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Post-transplant lymphoproliferative disorder
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Post-transplant lymphoproliferative disorder
Post-transplant lymphoproliferative disorder (PTLD) is the name given to a B cell proliferation due to therapeutic immunosuppression after organ transplantation. These patients may develop infectious mononucleosis-like lesions or polyclonal polymorphic B-cell hyperplasia. Some of these B cells may undergo mutations which will render them malignant, giving rise to a lymphoma.[citation needed]
In some patients, the malignant cell clone can become the dominant proliferating cell type, leading to frank lymphoma, a group of B cell lymphomas occurring in immunosuppressed patients following organ transplant.
Symptoms of PTLD are highly variable and nonspecific, and may include fever, weight loss, night sweats, and fatigue. Symptoms may be similar to those seen in infectious mononucleosis (caused by EBV). Pain or discomfort may result from lymphadenopathy or mass effect from growing tumors. Dysfunction may occur in organs affected by PTLD. Lung or heart involvement may result in shortness of breath.[citation needed]
Laboratory findings may show abnormally low white blood cell, red cell counts, and platelet counts. In addition, serum uric acid and lactate dehydrogenase levels may be elevated, while serum calcium levels may be decreased. All of these findings together can suggest tumor lysis syndrome.[citation needed]
The disease is an uncontrolled proliferation of B cell lymphocytes latently infected with Epstein–Barr virus (EBV). Production of an interleukin-10, an endogenous, pro-regulatory cytokine, has also been implicated.[citation needed]
In immunocompetent patients, Epstein-Barr virus can cause infectious mononucleosis in adolescents, which is otherwise asymptomatic in children during their childhood. However, in immunosuppressed transplant patients, the lack of T-cell immunosurveillance can lead to the proliferation of these EBV-infected B-lymphocytes.[citation needed]
However, calcineurin inhibitors (tacrolimus and ciclosporin), used as immunosuppressants in organ transplantation inhibit T cell function, and can prevent the control of the B cell proliferation.[citation needed]
Depletion of T cells by use of anti-T cell antibodies in the prevention or treatment of transplant rejection further increases the risk of developing post-transplant lymphoproliferative disorder. Such antibodies include ATG, ALG and OKT3 (muromonab-CD3).[citation needed]
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Post-transplant lymphoproliferative disorder AI simulator
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Post-transplant lymphoproliferative disorder
Post-transplant lymphoproliferative disorder (PTLD) is the name given to a B cell proliferation due to therapeutic immunosuppression after organ transplantation. These patients may develop infectious mononucleosis-like lesions or polyclonal polymorphic B-cell hyperplasia. Some of these B cells may undergo mutations which will render them malignant, giving rise to a lymphoma.[citation needed]
In some patients, the malignant cell clone can become the dominant proliferating cell type, leading to frank lymphoma, a group of B cell lymphomas occurring in immunosuppressed patients following organ transplant.
Symptoms of PTLD are highly variable and nonspecific, and may include fever, weight loss, night sweats, and fatigue. Symptoms may be similar to those seen in infectious mononucleosis (caused by EBV). Pain or discomfort may result from lymphadenopathy or mass effect from growing tumors. Dysfunction may occur in organs affected by PTLD. Lung or heart involvement may result in shortness of breath.[citation needed]
Laboratory findings may show abnormally low white blood cell, red cell counts, and platelet counts. In addition, serum uric acid and lactate dehydrogenase levels may be elevated, while serum calcium levels may be decreased. All of these findings together can suggest tumor lysis syndrome.[citation needed]
The disease is an uncontrolled proliferation of B cell lymphocytes latently infected with Epstein–Barr virus (EBV). Production of an interleukin-10, an endogenous, pro-regulatory cytokine, has also been implicated.[citation needed]
In immunocompetent patients, Epstein-Barr virus can cause infectious mononucleosis in adolescents, which is otherwise asymptomatic in children during their childhood. However, in immunosuppressed transplant patients, the lack of T-cell immunosurveillance can lead to the proliferation of these EBV-infected B-lymphocytes.[citation needed]
However, calcineurin inhibitors (tacrolimus and ciclosporin), used as immunosuppressants in organ transplantation inhibit T cell function, and can prevent the control of the B cell proliferation.[citation needed]
Depletion of T cells by use of anti-T cell antibodies in the prevention or treatment of transplant rejection further increases the risk of developing post-transplant lymphoproliferative disorder. Such antibodies include ATG, ALG and OKT3 (muromonab-CD3).[citation needed]
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