years. The authors suggest that previous reports of a lower incidence of PTLD late after OLT may warrant further examination as survival of OLT recipients improves.[29] A retrospective study of 431 adult liver transplant recipients by Zimmerman et al (2010) reported that 11 (2.6%) patients developed PTLD. Multivariate analysis in that study revealed that pretransplant steroid treatment and liver transplantation for autoimmune hepatitis were risk factors for developing PTLD.

More recent reports of PTLD in pediatric liver transplant recipients show rates that range from 3.8-4.7%. This is improved from earlier studies that reported PTLD rates as high as 5-15% for pediatric liver transplant (reviewed in Hartmann 2011). The initial observation that the use of tacrolimus was associated with a higher incidence of PTLD compared with cyclosporine[30] has more recently been attributed to the earlier practice of targeting higher tacrolimus levels. With greater experience using this immunosuppressive agent and targeting of lower therapeutic levels, tacrolimus no longer appears to be associated with a higher incidence of PTLD in pediatric liver transplant recipients.

Lung transplantation

Lung transplantation is associated with a relatively high rate of PTLD, with an incidence of approximately 5%. The median time to development of PTLD has been reported to be between 12 and 40 months, depending on the study. In one recent report of 705 lung transplant recipients, 34 cases of PTLD were identified, for an incidence of 4.8%.[31] Among the 17 patients diagnosed within 11 months of transplantation, 85% had polymorphic PTLD and the most common site involved was the allograft, in 71% of the patients. PTLD that developed late was typically monomorphic and was more likely to involve the GI tract (39%) than the lung allograft (28%). The US OPTN reports a rate of 5.72 cases of PTLD per 1000 post transplantation patient years, with most cases occurring less than 1 year post transplantation.


In the setting of HSCT, PTLD rates vary greatly depending on the conditioning regimen and the amount of T-cell depletion involved in either the conditioning or the product provided. Rates as high as 71% have been reported in the setting of very extreme T-cell depletion. More recently, however, rates of PTLD in adult HSCT range from 0.2% with no T-cell depletion to 1.7% with antithymocyte globulin treatment.[20]

Similar results are seen in pediatric HSCT. PTLD occurs in less than 1% of non–T-cell–depleted grafts from matched siblings, compared with as high as 30% of patients with unrelated or HLA-mismatched donors when extensive T-cell depletion of the donor bone marrow is performed. Other risk factors for PTLD in HSCT recipients include treatment of graft versus host disease with antithymocyte globulin or anti–T-cell monoclonal antibodies.[32]


Posttransplant lymphoproliferative disease (PTLD) represents a heterogenous group of tumors, ranging from B-cell hyperplasia to immunoblastic lymphoma, the latter portending a grim prognosis.[2, 33, 34] All PTLD, however, irrespective of histology, is potentially, life threatening. The presentation and clinical course for PTLD may be quite variable. At one end of the spectrum is fulminant disease with diffuse involvement, which may result in the rapid demise of the patient. At the other end of the spectrum are localized lesions that may be indolent and slow growing over months. The former tends to occur early post transplantation after primary EBV infection and often involves the allograft itself. Late-onset PTLD tends to be monoclonal, EBV-negative, and often more refractory to therapy.[18]

In a retrospective review of 32 adult and pediatric patients with PTLD, the 5-year survival rate was 59%.[33] Nearly half of the patients were diagnosed within the first year following transplantation. Six of 8 patients surgically treated remain alive and disease free. Characteristics associated with poorer survival were diagnosis within the first year post transplantation, monoclonal tumors, and presentation with an infectious mononucleosis–like syndrome.

While advances in the diagnosis and treatment of PTLD have improved outcomes for patients with PTLD, studies continue to report high rates of mortality from PTLD. A series of adult kidney and heart transplant recipients reported by Wasson et al in 2006 had a mortality rate of 26.6%. Similarly, a more recent report of pediatric kidney transplant patients also found a 25% mortality rate related to PTLD.[27]

Several studies have attempted to identify prognostic factors for PTLD outcomes. For example, Evens et al identified hypoalbuminemia as a strong prognostic factor in their multicenter study of 80 adult SOT recipients with PTLD. Similarly, Khedmat and Taheri performed a literature review and found evidence to suggest that CD20-positive PTLD portends earlier disease appearance and inferior outcome.

LeBlond et al applied the non-Hodgkin lymphoma International Prognostic Index (IPI) to a series of 61 adult patients with PTLD following kidney, lung, liver, or heart transplantation to analyze factors that may be predictive for shorter survival. In univariate analysis, the following were found to be poor prognostic features: performance status (PS) greater than or equal to 2, increased number of sites involved (ie, >1 vs 1), primary central nervous system (CNS) involvement, T-cell origin, monoclonality, nondetection of EBV in the tumor, and treatment based on chemotherapy (in addition to reduction in immunosuppression).

In multivariate analysis, PS less than 2 and decreased number of disease sites (ie, 1 vs >1) both were associated with improved survival. These determinants were used to identify 3 levels of risk stratification in terms of survival probability. For intermediate-risk patients (ie, PS ≥2 or 2 or more sites), median survival time with treatment was 34 months. For high-risk patients (ie, PS ≥2 and 2 or more sites), median survival time was 1 month. Survival time for low-risk patients (ie, PS < 2 and < 2 sites) was not defined. This risk stratification system was found to be more helpful in determining prognosis for PTLD patients than the IPI used for immunocompetent patients with non-Hodgkin lymphoma.

Although a number of prognostic scores have been proposed in different transplantation populations, none has been externally validated or widely adopted. The rarity and clinical diversity of the disease, as well as the nature of the reporting of PTLD cases, which is often retrospective and from single-institution studies, have contributed to the challenge of developing and validating a universally accepted system of risk classification.

Contributor Information and Disclosures

Phillip M Garfin, MD, PhD California Institute of Regenerative Medicine MD Training Scholar, Clinical Instructor, Section of Hematology, Oncology, Stem Cell Transplantation, and Cancer Biology, Department of Pediatrics, Stanford University School of Medicine

Phillip M Garfin, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Society of Hematology, American Society of Pediatric Hematology/Oncology

Disclosure: Nothing to disclose.


Clare J Twist, MD Associate Professor of Pediatrics, Division of Hematology/Oncology, Medical Center Line, Stanford University School of Medicine; Medical Staff, Lucile Packard Children’s Hospital and Stanford University Medical Center

Clare J Twist, MD is a member of the following medical societies: American Society of Hematology, American Society of Pediatric Hematology/Oncology, Children's Oncology Group, American Society of Clinical Oncology

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: Received salary from Medscape for employment. for: Medscape.

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, SWOG

Disclosure: Partner received none from No financial interests for none.

Chief Editor

Ron Shapiro, MD Professor of Surgery, Robert J Corry Chair in Transplantation Surgery, Associate Clinical Director, Thomas E Starzl Transplantation Institute, University of Pittsburgh Medical Center

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

Disclosure: Nothing to disclose.


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

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

Mary Prendergast, MD Department of 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.

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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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