Cytomegalovirus reactivation following autologous peripheral blood stem cell transplantation for multiple myeloma in the era of novel chemotherapeutics and tandem transplantation.
Cytomegalovirus (CMV) is an important pathogen after allogeneic transplantation. However, few studies have examined CMV reactivation after autologous peripheral blood stem cell transplantation (APBSCT) to treat multiple myeloma (MM), especially in the setting of the newer chemotherapeutic agents and/or 2 sequential APBSCTs (ie, tandem transplantation). A retrospective chart review of patients with MM who underwent either single APBSCT or tandem transplantation was conducted to evaluate the incidence, risk factors, and outcomes of CMV infection at a single institution. A total of 104 patients with MM underwent transplantation during the study period, including 66 patients who received tandem transplantation. The majority of patients (66 of 104; 63.5%) were CMV-seropositive, and CMV viremia was frequently detected in this subgroup (32 of 66; 48.5%). No primary CMV infections were identified. CMV reactivation was more common in recipients of tandem transplantation than in recipients of single APBSCT (P < .001). In addition, patients who developed CMV viremia were more likely to have received conditioning therapy with melphalan, bortezomib, dexamethasone, and thalidomide compared with those without CMV reactivation (P = .015). However, on multiple logistic regression analysis, only receipt of tandem transplantation was significantly associated with CMV reactivation (odds ratio, 5.112; 95% confidence interval, 1.27-20.60; P = .022). Febrile episodes of CMV viremia were observed in 17 patients (17 of 32; 53.1%), and invasive CMV disease was diagnosed in 1 patient. Our data suggest that CMV reactivation after APBSCT for MM is relatively common, and that viremia is often associated with fever. CMV surveillance should be considered, especially when tandem transplantation is performed using combination chemotherapy with high-dose melphalan.
Division of Infectious Diseases, Department of Internal Medicine, University of Utah, Salt Lake City, Utah 84132, USA. jong.kim@hsc.utah.edu
Jong Hun
JH
Kim
Claudia
C
Goulston
Stephanie
S
Sanders
Mary
M
Lampas
Maurizio
M
Zangari
Guido
G
Tricot
Kimberly E
KE
Hanson
D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use; D001897:Boronic Acids / Q000627:therapeutic use; D000069286:Bortezomib; D003587:Cytomegalovirus / Q000187:drug effects / Q000502:physiology; D003586:Cytomegalovirus Infections / Q000188:drug therapy* / Q000209:etiology / Q000821:virology; D005260:Female; D006801:Humans; D008297:Male; D008558:Melphalan / Q000627:therapeutic use; D008875:Middle Aged; D009101:Multiple Myeloma / Q000276:immunology / Q000628:therapy*; D019653:Myeloablative Agonists / Q000627:therapeutic use*; D036102:Peripheral Blood Stem Cell Transplantation / Q000009:adverse effects / Q000379:methods* / Q000401:mortality; D011719:Pyrazines / Q000627:therapeutic use; D012189:Retrospective Studies; D012307:Risk Factors; D013792:Thalidomide / Q000627:therapeutic use; D019172:Transplantation Conditioning; D014182:Transplantation, Autologous; D019562:Viral Load / Q000187:drug effects; D014766:Viremia / Q000188:drug therapy* / Q000209:etiology / Q000821:virology; D014775:Virus Activation
D000998:Antiviral Agents; D001897:Boronic Acids; D019653:Myeloablative Agonists; D011719:Pyrazines; D013792:Thalidomide; D000069286:Bortezomib; D008558:Melphalan