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Hematopoietic stem cell transplant (HSCT) recipients are at an increased risk of bacterial, viral, fungal and parasitic infections. Past exposures to infections, the degree of immunosuppression, prolonged neutropenia and presence of graft versus host disease (GVHD) are some of the factors which make HSCT recipients more susceptible to infections. Viral infections have emerged as a major challenge causing high morbidity and mortality in stem cell transplant recipients. Myeloablative conditioning regimens and GVHD prevention strategies which may delay immune reconstitution and serologic status of donors and recipients affect the incidence of viral infections. Community-acquired respiratory and gastrointestinal viral infections like respiratory syncytial virus (RSV), rhinovirus, adenovirus, influenza, norovirus and reactivation of latent viruses like herpes simplex virus (HSV), cytomegalovirus (CMV) are some of the important pathogens increasing the morbidity and mortality in transplant recipients. Clinical manifestations range from asymptomatic carriage to severe disease. Due to lack of effective agents to treat viral infections and emerging resistance patterns, preventive and prophylactic strategies are valuable. Our review article provides an overview of commonly encountered viral infections and their management in an allogeneic stem cell transplant setting in the adult age group. KeywordsViral infections; allogeneic stem cell transplants; hematopoietic stem cell transplants IntroductionViral infections can be asymptomatic or subclinical or even lead to severe disease in allogeneic HSCT recipients. Viral diseases of importance in HSCT include herpes simplex virus (HSV), varicellazoster virus (VZV), human herpesvirus 6 (HHV-6), cytomegalovirus (CMV), Epstein-Barr virus (EBV) and respiratory viruses (eg, respiratory syncytial virus, adenovirus, influenza, parainfluenza). Most of these viral infections are opportunistic in nature and are related to factors influencing engraftment and immune reconstitution [1]. Increase in HLA mismatched donor allogeneic transplants and using anti-thymocyte globulin (ATG) for GVHD prevention are few factors which predispose recipients to viral infections [2,3]. Fortunately, based on molecular diagnostic methods, a polymerase chain reaction can offer an early diagnosis of these infections [4,5]. Early diagnosis facilitates timely intervention controlling infection associated complications. Many prophylactic and pre-emptive treatment strategies are also aimed at decreasing viral infection-related complications [6]. Immunotherapy to restore virus-specific immunity are proven to be effective in treating CMV, EBV and adenovirus infections [7]. In our review article, we have made an attempt to discuss risk factors for post-HSCT viral infections, preventive strategies and treatment options. Risk Factors for Viral Infections Source of Stem CellsPeripheral blood stem cells achieve faster hematopoietic and immune reconstitution compared to bone marrow and cord blood source. Hence, this is asso...

Hodgkin lymphoma (HL) is a lymphoid neoplasm characterized by malignant lymphocytes, known as Reed-Sternberg cells, on a background of non-neoplastic inflammatory cells. Lugano staging determines the stage of Hodgkin lymphoma, which, in turn, determines the treatment and prognosis. Limited-stage disease is defined as Stage I and Stage II, which is diagnosed in more than 50% of patients. Pre-treatment risk stratification, PET-adapted therapy, and combined modality treatment have significantly improved cure rates, making limited-stage HL one of the most curable malignancies. In this article, we discuss the current approach to managing limited-stage HL.

Plasmablastic lymphoma is a rare subtype of large B-cell lymphoma characterised by an aggressive clinical course with frequent relapses and refractoriness to chemotherapy. It is usually associated with HIV, however, it can also be seen in immunocompetent patients. It has distinct pathological characteristics, such as plasmablastic morphology and lack of CD20 expression. These characteristics pose a clinical and pathological challenge. There is no standard of care established in this entity. In this case report, we described a novel bortezomib-based plasma cell targeted regimen in a HIV-negative patient refractory to chemotherapy.

Introduction: MM remains incurable but therapeutic advances has resulted in improved overall survival (OS) particularly for younger pts who are eligible for ASCT. Regardless OS improvements have been heterogeneous and it is well known that relapse within one year of ASCT is an independent negative prognostic factor. A particularly worse subgroup is pts who relapse and die of MM within a year of ASCT. There is limited data describing this subgroup of pts, the risk factors associated with their early relapse post ASCT and characteristics at relapse. Objective: Describe patient and disease related characteristics among MM pts who underwent ASCT and died of relapsed MM within the first year post ASCT in the era of novel agents. Methods: Pts were identified from the Leukemia/BMT Program of B.C. database, underwent ASCT between January 1st 2007 and July 31st 2016 and died of MM related causes within 365 days post ASCT. During this time period bortezomib (BORT) and lenalidomide (LEN) were available as second line therapy and BORT was available as induction pre-transplant for defined circumstances including high risk cytogenetics. Out of 752 ASCTs, 702 were performed as a part of initial therapy. The remaining ASCTs were performed as salvage or were the second of planned tandem ASCTs. Among the remaining 702 pts 37(5.3%) died within the first 365 days post ASCT. Of the 37 pts, 32 died from MM and related causes, 2 died of TRM from ASCT and 3 died from other causes not related to MM or ASCT. The 32 pts (4.6% of the total) who died of MM and related causes were matched with 64 controls (2:1 ratio) who were selected randomly from the remaining patient cohort and matched for age, gender, and year of transplantation. Results: There was no difference in Age at diagnosis (Median: case 61 VS control 60, P= .97) or gender (Male case 40.6% VS control 35.9%, P= .66). There was no significant difference in the prevalence of anemia, renal dysfunction, or hypercalcemia between both groups at diagnosis (table). Pts who died within the first year of ASCT had a more advanced stage at diagnosis compared to the control group (ISS Stage III: 53.1% vs 18.8%, P= .003). BORT based induction therapy was used in 84.4% of the cases compared to 53.1% in the control group, P= .001. The majority of pts in both groups had partial response or better to frontline therapy (Cases: 81.2% VS Controls 79.7%, P= .5). Only 9.4% of cases and 4.7% of controls had evidence of disease progression at the time of ASCT. High risk cytogenetics (t(4;14), t(14;16), or del 17p) were significantly more prevalent among pts who died within the first year post ASCT compared to the control (58.82% vs 31.67%, P= .009). There was no difference in the monoclonal protein subtype between the cases and controls, P= .55. The median time from ACST to disease relapse was 118 days (40-319) for the case group compared to 511 (107-1958) in the control group. Within the case group, 19 (59.3%) received LEN based therapy as second line therapy and 9 (28.1%) received BORT based therapy. Three patients (9.37%) were not candidates for any further therapy due to acute illness (2 sepsis, 1 subdural hemorrhage) related to fulminant MM relapse and one patient (3.1%) decided not to proceed with therapy due to functional decline. Overall, 17 pts (53.1%) received both BORT and LEN during the disease course, 12 (37.5%) received BORT only, 2 (6.25%) received LEN only and one received neither (3.1%). At the time of disease relapse, 9 (28.1%) had Hb level <85 g/l, 1 (3.1%) ANC<1000/mm3, 9 (28.1%) Plt <50/mm3, 9 (28.1%) GFR <20 ml/min, and 20 (62.5%) had at least one abnormal value (Hb, ANC, Plt, or Cr) and were not candidates for inclusion to clinical trials. Median OS (months) was Case 7.3 vs Control 63.8, P<.001. Conclusion: Approximately 5% of pts with MM who are ASCT eligible will die of MM within the first year post transplant. High risk cytogenetics (t(4;14), t(14;16), or del 17p) and advanced stage disease (ISS III) are risk factors for early mortality post ASCT for MM pts. These patient who relapse early typically have fulminant relapse with hematological and biochemical parameters outside of the range which would allow them to be enrolled on clinical trials and/or results in challenging standard of care management. Even in the era of novel agents, such pts do particularly poorly and represent a true unmet need in the treatment of MM. Further studies to understand the biology of their MM is required for identifying more potent therapeutic targets and protocols. Disclosures No relevant conflicts of interest to declare.