Post-transplant lymphoproliferative disorder (PTLD) is the name given to a group of B cell lymphoma occurring in Immunosuppression patients following organ transplant. It is an uncommon condition occurring in 0.2% of patients within one year of transplant, with an annual incidence of 0.04% thereafter. The risk of developing the disease is higher in children and recipients of heart transplants. The disease is an uncontrolled proliferation of B cell lymphocytes following infection with Epstein-Barr virus. Production of an interleukin-10, an endogenous anti-T cell cytokine, has also been implicated. In immunocompetent patients, Epstein-Barr virus causes infectious mononucleosis, characterised by a proliferation of B-lymphocytes which is controlled by Suppressor T cells. However, calcineurin inhibitors (tacrolimus and cyclosporine) used as immunosuppressants in organ transplantation inhibit T cell function, and can prevent the control of the B cell proliferation. Depletion of T cells by use of anti-T cell Antibody in the prevention or treatment of transplant rejection further increases the risk of developing post-transplant lymphoproliferative disorder. Such antibodies include Anti-thymocyte_globulin, Anti-lymphocyte_globulin and OKT3. Polyclonal PTLD may form tumour masses and present with symptoms due to a mass effect, e.g. symptoms of bowel obstruction. Monoclonal forms of PTLD tend to form a disseminated maligant lymphoma. PTLD may spontaneously regress on reduction or cessation of Immunosuppression medication, and can also be treated with addition of anti-viral therapy. In some cases it will progress to non-Hodgkin's lymphoma and may be fatal. Transplantation medicine
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Post-transplant lymphoproliferative disorder
Post-transplant lymphoproliferative disorder (PTLD) is the name given to a group of B cell lymphoma occurring in Immunosuppression patients following organ transplant. It is an uncommon condition occurring in 0.2% of patients within one year of transplant, with an annual incidence of 0.04% thereafter. The risk of developing the disease is higher in children and recipients of heart transplants. The disease is an uncontrolled proliferation of B cell lymphocytes following infection with Epstein-Barr virus. Production of an interleukin-10, an endogenous anti-T cell cytokine, has also been implicated. In immunocompetent patients, Epstein-Barr virus causes infectious mononucleosis, characterised by a proliferation of B-lymphocytes which is controlled by Suppressor T cells. However, calcineurin inhibitors (tacrolimus and cyclosporine) used as immunosuppressants in organ transplantation inhibit T cell function, and can prevent the control of the B cell proliferation. Depletion of T cells by use of anti-T cell Antibody in the prevention or treatment of transplant rejection further increases the risk of developing post-transplant lymphoproliferative disorder. Such antibodies include Anti-thymocyte_globulin, Anti-lymphocyte_globulin and OKT3. Polyclonal PTLD may form tumour masses and present with symptoms due to a mass effect, e.g. symptoms of bowel obstruction. Monoclonal forms of PTLD tend to form a disseminated maligant lymphoma. PTLD may spontaneously regress on reduction or cessation of Immunosuppression medication, and can also be treated with addition of anti-viral therapy. In some cases it will progress to non-Hodgkin's lymphoma and may be fatal. Transplantation medicine
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