Abstract
The Epstein-Barr virus (EBV) associated Post-Transplant Lymphoproliferative Disorders (PTLD) are increasingly recognized as a fatal complication of hematological stem cell transplantation (HSCT). Thoracic involvement, that may be isolated or part of a disseminated disease, usually encompasses pulmonary nodules or masses and mediastinal lymph node enlargement. The current case study presents 2 patients who underwent HSCT, one allogenic and the other autologous, who developed an exceptional endobronchial EBV related PTLD. The first patient had a fleshy white endobronchial mass resulting in a right upper lobe atelectasis and the second had an extensive necrotising mucosa from trachea to both basal bronchi without any significant change of lung parenchyma on the CT scan. In both cases, the diagnosis was made by bronchial biopsies. Physicians should be aware of an endobronchial pattern of EBV associated PTLD after HSCT to permit quick diagnosis and therapeutic intervention.
Highlights
Post-transplant lymphoproliferative disorders (PTLD) are rare and life-threatening complications of prolonged immunosuppression that is usually derives from the proliferation of Epstein-Barr virus (EBV) infected B-cells.[1]
An exceptional presentation of thoracic EBV related PTLD with endobronchial localization occurring in 2 hematological stem cell transplant recipients whose diagnosis was made by flexible bronchoscopy
PTLD may occur after hematological stem cell transplantation
Summary
Post-transplant lymphoproliferative disorders (PTLD) are rare and life-threatening complications of prolonged immunosuppression that is usually derives from the proliferation of Epstein-Barr virus (EBV) infected B-cells.[1]. Systematic quantitative EBV PCR performed for blood samples became positive 34 days after cord blood stem cell transplantation (65000 copies/mL) At this time, the patient had a normal lung CT scan. As the result of a post transplant EBV reactivation, rituximab (administered at a dose of 375 mg/m2) was introduced with 4 subsequent weekly courses until December 2004, when PCR analysis of blood samples for EBV were significantly decreased (7500 copies/mL) He was hospitalised in January 2005 for a fever associated with a productive cough while he was still taking cyclosporine (250 mg/d) and prednisone (50 mg/d) as immunosuppressive treatment. He relapsed in December 2004, with abdominal and inguinal adenopathies, as confirmed by the cytological analysis of an inguinal lymph node, characteristic of follicular lymphoma. Despite focussed antibiotics and one cycle of rituximab, the patient died a few weeks later
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