demonstrated in AITL samples, these may not actually be the precursors to the subsequent DLBCLs these patients develop. Several clonal B-cell populations may develop during the course of the disease, and these may be transient, with many disappearing subsequently. Hence, when a proportion of AITL patients subsequently develop a full-blown DLBCL or EBV- cHL, one may or may not be able to establish clonal ancestry to ‘precursor’ cells seen in an earlier biopsy. K. N. Naresh 1 L. P. Menasce 2 P. Shenjere 2 S. S. Banerjee 2 1 Department of Histopathology, Hammersmith Hospital and Imperial College, London, and 2 Christie Hospital, Manchester, UK. E-mail: k.naresh@imperial.ac.uk References Attygalle, A.D., Chuang, S.S., Diss, T.C., Du, M.Q., Isaacson, P.G. & Dogan, A. (2007a) Distinguishing angioimmunoblastic T-cell lym- phoma from peripheral T-cell lymphoma, unspecified, using mor- phology, immunophenotype and molecular genetics. Histopathology, 50, 498–508. Attygalle, A.D., Kyriakou, C., Dupuis, J., Grogg, K.L., Diss, T.C., Wotherspoon, A.C., Chuang, S.S., Cabec ¸adas, J., Isaacson, P.G., Du, M.Q., Gaulard, P. & Dogan, A. (2007b) Histologic evolution of angioimmunoblastic T-cell lymphoma in consecutive biopsies: clinical correlation and insights in to natural history and disease progression. American Journal of Surgical Pathology, 31, 1077–1088. Browne, P., Petrosyan, K., Hernandez, A. & Chan, J.A. (2003) The B-cell transcription factors BSAP, Oct-2, and BOB.1 and the pan-B- cell markers CD20, CD22, and CD79a are useful in the differential diagnosis of classic Hodgkin lymphoma. American Journal of Clinical Pathology, 120, 767–777. Quintanilla-Martinez, L., Fend, F., Moguel, L.R., Spilove, L., Beaty, M.W., Kingma, D.W., Raffeld, M. & Jaffe, E.S. (1999) Peripheral T-cell lymphoma with Reed-Sternberg-like cells of B-cell phenotype and genotype associated with Epstein-Barr virus infection. American Journal of Surgical Pathology, 23, 1233–1240. Ranganathan, S., Webber, S., Ahuja, S. & Jaffe, R. (2004) Hodgkin-like posttransplant lymphoproliferative disorder in children: does it differ from posttransplant Hodgkin lymphoma? Pediatric and Developmental Pathology, 7, 348–360. Tzankov, A., Bourgau, C., Kaiser, A., Zimpfer, A., Maurer, R., Pileri, S.A., Went, P. & Dirnhofer, S. (2005) Rare expression of T-cell markers in classical Hodgkin’s lymphoma. Modern Pathology, 18, 1542–1549. Willenbrock, K., Brauninger, A. & Hansmann, M.L. (2007) Frequent occurrence of B-cell lymphomas in angioimmunoblastic T-cell lymphoma and proliferation of Epstein-Barr virus-infected cells in early cases. British Journal Haematology, 138, 733–739. Keywords: lymphomas, lymphoid malignancies, Epstein–Barr virus. doi:10.1111/j.1365-2141.2008.07004.x Clinical effectiveness of decitabine in severe sickle cell disease The haemolytic anaemia in sickle cell disease (SCD) may be exacerbated acutely and chronically by aplastic crises, splenic or hepatic sequestration, folate or iron deficiency, erythropoi- etin deficiency, bone marrow scarring, delayed haemolytic transfusion reactions, autoimmune haemolysis or hyper- haemolysis of unknown aetiology. Progressive and acute anaemia exacerbations can be life-threatening and standard management options, such as transfusion, hydroxycarbamide and erythropoietin therapy may fail to rescue patients from clinical decline and early death. The DNA hypomethylating agent 5-aza-2’-deoxycytidine (decitabine) has been studied as a potential disease modifying agent for SCD. In phase I/II studies, decitabine produced clinically significant increases in total and fetal haemoglobin (HbF) and improvements in a range of surrogate clinical end-points (Koshy et al, 2000; DeSimone et al, 2002; Saun- thararajah et al, 2003). However, relatively short-term drug administration limited the ability to measure definitive clinical improvement. We describe the outcomes of decitabine treat- ment for four patients with deteriorating clinical courses and severe illness despite maximized standard of care. The severe clinical status and trends prior to decitabine initiation and the duration of follow-up enabled persuasive documentation of clinical improvement. Decitabine is approved by the US Food and Drug Admin- istration for the treatment of myelodysplastic syndrome. Therefore, decitabine administration in SCD is ‘off-label’. The off-label prescription was to provide direct benefit to these patients and not for research. Decitabine was considered because of clinical deterioration and life-threatening compli- cations despite hydroxycarbamide therapy, erythropoietin for relative reticulocytopenia (haemoglobin <90 g/l, reticulocytes £250 · 10 9 /l), decreased availability and increased transfusion risks from ‡5 red blood cell (RBC) allo-antibodies and autoantibodies, and ineligibility for available protocol therapy. The rationale for decitabine use and its potential risks were discussed with patients and family members with appropriate documentation in the medical chart. Females of child-bearing Correspondence ª 2008 The Authors 126 Journal Compilation ª 2008 Blackwell Publishing Ltd, British Journal of Haematology, 141, 120–131