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No other clinical abnormality was noted, except for recent weight loss. His biological data were normal. A computed tomography (CT) scan detected lymphadenopathies (left supraclavicular, left axillary and mesenteric), splenomegaly with nodules and a left kidney tumor. The bone marrow biopsy was normal. The 18 FDG PET image and SUV are presented in figure 1 . Left axillary lymphadenectomy revealed an NLPHL. Because of weight loss and disease diffusion, a splenectomy was performed to test for high-grade lymphoma transformation. The macroscopic examination revealed a 16.5 ! 10.5 ! 6.5-cm splenomegaly with two nodules. The performed histological and immunophenotypical analyses confirmed the diagnosis of diffuse large B cell lymphoma (DLBCL). The patient was treated by eight RCHOP cycles. Complete remission was still observed 42 months later. Nodular lymphocyte predominant Hodgkin’s lymphoma (NLPHL) has been clearly individualized from classic Hodgkin’s lymphoma [1] . In the absence of a bulky tumor, the outcome is favorable [2] . However, with a median follow-up time of 6.5 years, up to 14% of patients experience a high-grade non-Hodgkin’s lymphoma (NHL) transformation [3] . This event usually imposes a new biopsy that may be guided by 18 fluorodeoxyglucose positron emission tomography ( 18 FDG PET), which has been proposed to discriminate between lowgrade and high-grade NHL [4, 5] . Schoder et al. [4] showed that the standardized uptake value (SUV, fig. 1) was lower in indolent than in aggressive NHL: 7.0 8 3.1 and 19.6 8 9.3, respectively. The suggested cut-off value for the distinction between indolent and high-grade lymphoma, with 100% specificity, was 13, using a receiver operating characteristic (ROC) technique. In a large series of NLPHL, the median SUV was 6.1 (range, 1.2–20.1) [6] . No SUV data were available concerning an aggressive transformation. So we report, for the first time, two cases of NLPHL high-grade transformation with 18 FDG PET SUV data. First case: a 51-year-old man presented in April 2008 with a 10-year history of left axillary lymphadenopathy. Received: June 12, 2012 Accepted after revision: October 14, 2012 Published online: January 11, 2013

Thrombotic thrombocytopenic purpura (TTP) and hemolytic-uremic syndrome have recently been observed in patients undergoing interferon alpha (IFN-α) therapy. However, the relationship between disease and therapy has not been established, essentially because of concomitant treatment or previous bone marrow transplantation. We present a case of TTP developing during IFN-α therapy for chronic myelogenous leukemia. In this case, IFN-α seems to be the only etiological agent.