Post transplant lymphoproliferative disorder

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vamsikrishna Gunnam M.B.B.S[2] Maria Fernanda Villarreal, M.D. [3]

Synonyms and Keywords: PTLD;

Overview

Post-transplant lymphoproliferative disorder (also known as PTLD) is defined as a lymphoid (immune cells) and/or plasmacytic proliferations (rapid increase) due to therapeutic immunosuppression after organ transplantation especially in the patients who are undergoing solid organ or allogeneic (donor) hematopoietic stem cell transplantation. Post transplant lymphoproliferative disorder was first discovered by Denis Parsons Burkitt, an Irish physician, in 1965. According to World Health Organization (WHO) classification system, post transplant lymphoproliferative disorder may be classified into 4 subtypes: early hyperplastic lesions, polymorphic lesions, monomorphic lesions, and classic Hodgkin-type lymphomas. Patients with post-transplant lymphoproliferative disorder may develop serious complications of transplantation with infectious mononucleosis-like lesions due to Epstein-Barr virus (EBV) or polyclonal polymorphic B-cell hyperplasia. In some cases, B-cells may undergo mutations which will render them malignant, giving rise to a lymphoma. The malignant cell clone can become the dominant proliferating cell type, leading to a group of B cell lymphomas occurring in immunosuppressed patients following organ transplant. Post transplant lymphoproliferative disorder arises from germinal center or post-germinal center B cells (B-PTLD), which are normally involved the production of antibodies and durable memory B cells. Post transplant lymphoproliferative disorder is very rare, and the prevalence of post transplant lymphoproliferative disorder remains unknown. Post transplant lymphoproliferative disorder is more commonly observed among young patients. The medical treatment for post transplant lymphoproliferative disorder, includes: immunosuppression, antiviral therapy, interferon alpha therapy, CD20 antibody therapy, and chemotherapy.

Historical Perspective

  • Post transplant lymphoproliferative disorder was first discovered by Denis Parsons Burkitt, an Irish physician, in 1965.
  • Post transplant lymphoproliferative disorder was first introduced in 1984 by Starzl.[1]

Classification

Category Subtype
Early hyperplastic lesions
Polymorphic lesions
Monomorphic lesions B-cell lymphomas

T-cell lymphomas

Other types

Pathophysiology

  • It is understood that post transplant lymphoproliferative disorder is the result of B cell proliferation induced by Epstein-Barr virus (EBV) infection.[4][5][6]
  • 90 to 95 percent of patients with post transplant lymphoproliferative disorder shows positive serologic of infection especially with Epstein-Barr virus (EBV) infection.[7]
  • Membrane proteins associated with EBV plays a major role in contribute to B cell growth and survival.[8][9][10][11][12][13]
    • LMP-1-Latent membrane protein 1
    • LMP-2A-Latent membrane protein 2
    • EBNA-2 (Epstein-Barr nuclear antigen 2) and
    • EBNA-LP (Epstein-Barr nuclear antigen 2 ladder protein)
  • The overexpression of bcl-2 has been associated with the development of post transplant lymphoproliferative disorder.
  • On gross pathology, characteristic findings of post transplant lymphoproliferative disorder, include:

Causes

Differentiating Post Transplant Lymphoproliferative Disorder from Other Diseases

Epidemiology and Demographics

Incidence

  • The incidence of post transplant lymphoproliferative disorder is approximately 20,000 in 100,000 of all cancers especially with solid organ transplantation.[20][21][22][23][24][25]
  • The incidence of post transplant lymphoproliferative disorder in liver transplants is approximately 1000 to 2000 in 100,000 patients.
  • The incidence of post transplant lymphoproliferative disorder in renal transplant is approximately 1000 to 3000 in 100,000 patients.
  • The incidence of post transplant lymphoproliferative disorder in heart transplant is approximately 2000 to 6000 in 100,000 patients.
  • The incidence of post transplant lymphoproliferative disorder in lung transplant is approximately 2000 to 9000 in 100,000 patients.
  • The incidence of post transplant lymphoproliferative disorder in intestinal or multi organ transplants is approximately as high as 11,000 to 33,000 in 100,000 patients.

Prevalence

  • The prevalence of post transplant lymphoproliferative disorder remains unknown.

Age

  • Post transplant lymphoproliferative disorder is more commonly observed among young patients.[26]

Gender

  • Females are slightly more affected with post transplant lymphoproliferative disorder than men.[27]

Race

  • There is no racial predilection for post transplant lymphoproliferative disorder.[28]

Risk Factors

Natural History, Complications and Prognosis

Natural History

  • The majority of patients with post transplant lymphoproliferative disorder are symptomatic at the time of diagnosis.
  • Early clinical features include fatigue, fever, and weight-loss.

Complications

  • If left untreated, patients with post transplant lymphoproliferative disorder may progress to develop organ failure.
  • The most common complication of post transplant lymphoproliferative disorder is fatal infection.

Prognosis

  • Depending on the extent of the disease progression at the time of diagnosis, the prognosis may vary in post transplant lymphoproliferative disorder patients due to heterogeneity of the disease.[35][36]
  • Prognosis also depends on what type of PTLD the patient is presenting.
  • Prognosis is generally poor, and the 5-year survival rate of patients with post transplant lymphoproliferative disorder is approximately 37- 61%.
  • In post transplant lymphoproliferative disorder patients estimated average survival rates range from 25%–60%.

Diagnosis

Symptoms

  • Symptoms in post transplant lymphoproliferative disorder patients are highly variable.[18]
  • Symptoms are depends on type of post transplant lymphoproliferative disorder patient present with, and the organs involved.
  • Symptoms of post transplant lymphoproliferative disorder may include the following:[37]

Physical Examination

Laboratory Findings

Laboratory findings consistent with the diagnosis of post transplant lymphoproliferative disorder include:

Imaging Findings

Treatment

Medical Therapy

  • According to following guidelines proposed post transplant lymphoproliferative disease is treated:[56][57][58][59][60]
    • American Society of Transplantation (AST).
    • World Health Organization (WHO).
    • NCCN: National Comprehensive Cancer Network.
    • European best practice guidelines for renal transplantation.
    • British Committee for Standards in Haematology.
    • British Transplantation Society.
  • Pharmacologic medical therapies for post transplant lymphoproliferative disorder highly varied based on the subtype and type of transplant.[61]
  • In post transplant lymphoproliferative disorder patients standardized therapeutic approach cannot be applied to all patients.
  • The medical treatment for post transplant lymphoproliferative disorder, include the followings.[62]

Immunosuppression

Early lesions

  • Pharmacologic medical therapies for early lesions in post transplant lymphoproliferative disorder include:[70][71]

Polymorphic PTLD

  • Pharmacologic medical therapies for polymorphic post transplant lymphoproliferative disorder include:

Monomorphic PTLD

Classic Hodgkin lymphoma-like PTLD

  • Pharmacologic medical therapies for classic hodgkin lymphoma like post transplant lymphoproliferative disorder include:

Rituximab

Chemoimmunotherapy

Surgery

  • Surgery is not recommended for patients with post transplant lymphoproliferative disorder.[18]

Prevention

References

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  2. LaCasce, A. S. (2006). "Post-Transplant Lymphoproliferative Disorders". The Oncologist. 11 (6): 674–680. ISSN 1083-7159. doi:10.1634/theoncologist.11-6-674. 
  3. Petrara, Maria Raffaella; Giunco, Silvia; Serraino, Diego; Dolcetti, Riccardo; De Rossi, Anita (2015). "Post-transplant lymphoproliferative disorders: From epidemiology to pathogenesis-driven treatment". Cancer Letters. 369 (1): 37–44. ISSN 0304-3835. doi:10.1016/j.canlet.2015.08.007. 
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