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Post-transplant lymphoproliferative disorder (PTLD) is a serious complication after solid-organ transplantation. We report a lung transplant recipient presenting with lower limb weakness as a result of extradural cord compression from PTLD. Diagnosis was made by laminectomy of T-3 with partial removal of the epidural mass. Further treatment consisted of chemoradiotherapy. The patient recovered completely. To our knowledge, this is the first reported case of PTLD presenting with signs and symptoms of spinal cord compression. The differential diagnosis of spinal cord compression in a patient who has had a transplant should include primary presentation of PTLD.

Background: Monitoring of the Epstein-Barr virus-DNA load is frequently used to identify patients at risk for post-transplant lymphoproliferative disease (PTLD). Epstein-Barr virus DNA can be measured in the plasma and whole blood serum compartments., Methods: We compared levels of Epstein-Barr virus DNA in whole blood and plasma using a real-time TaqMan polymerase chain reaction assay in 100 consecutive paired whole blood and plasma samples from 25 lung and heart-lung transplant recipients with detectable whole blood Epstein-Barr virus-DNA load (>2,000 copies/ml)., Results: A correlation (r2) of 0.58 (p < 0.001) was observed between both measurements, whereas of the positive whole blood samples (>2,000 copies/ml), only 17 samples (18%) were also positive in plasma., Conclusion: These results indicate that by virtue of its sensitivity, whole blood rather than plasma may be the preferable specimen for the detection of Epstein-Barr virus DNA in lung transplant recipients.

Post-transplant lymphoproliferative disease (PTLD) is a major complication after solid organ transplantation. We analyzed incidence, patient characteristics, clinical presentation, and prognostic factors for treatment outcome and survival of PTLD patients transplanted at our center. Records from adult kidney and lung transplant recipients, transplanted between January 1985 and December 2002 with a histologically confirmed diagnosis of PTLD, were retrieved. Histology was reviewed and prognostic factors for treatment outcome were evaluated by multivariable analysis. Of 1354 kidney and 206 lung transplants, PTLD was diagnosed in 40 transplant recipients (2.6%). Lung transplant recipients had a significantly higher incidence of PTLD (8.3%) than kidney transplant recipients (1.7%). Sites of presentation were highly heterogeneous. Notably, PTLD localized in the allograft occurred significantly earlier after transplantation than PTLD localized outside the allograft (p = 0.001). This was true for lung (p = 0.006) as well as for kidney transplant recipients (p = 0.03). In multivariable Cox regression, performance status (p = 0.01) and advanced stage (p = 0.04) were factors negatively predictive for response to first-line treatment. Only performance status remained as negative predictive factor for survival (p = 0.002) and freedom from tumor progression (p = 0.01). In conclusion, the allograft is significantly more often involved as primary site of PTLD presentation during the first post-transplant year. This may have clinical consequences and give new insights in pathogenesis of PTLD. Performance status and stage are important risk factors for outcome of PTLD.

Background: Rituximab, a humanized anti-CD20 monoclonal antibody, is a promising new tool for the treatment of posttransplant lymphoproliferative disease (PTLD), especially for patients transplanted with rejection prone transplants of vital organs, such as patients after lung transplantation. Thus far, no major complications have been described. We treated three lung transplant recipients with Rituximab because of PTLD., Methods: Patients were treated with four weekly doses of 375 mg/m2 of Rituximab. Epstein-Barr virus (EBV) DNA was monitored with quantitative-competitive polymerase chain reaction and circulating B cells with flow cytometry., Results: Treatment with Rituximab resulted in a complete remission in all patients without signs of or progression of bronchiolitis obliterans syndrome. Patient 1 relapsed after 2 months with a partly CD20-negative PTLD but is in stable remission after radiotherapy. Patient 2 is in complete remission 16 months after treatment, but patient 3 developed a hypogammaglobulinemia and died of invasive aspergillosis after 6 months. EBV DNA was detectable in the blood samples of patients 2 and 3 before treatment with Rituximab and became negative instantly after Rituximab. In all three patients, B cells are absent in the peripheral blood 7 months (at death), 16 months, and 16 months after treatment with Rituximab. Antiproliferating agents, such as mycophenolate mofetil (MMF), might prolong B-cell depletion., Conclusions: Rituximab was effective for the treatment of PTLD without progression of transplant dysfunction in our patients. Complications were a partly CD20-negative relapse of PTLD and a hypogammaglobulinemia. Attention should be paid to immunoglobulin G (IgG) levels, especially in patients treated with antiproliferating agents such as MMF.