Posttransplant Lymphoproliferative Disease Clinical Presentation

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

History

Whether PTLD presents as localized or disseminated disease, the tumors are aggressive and rapidly progressive and often are fatal. Clinical presentation is very variable and includes fever (57%), lymphadenopathy (38%), gastrointestinal symptoms (27%), infectious mononucleosis–like syndrome that can be fulminant (19%), pulmonary symptoms (15%), CNS symptoms (13%), and weight loss (9%). Patients may report fever, weight loss, anorexia, lethargy, sore throat, swollen glands, diarrhea, abdominal pain, shortness of breath, neurological symptoms, or symptoms that initially would not suggest a diagnosis of PTLD.

The most common sites for involvement are lymph nodes (59%), liver (31%), lung (29%), kidney (25%), bone marrow (25%), small intestine (22%), spleen (21%), CNS (19%), large bowel (14%), tonsils (10%), and salivary glands (4%). T-cell lymphoproliferative disorders not associated with EBV infection tend to occur at extranodal sites. Reports exist of PTLD presenting in the oral cavity.

Raut et al described a patient who received an allogeneic bone marrow transplant for chronic myeloid leukemia complicated by severe chronic graft versus host disease, for which he was treated with cyclophosphamide and mycophenolate mofetil.[7] The patient reported soreness of the gum. Biopsy results of the tissue revealed a diagnosis of non-Hodgkin lymphoma. For patients who have received either solid organ transplantation or allogeneic bone marrow transplantation and who are immunosuppressed as prophylaxis against graft rejection or graft versus host disease, a high index of suspicion and vigilance is required for prompt and timely diagnosis. A diagnosis of PTLD is entertained more easily in a patient who has undergone transplantation recently and who presented with fever, unexplained weight loss, lymphadenopathy, and hepatosplenomegaly.

The incidence of PTLD varies with the type of transplanted allograft. It is much higher in heart or heart-lung transplants, presumably reflecting the need for more intense immunosuppression in these patients. In terms of lymphoproliferative disease occurring in the allograft itself, it depends on the graft in question. The lungs very frequently are a site of involvement in patients undergoing heart-lung, or heart alone, transplant. In cardiac transplant, the heart itself seldom is involved. In renal allografts, the graft kidney is affected approximately one third of the time, which is similar to graft involvement rates in liver and bone marrow transplant cases.

In patients who undergo bone marrow transplantation, risk factors for the development of PTLD include the development of graft versus host disease treated with antithymocyte globulin or monoclonal antibodies, total-body irradiation, T-cell depletion of donor marrow, and human leukocyte antigen (HLA) mismatch.

Higher risk of developing PTLD and earlier occurrence posttransplantation have been shown to occur with more intense immunosuppression. The total burden of immunosuppression appears to be a very significant factor in determining risk. Swinnen et al (1990) examined the incidence of PTLD in patients undergoing cardiac transplant and using OKT3 (murine monoclonal anti-CD3 antibody) as immunosuppression and found an incidence of 6.2% in patients who had received a dose of 75 mg or less. The mean time to development of PTLD was 11 months, compared with an incidence of 35.25% and a mean interval of 1.5 months in patients who received doses of greater than 75 mg. With prednisolone and azathioprine alone, the mean time to developing PTLD is 50 months. Cyclosporin therapy reduced this to 5 months. Use of tacrolimus and use of antilymphocyte globulins have been associated with much earlier and more frequent presentation of PTLD.

A retrospective study of 431 liver transplant recipients by Zimmerman et al (2010) reported that 11 (2.6%) patients developed PTLD.[8] By multivariate analysis, risk factors for PTLD were pretransplant steroid treatment and liver transplantation for autoimmune hepatitis.

Cox et al addressed the incidence PTLD in pediatric patients undergoing liver transplant and found that the use of tacrolimus was associated with a higher incidence of PTLD (19% versus 3%) compared to cyclosporin.[9]

Other risk factors that have been identified as predictive for the development of PTLD include recipient pretransplant EBV seronegativity and donor EBV seropositivity. The incidence of PTLD has been found to be significantly higher in patients who are EBV seronegative pretransplant, compared with those who are seropositive (23.1% versus 0.7% in Cockfield's 1993 analysis[10] ). Presumably, EBV is transmitted from donor to recipient via the graft at a time of considerable immunosuppression for the recipient, or the patient develops primary EBV infection unrelated to donor EBV status. However, experience at the University of Pittsburgh indicates that, in the case of intestinal transplantation, the incidence of PTLD is as high in patients who are EBV seropositive pretransplantation as in patients who are seronegative.

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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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