Summary. We determined the hepatitis C virus (HCV) antibodies (anti-HCV) and the hepatitis B virus (HBV) surface antigen (HBsAg) in a cohort of 68 consecutive non-Hodgkin's lymphoma (NHL) patients diagnosed and treated in our institution between December 1997 and March 1999. 27 cases were diagnosed as low-grade, 33 as intermediate-grade, and eight as high-grade NHL. In 35 cases (51´4%) we found evidence of either HCV or HBV infection. Anti-HCV antibodies were found in 20 patients (29´5%) and HBsAg was found in 21 patients (30´8%). In six patients both anti-HCV and HBsAg were present. Anti-HCV were present in 12/27 low-grade NHL cases (44´4%) and in 8/41 intermediate/high-grade (aggressive) NHL cases (19´5%, P < 0´03). HBsAg was found in 10/27 low-grade NHL cases (37%) and in 11/41 aggressive NHL cases (26´8%). Evidence of liver disease, as re¯ected by elevated aminotransferases or typical alterations at liver biopsy, was present in eight patients. Cryoglobulins were present in six patients, all anti-HCV positive and with low-grade NHL. The prevalence of both HCV antibodies and HBsAg was signi®cantly higher (P < 0´0001) in our NHL cases than in a sample of the general Romanian population, where the prevalence of anti-HCV was 4´9% and that of HBsAg was 6´3%. It is dif®cult to say whether either HCV or HBV had actually been involved in lymphomagenesis or if a-interferon treatment would be effective in this subset of patients.

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Large granular lymphocytic leukemia (LGLL) is a rare lymphoproliferative disorder of transformed natural killer or T-cells attributed to chronic exposure to the proinflammatory cytokine IL-15. Diagnosis of the majority of T-cell LGLL is established by documenting clonal large granular lymphocytes (LGLs) in peripheral blood, by morphology and immunophenotype. The proteasome inhibitor bortezomib is known to target molecular pathways downstream of the IL-15 receptor signaling and has been proposed as a therapy in these patients. We report an uncommon presentation of LGLL with chronic neutropenia lacking typical blood LGLs, which failed to respond to bortezomib but obtained a very good partial remission with a classical methotrexate regimen.

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The coexistence of both myeloproliferative and lymphoproliferative neoplasms in the same patient is an uncommon finding. We report two patients who presented such an association. The first patient was initially diagnosed with essential thrombocythemia, developing a clinical and haematological picture consistent with chronic lymphocytic leukaemia several years afterwards. The second patient was diagnosed concomitantly with polycythaemia vera and chronic lymphocytic leukaemia. Both patients were positive for the JAK2 V617F mutation. In the first patient the chronic lymphocytic leukaemia was asymptomatic, stage A, and did not require any additional treatment, while the second patient presented with generalized large lymphadenopathy (stage B) and chronic lymphocytic leukaemia-related symptoms, requiring chronic lymphocytic leukaemia-directed treatment. It is unclear whether there is a pathogenetic link between the myeloproliferative and lymphoproliferative diseases encountered in these patients, both being probably the result of random mutations occurring in distinct initiating cells. However, given the higher risk of lymphoproliferative neoplasms development in myeloproliferative neoplasms patients reported in larger studies, the genomic instability characteristic to myeloproliferative neoplasms may play a role in subsequent lymphoproliferative neoplasms occurrence.

Morphological and immuno-flow cytometry assisted analysis of peripheral blood and bone marrow are mandatory investigations in the diagnosis