A well-known side effect of allogeneic hematopoietic stem cell transplantation (HSCT) and solid organ transplantation (SOT) is posttransplant lymphoproliferative disorder (PTLD).
Epstein-Barr virus (EBV) infection of B-cells is linked to PTLD because of original EBV infection or because of posttransplant virus reactivation.
Most T-cell lymphoproliferative diseases following SOT and HSCT are B-cell proliferations, while T-cell lymphoproliferative disorders that are not usually linked to EBV infection.
It includes a various of plasmacytic and lymphoid proliferations from malignant lymphoma to benign hyperplasia.
Reduction or removal of immunosuppression is the primary goal of initial care of PTLD, and it may reverse the lymphoproliferative process in certain circumstances.
PTLD is different from neoplastic lymphoproliferative diseases that affect immunocompetent people due to its potential for reversibility with a reduction in immunosuppression.
Depending on the transplanted organ or clinical circumstance, reducing immunosuppression may not always possible and involves the risk of causing allograft malfunction.
Epidemiology
Immunosuppression required for the specific transplant and the type of transplant received are major factors in the incidence of posttransplant lymphoproliferative disorder (PTLD).
The most important risk factor for developing PTLD is EBV infection, which can occur in an EBV-seronegative recipient who receives an allograft from an EBV-seropositive donor.
As a result, it is not shocking that pediatric transplant recipients generally have higher reported PTLD rates than adult transplant recipients.
In comparison to kidney and liver transplants, reported rates are greater for heart, heart-lung, and small bowel transplants.
The prevalence of PTLD in adult HSCT varies from 0.2% in the absence of T-cell depletion to 1.7% in the presence of antithymocyte globulin.
Anatomy
Pathophysiology
A childhood EBV primary infection causes a mild and self-limiting sickness. An EBV infection results in infectious mononucleosis in older, immunocompetent children and adults.
Latent in B-cell lymphocytes and continuously reproducing in oropharyngeal cells, the virus remains in a person for the duration of their life
EBV has also been linked to nasopharyngeal cancer in Asian people and non-Hodgkin lymphoma and oral hairy leukoplakia in HIV-positive patients.
Approximately 100 viral proteins that are expressed during replication are encoded by the linear DNA molecule known as the EBV genome.
Continuous proliferation and B-cell activation are linked to cell transformation. In immunocompetent patients, cytotoxic T cells regulate the growth of changed B cells.
Etiology
The causes of PTLD are as follows:
EBV infection
Immunosuppression
EBV-negative pathways
Transplant type
Host/donor serostatus
Genetics
Prognostic Factors
The clinical course and appearance of PTLD might vary greatly. The patient may die quickly from fulminant disease with diffuse involvement, which is at one extreme of the spectrum.
The 5-year survival rate was 59% in a retrospective analysis of 32 SOT patients with PTLD, both adults and children. In the year after transplantation, about half of the patients received a diagnosis.
Studies continue to show significant rates of PTLD-related death, despite improvements in patient outcomes caused by advancements in diagnosis and therapy.
Clinical History
Clinical History:
Collect details including the timing of onset, presenting symptoms, and clinical history to understand clinical history of patients.
The treatment of PTLD is still difficult and there is no one-size-fits-all therapeutic strategy.
When compared to patients with clinically aggressive PTLD, people with less aggressive or polyclonal PTLD typically react better to this therapeutic strategy.
The humanized anti-CD20 monoclonal antibody rituximab has set the standard of care for individuals who do not respond well to immunosuppression reduction.
In the treatment of CD20-expressing PTLD, reports have shown that single-agent rituximab is safe and effective, with a response rate of about.
Rituximab monotherapy is safe for patients who achieve complete remission with rituximab induction therapy or who have fewer than three international prognostic index (IPI) risk factors at diagnosis and achieve partial remission.
Due to end-organ toxicity or the possibility of allograft malfunction, SOT patients frequently cannot handle full-dose chemotherapy. Doxorubicin doses for heart transplant recipients are frequently lowered due to worries about myocardial damage.
A Children’s Oncology Group phase II trial with low-dose cyclophosphamide, prednisone, and rituximab was carried out to further evaluate the effectiveness of this regimen.
Patients with PTLD are typically on long-term immunosuppressive therapy, which increases their vulnerability to opportunistic infections.
In hospital settings, patients may require protective isolation or placement in high-efficiency particulate air (HEPA)-filtered rooms, particularly when undergoing chemotherapy.
If the patient resides in a rural or high-risk area for endemic pathogens, relocation or stricter environmental controls may be considered.
Proper awareness about PLTD should be provided and its related causes with management strategies.
Appointments with hematology specialists and preventing recurrence of disorder is an ongoing life-long effort.
Use of Immunosuppressive Agents
Cyclosporine:
It suppresses humoral immunity and humoral immunity.
Mycophenolate:
It inhibits inosine monophosphate dehydrogenase and suppresses de novo purine synthesis.
Prednisone:
It reduces inflammation that reverses increased capillary permeability and suppress PMN activity.
Use of Antiviral Agents
Acyclovir:
It suppresses HSV-1 and HSV-2 activity that binds to viral thymidine kinase.
Ganciclovir:
It is a 2′-deoxyguanosine acyclic nucleoside analog that prevents herpes virus proliferation in both in vitro and in vivo settings.
Use of Immunomodulator Agent
Rituximab:
The hybrid murine/human monoclonal antibody targets the CD20 antigen present on the surface of both healthy and cancerous B cells.
Interferon alfa-2b:
A protein called interferon alfa-2b is produced using recombinant DNA technology.
Use of Antineoplastic Agents
Cyclophosphamide:
Their mode of action might involve DNA cross-linking, which could interfere the proliferation of both healthy and malignant cells.
Doxorubicin:
It creates free radicals to inhibits topoisomerase II as both have the potential to destroy DNA.
Vincristine:
There could be a rise in platelet formation or a decrease in reticuloendothelial cell activity.
Etoposide:
In the late S or early G2 phases of the cell cycle, it prevents cell growth by inhibiting topoisomerase II and breaking DNA strands.
Methotrexate:
In cancerous cells, it prevents DNA synthesis and cell division by blocking dihydrofolate reductase.
»
Home » CAD » Posttransplant Lymphoproliferative Disease
Posttransplant Lymphoproliferative Disease
Updated :
December 3, 2025
A well-known side effect of allogeneic hematopoietic stem cell transplantation (HSCT) and solid organ transplantation (SOT) is posttransplant lymphoproliferative disorder (PTLD).
Epstein-Barr virus (EBV) infection of B-cells is linked to PTLD because of original EBV infection or because of posttransplant virus reactivation.
Most T-cell lymphoproliferative diseases following SOT and HSCT are B-cell proliferations, while T-cell lymphoproliferative disorders that are not usually linked to EBV infection.
It includes a various of plasmacytic and lymphoid proliferations from malignant lymphoma to benign hyperplasia.
Reduction or removal of immunosuppression is the primary goal of initial care of PTLD, and it may reverse the lymphoproliferative process in certain circumstances.
PTLD is different from neoplastic lymphoproliferative diseases that affect immunocompetent people due to its potential for reversibility with a reduction in immunosuppression.
Depending on the transplanted organ or clinical circumstance, reducing immunosuppression may not always possible and involves the risk of causing allograft malfunction.
Immunosuppression required for the specific transplant and the type of transplant received are major factors in the incidence of posttransplant lymphoproliferative disorder (PTLD).
The most important risk factor for developing PTLD is EBV infection, which can occur in an EBV-seronegative recipient who receives an allograft from an EBV-seropositive donor.
As a result, it is not shocking that pediatric transplant recipients generally have higher reported PTLD rates than adult transplant recipients.
In comparison to kidney and liver transplants, reported rates are greater for heart, heart-lung, and small bowel transplants.
The prevalence of PTLD in adult HSCT varies from 0.2% in the absence of T-cell depletion to 1.7% in the presence of antithymocyte globulin.
A childhood EBV primary infection causes a mild and self-limiting sickness. An EBV infection results in infectious mononucleosis in older, immunocompetent children and adults.
Latent in B-cell lymphocytes and continuously reproducing in oropharyngeal cells, the virus remains in a person for the duration of their life
EBV has also been linked to nasopharyngeal cancer in Asian people and non-Hodgkin lymphoma and oral hairy leukoplakia in HIV-positive patients.
Approximately 100 viral proteins that are expressed during replication are encoded by the linear DNA molecule known as the EBV genome.
Continuous proliferation and B-cell activation are linked to cell transformation. In immunocompetent patients, cytotoxic T cells regulate the growth of changed B cells.
The causes of PTLD are as follows:
EBV infection
Immunosuppression
EBV-negative pathways
Transplant type
Host/donor serostatus
The clinical course and appearance of PTLD might vary greatly. The patient may die quickly from fulminant disease with diffuse involvement, which is at one extreme of the spectrum.
The 5-year survival rate was 59% in a retrospective analysis of 32 SOT patients with PTLD, both adults and children. In the year after transplantation, about half of the patients received a diagnosis.
Studies continue to show significant rates of PTLD-related death, despite improvements in patient outcomes caused by advancements in diagnosis and therapy.
Clinical History:
Collect details including the timing of onset, presenting symptoms, and clinical history to understand clinical history of patients.
The treatment of PTLD is still difficult and there is no one-size-fits-all therapeutic strategy.
When compared to patients with clinically aggressive PTLD, people with less aggressive or polyclonal PTLD typically react better to this therapeutic strategy.
The humanized anti-CD20 monoclonal antibody rituximab has set the standard of care for individuals who do not respond well to immunosuppression reduction.
In the treatment of CD20-expressing PTLD, reports have shown that single-agent rituximab is safe and effective, with a response rate of about.
Rituximab monotherapy is safe for patients who achieve complete remission with rituximab induction therapy or who have fewer than three international prognostic index (IPI) risk factors at diagnosis and achieve partial remission.
Due to end-organ toxicity or the possibility of allograft malfunction, SOT patients frequently cannot handle full-dose chemotherapy. Doxorubicin doses for heart transplant recipients are frequently lowered due to worries about myocardial damage.
A Children’s Oncology Group phase II trial with low-dose cyclophosphamide, prednisone, and rituximab was carried out to further evaluate the effectiveness of this regimen.
Hematology
Patients with PTLD are typically on long-term immunosuppressive therapy, which increases their vulnerability to opportunistic infections.
In hospital settings, patients may require protective isolation or placement in high-efficiency particulate air (HEPA)-filtered rooms, particularly when undergoing chemotherapy.
If the patient resides in a rural or high-risk area for endemic pathogens, relocation or stricter environmental controls may be considered.
Proper awareness about PLTD should be provided and its related causes with management strategies.
Appointments with hematology specialists and preventing recurrence of disorder is an ongoing life-long effort.
Hematology
Cyclosporine:
It suppresses humoral immunity and humoral immunity.
Mycophenolate:
It inhibits inosine monophosphate dehydrogenase and suppresses de novo purine synthesis.
Prednisone:
It reduces inflammation that reverses increased capillary permeability and suppress PMN activity.
Hematology
Acyclovir:
It suppresses HSV-1 and HSV-2 activity that binds to viral thymidine kinase.
Ganciclovir:
It is a 2′-deoxyguanosine acyclic nucleoside analog that prevents herpes virus proliferation in both in vitro and in vivo settings.
Hematology
Rituximab:
The hybrid murine/human monoclonal antibody targets the CD20 antigen present on the surface of both healthy and cancerous B cells.
Interferon alfa-2b:
A protein called interferon alfa-2b is produced using recombinant DNA technology.
Hematology
Cyclophosphamide:
Their mode of action might involve DNA cross-linking, which could interfere the proliferation of both healthy and malignant cells.
Doxorubicin:
It creates free radicals to inhibits topoisomerase II as both have the potential to destroy DNA.
Vincristine:
There could be a rise in platelet formation or a decrease in reticuloendothelial cell activity.
Etoposide:
In the late S or early G2 phases of the cell cycle, it prevents cell growth by inhibiting topoisomerase II and breaking DNA strands.
Methotrexate:
In cancerous cells, it prevents DNA synthesis and cell division by blocking dihydrofolate reductase.
Hematology
Procedural interventions in PTLD are essential for diagnosis, staging, symptom relief, and occasionally curative intent in localized disease.
The diagnostic procedures include tissue Biopsy, while therapeutic procedures include endoscopy and thoracentesis.
Hematology
In the initial assessment and diagnosis phase, the goal is to confirm diagnosis and classify PTLD subtype.
In planning phase, the goal is to determine PTLD severity and risk along with selection treatment approach.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional procedures.
The regular follow-up visits with the hemtology specialist are scheduled to check the improvement of patients along with treatment response.
A well-known side effect of allogeneic hematopoietic stem cell transplantation (HSCT) and solid organ transplantation (SOT) is posttransplant lymphoproliferative disorder (PTLD).
Epstein-Barr virus (EBV) infection of B-cells is linked to PTLD because of original EBV infection or because of posttransplant virus reactivation.
Most T-cell lymphoproliferative diseases following SOT and HSCT are B-cell proliferations, while T-cell lymphoproliferative disorders that are not usually linked to EBV infection.
It includes a various of plasmacytic and lymphoid proliferations from malignant lymphoma to benign hyperplasia.
Reduction or removal of immunosuppression is the primary goal of initial care of PTLD, and it may reverse the lymphoproliferative process in certain circumstances.
PTLD is different from neoplastic lymphoproliferative diseases that affect immunocompetent people due to its potential for reversibility with a reduction in immunosuppression.
Depending on the transplanted organ or clinical circumstance, reducing immunosuppression may not always possible and involves the risk of causing allograft malfunction.
Immunosuppression required for the specific transplant and the type of transplant received are major factors in the incidence of posttransplant lymphoproliferative disorder (PTLD).
The most important risk factor for developing PTLD is EBV infection, which can occur in an EBV-seronegative recipient who receives an allograft from an EBV-seropositive donor.
As a result, it is not shocking that pediatric transplant recipients generally have higher reported PTLD rates than adult transplant recipients.
In comparison to kidney and liver transplants, reported rates are greater for heart, heart-lung, and small bowel transplants.
The prevalence of PTLD in adult HSCT varies from 0.2% in the absence of T-cell depletion to 1.7% in the presence of antithymocyte globulin.
A childhood EBV primary infection causes a mild and self-limiting sickness. An EBV infection results in infectious mononucleosis in older, immunocompetent children and adults.
Latent in B-cell lymphocytes and continuously reproducing in oropharyngeal cells, the virus remains in a person for the duration of their life
EBV has also been linked to nasopharyngeal cancer in Asian people and non-Hodgkin lymphoma and oral hairy leukoplakia in HIV-positive patients.
Approximately 100 viral proteins that are expressed during replication are encoded by the linear DNA molecule known as the EBV genome.
Continuous proliferation and B-cell activation are linked to cell transformation. In immunocompetent patients, cytotoxic T cells regulate the growth of changed B cells.
The causes of PTLD are as follows:
EBV infection
Immunosuppression
EBV-negative pathways
Transplant type
Host/donor serostatus
The clinical course and appearance of PTLD might vary greatly. The patient may die quickly from fulminant disease with diffuse involvement, which is at one extreme of the spectrum.
The 5-year survival rate was 59% in a retrospective analysis of 32 SOT patients with PTLD, both adults and children. In the year after transplantation, about half of the patients received a diagnosis.
Studies continue to show significant rates of PTLD-related death, despite improvements in patient outcomes caused by advancements in diagnosis and therapy.
Clinical History:
Collect details including the timing of onset, presenting symptoms, and clinical history to understand clinical history of patients.
The treatment of PTLD is still difficult and there is no one-size-fits-all therapeutic strategy.
When compared to patients with clinically aggressive PTLD, people with less aggressive or polyclonal PTLD typically react better to this therapeutic strategy.
The humanized anti-CD20 monoclonal antibody rituximab has set the standard of care for individuals who do not respond well to immunosuppression reduction.
In the treatment of CD20-expressing PTLD, reports have shown that single-agent rituximab is safe and effective, with a response rate of about.
Rituximab monotherapy is safe for patients who achieve complete remission with rituximab induction therapy or who have fewer than three international prognostic index (IPI) risk factors at diagnosis and achieve partial remission.
Due to end-organ toxicity or the possibility of allograft malfunction, SOT patients frequently cannot handle full-dose chemotherapy. Doxorubicin doses for heart transplant recipients are frequently lowered due to worries about myocardial damage.
A Children’s Oncology Group phase II trial with low-dose cyclophosphamide, prednisone, and rituximab was carried out to further evaluate the effectiveness of this regimen.
Hematology
Patients with PTLD are typically on long-term immunosuppressive therapy, which increases their vulnerability to opportunistic infections.
In hospital settings, patients may require protective isolation or placement in high-efficiency particulate air (HEPA)-filtered rooms, particularly when undergoing chemotherapy.
If the patient resides in a rural or high-risk area for endemic pathogens, relocation or stricter environmental controls may be considered.
Proper awareness about PLTD should be provided and its related causes with management strategies.
Appointments with hematology specialists and preventing recurrence of disorder is an ongoing life-long effort.
Hematology
Cyclosporine:
It suppresses humoral immunity and humoral immunity.
Mycophenolate:
It inhibits inosine monophosphate dehydrogenase and suppresses de novo purine synthesis.
Prednisone:
It reduces inflammation that reverses increased capillary permeability and suppress PMN activity.
Hematology
Acyclovir:
It suppresses HSV-1 and HSV-2 activity that binds to viral thymidine kinase.
Ganciclovir:
It is a 2′-deoxyguanosine acyclic nucleoside analog that prevents herpes virus proliferation in both in vitro and in vivo settings.
Hematology
Rituximab:
The hybrid murine/human monoclonal antibody targets the CD20 antigen present on the surface of both healthy and cancerous B cells.
Interferon alfa-2b:
A protein called interferon alfa-2b is produced using recombinant DNA technology.
Hematology
Cyclophosphamide:
Their mode of action might involve DNA cross-linking, which could interfere the proliferation of both healthy and malignant cells.
Doxorubicin:
It creates free radicals to inhibits topoisomerase II as both have the potential to destroy DNA.
Vincristine:
There could be a rise in platelet formation or a decrease in reticuloendothelial cell activity.
Etoposide:
In the late S or early G2 phases of the cell cycle, it prevents cell growth by inhibiting topoisomerase II and breaking DNA strands.
Methotrexate:
In cancerous cells, it prevents DNA synthesis and cell division by blocking dihydrofolate reductase.
Hematology
Procedural interventions in PTLD are essential for diagnosis, staging, symptom relief, and occasionally curative intent in localized disease.
The diagnostic procedures include tissue Biopsy, while therapeutic procedures include endoscopy and thoracentesis.
Hematology
In the initial assessment and diagnosis phase, the goal is to confirm diagnosis and classify PTLD subtype.
In planning phase, the goal is to determine PTLD severity and risk along with selection treatment approach.
In supportive care and management phase, patients should receive required attention such as lifestyle modification and interventional procedures.
The regular follow-up visits with the hemtology specialist are scheduled to check the improvement of patients along with treatment response.
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