A. Paviglianiti, Tânia Maia, Joël-Meyer Gozlan, E. Brissot, F. Malard, Anne Banet, Zoé Van de Wyngaert, T. Ledraa, R. Belhocine, S. Sestili, Antoine Capes, Nicolas Stocker, Agnès Bonnin, A. Vekhoff, Ollivier Legrand, M. Mohty, R. Duléry
{"title":"Human herpesvirus type 6 reactivation after haploidentical hematopoietic cell transplantation with post-transplant cyclophosphamide and antithymocyte globulin: risk factors and clinical impact","authors":"A. Paviglianiti, Tânia Maia, Joël-Meyer Gozlan, E. Brissot, F. Malard, Anne Banet, Zoé Van de Wyngaert, T. Ledraa, R. Belhocine, S. Sestili, Antoine Capes, Nicolas Stocker, Agnès Bonnin, A. Vekhoff, Ollivier Legrand, M. Mohty, R. Duléry","doi":"10.46989/001c.92525","DOIUrl":"https://doi.org/10.46989/001c.92525","url":null,"abstract":"Human herpesvirus type 6 (HHV6) reactivation after haploidentical hematopoietic cell transplantation (HCT) with post-transplant cyclophosphamide (PT-Cy) has been scarcely studied, especially when antithymocyte globulin (ATG) is added to the graft-versus-host disease (GvHD) prophylaxis. We conducted a retrospective cohort study in 100 consecutive patients receiving haploidentical HCT with PT-Cy. We systematically monitored HHV6 DNA loads in blood samples on a weekly basis using quantitative PCR until day +100. The 100-day cumulative incidence of HHV6 reactivation was 54%. Clinically significant HHV6 infections were rare (7%), associated with higher HHV6 DNA loads, and had favorable outcomes after antiviral therapy. The main risk factor for HHV6 reactivation was a low absolute lymphocyte count (ALC) < 290/µL on day +30 (68% versus 40%, p = 0.003). Adding ATG to PT-Cy did not increase the incidence of HHV6 reactivation (52% with ATG versus 79% without ATG, p = 0.12). Patients experiencing HHV6 reactivation demonstrated delayed platelet recovery (HR 1.81, 95% CI 1.07-3.05, p = 0.026), higher risk of acute grade II-IV GvHD (39% versus 9%, p < 0.001) but similar overall survival and non-relapse mortality to the other patients. In conclusion, our findings endorse the safety of combining ATG and PT-Cy in terms of the risk of HHV6 reactivation and infection in patients undergoing haploidentical HCT. Patients with a low ALC on day +30 face a higher risk of HHV6 reactivation and may require careful monitoring.","PeriodicalId":503947,"journal":{"name":"Clinical Hematology International","volume":"37 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139810022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Considerations for the treatment of frail multiple myeloma patients","authors":"M. Mohty, S. V. Rajkumar","doi":"10.46989/001c.92586","DOIUrl":"https://doi.org/10.46989/001c.92586","url":null,"abstract":"","PeriodicalId":503947,"journal":{"name":"Clinical Hematology International","volume":"739 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140476527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Celebrating five years of “Hematology without Borders” by the International Academy for Clinical Hematology (IACH)","authors":"M. Mohty, A. Nagler, Bipin P Savani","doi":"10.46989/001c.91538","DOIUrl":"https://doi.org/10.46989/001c.91538","url":null,"abstract":"","PeriodicalId":503947,"journal":{"name":"Clinical Hematology International","volume":"20 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139383958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
M. Rehman, Maha Hameed, Z. Shah, Omer S Ashruf, R. Ali, Fatima Faraz, J. Basit, Israr Khan, Faizan Fazal, Ahmad Iftikhar, A. Nashwan, Muhammad Salman Faisal, F. Anwer
{"title":"Incidence and Risk of Secondary Malignancy in Patients with Waldenström Macroglobulinemia: A Population-Based Analysis","authors":"M. Rehman, Maha Hameed, Z. Shah, Omer S Ashruf, R. Ali, Fatima Faraz, J. Basit, Israr Khan, Faizan Fazal, Ahmad Iftikhar, A. Nashwan, Muhammad Salman Faisal, F. Anwer","doi":"10.46989/001c.90436","DOIUrl":"https://doi.org/10.46989/001c.90436","url":null,"abstract":"Waldenström macroglobulinemia (WM) is a rare lymphoplasmacytic lymphoma which may predispose individuals to development of secondary malignancies (SMs). The Surveillance, Epidemiology, and End Results (SEER) database is a comprehensive registry of cancer patients in the United States reporting on a wide set of demographic variables. Using the SEER-18 dataset, analyzing patients from 2000 to 2018, we aimed to assess the incidence of SMs in WM patients. Patient characteristics such as gender, age, race, and latency were identified, and respective standardized incidence ratios (SIRs) and absolute excess risks (AERs) were calculated to compare to the general population. Of the 4,112 eligible WM patients identified, SMs were reported in 699 (17%) patients. The overall risk of developing SM, second primary malignancy, and secondary hematological malignancy was significantly higher in WM patients compared to the general population. Our findings show that WM patients had a 53% higher risk of SMs relative to the general population, and an AER of 102.69 per 10,000. Although the exact mechanism is unclear, the risk of SM development may be due to genetic predisposition, immune dysregulation, or treatment-induced immune suppression.","PeriodicalId":503947,"journal":{"name":"Clinical Hematology International","volume":"2 2","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139383971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}