Fulminant post-transplant lymphoproliferative disorder presenting with lactic acidosis and acute liver failure.

Post-transplant lymphoproliferative disorder (PTLD) is the most common non-cutaneous malignancy in solid organ transplant recipients and is associated with significant mortality. In renal transplant recipients the incidence has been estimated to be between 0.2 and 2.3% [1,2]. Most PTLD is driven by Epstein–Barr virus (EBV) infection. The risk of lymphoma in transplant recipients is up to 40 times that of the general population [1]. A spectrum of severity is seen and this reflects the degree of additional oncogene activation and the associated transition from a polyclonal to a monoclonal disease [3]. Extra-nodal disease is common and as a consequence the presentation is often subtle and the diagnosis delayed. There are two principle risk factors for the development of PTLD: the intensity of immunosuppression and the EBV status of the donor and recipient. High dose immunosuppression with ciclosporin, tacrolimus, or anti-lymphocyte antibodies are all associated with increased risk [1]. EBV naı̈ve recipients receiving EBV positive grafts are at greatly increased risk [4,5]. Such patients acquire a primary infection in the context of high dose immunosuppression during the early posttransplant period when cytotoxic T-cell responses to EBV are undetectable [6]. This report describes a minimally immunosuppressed patient who developed PTLD very early in the posttransplant period. The clinical presentation was catastrophic and to the best of our knowledge has not been described before. Case