Letter to the Editor: “Burkitt Lymphoma in Renal Transplant Recipient”

Malignancy is a well-defined complication of chronic immunosuppression. Post-transplant lymphoproliferative disorder (PTLD) is a well-recognized complication of solid organ transplantation. There is a wide range of pathological presentations, from plasmocytic hyperplasia to high-grade lymphoma. Most PTLDs are due to Epstein-Barr virus (EBV) infection and occur during the early phase of transplantation, when marked immunosuppression is given to the patient. Regarding EBV-induced B-cell proliferation, Burkitt lymphoma has been rarely reported in solid organ transplantation, raising specific problems of prognosis and therapy. Burkitt's lymphoma is a highly aggressive lymphoma identified and described in the last century by Denis Burkitt in Africa. Since its description in African children, it has been recognized outside areas with endemic malaria, in children as well as among individuals with an underlying immunodeficiency. This article reports the clinical, laboratory findings and treatment of a patient who developed Burkitt's lymphoma (BL) after renal transplant and some issues about lymphoproliferative disorders after transplantation.[1],[2]

The case report is of a 26-year-old man who had previously been healthy with renal transplant, but who had developed disseminated Burkitt's lymphoma 38 months after transplantation.

The patient was admitted to the clinic with headache, left eye pain, diplopia, and complete ptosis. Left eye examination disclosed complete third nerve palsy with pupillary involvement. Neurological examination showed a positive bilateral Babinsky sign but otherwise was normal. Immunosuppressive therapy had consisted of prednisolone, cyclosporine, and azathioprine.

Initiation laboratory parameters were as follows: leukocyte, 8260; neutrophil, 5560; lymphocyte, 1190; monocyte, 1200; Hb, 15.4g/dL; MCV, 91.4; Plt, 19700; sedimentation, 39mm/h; CRP, 11.3. Regarding bone marrow aspiration: hypercellular, massive (>90%) L3 type of lymphoid blast cell infiltration, PAS: (+), MPO: (−), TDT (−),CD₂₀: 83%, CD₃: 2%, CALLA: (+). Laboratory parameters were urea, 41 mg/dL; creatinine, 1.18 mg/dL; glucose, 83 mg/dL; AST, 27 U/L; ALT, 32 U/L; total protein, 7.7 g/dL; albumine, 4.5g/dL; LDH, 2310–4640–6428mg/dL. Left transverse sinus was not obtained with cranial MRI and diffuses segmental dural thickening. Examination of the CSF was normal.

Due to the high level of LDH, CSF examination was performed, but it was found to be normal. Diagnosis of leukemia was done by blood smear and bone marrow biopsy. Histologic and immunohistologic examinations revealed diffuse large B-cell lymphoma. A potential risk factor of the patient may be the immunosuppressive therapy. EBV infection could be important risk factor, which is also reported in the literature.[3] Treatment of PTLD should be initiated with immunosuppression reduction. Standard dose chemotherapy leads to significant morbidity. Several strategies have been postulated to minimize the occurrence of malignancy, including ganciclovir prophylaxis for the prevention of PTLD and the use of mycophenolic acid and TOR inhibitor maintenance to diminish the incidence of PTLD and solid malignancies.[4]

Notes

*There is no conflict of interest regarding this manuscript.