Summary De novo diffuse large B‐cell lymphoma (DLBCL) presenting with synchronous central nervous system (CNS) and systemic disease (synDLBCL) is not well described and is excluded from clinical trials. We performed a retrospective analysis of 80 synDLBCL patients treated across 10 Australian and UK centres. Of these patients, 96% had extranodal systemic disease. CNS‐directed treatment with combination intravenous cytarabine and high‐dose methotrexate (“CNS‐intensive”) (n = 38) was associated with favourable survival outcomes compared with “CNS‐conservative” strategies such as intravenous high‐dose methotrexate monotherapy, intrathecal therapy and/or radiotherapy (2‐year progression‐free survival [PFS] 50% vs. 31%, P = 0·006; 2‐year overall survival [OS] 54% vs. 44%, P = 0·037). Outcomes were primarily dictated by the ability to control the CNS disease, with 2‐year cumulative CNS relapse incidence of 42% and non‐CNS relapse 21%. Two‐year OS for CNS‐relapse patients was 13% vs. 36% for non‐CNS relapses (P = 0·02). Autologous stem cell transplantation as consolidation (n = 14) was not observed to improve survival in those patients who received CNS‐intensive induction when matched for induction outcomes (2‐year PFS 69% vs. 56%, P = 0·99; 2‐year OS 66% vs. 56%, P = 0·98). Hyperfractionated or infusional systemic treatment did not improve survival compared to R‐CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) (2‐year OS 49% for both groups). Our study suggests that adequate control of the CNS disease is paramount and is best achieved by intensive CNS‐directed induction.

Cytomegalovirus (CMV) infection has been associated with higher overall and non-relapse mortality after allogeneic haematopoietic stem cell transplant (HSCT) and remains an important risk factor for poor outcomes. 1,2 The majority of patients with CMV infection following allogeneic HSCT have infection of latent virus, rather than primary infection, and the strongest risk factor is positive recipient serostatus. 3,4 Other established risk factors include a seropositive donor, umbilical cord blood donor, haploidentical donor, T-cell depletion, graft-versus-host-disease (GVHD), steroid use, and delayed Tcell recovery. 3,5,6 Potential mechanisms for the detrimental effect of CMV infection on patient outcomes include increased co-infections, organ failure (from CMV or side effects of anti-viral treatment) and graft-versus-host disease. 1 CMV infection should be distinguished from CMV disease, which in allogeneic HSCT recipients can affect almost any organ and has a high mortality. 5 In the era of sensitive, accurate and rapid viral load monitoring by quantitative polymerase chain reaction (qPCR), many centres have adopted a strategy of pre-emptive treatment in response to a rising viral load in order to prevent CMV disease. Unlike universal antiviral prophylaxis, this avoids exposing patients who do not have CMV infection to the toxicity of anti-viral medications. Initial viral load, viral load doubling time and peak viral load are

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