Cytomegalovirus reactivation after bortezomib treatment for multiple myeloma and light chain amyloidosis. (10th January 2020)

• Record Type: Journal Article
• Authors: Sharpley, Faye A; De‐Silva, Dunnya; Mahmood, Shameem; Sachchithanantham, Sajitha; Ramsay, Isobel; Garcia Mingo, Ana; Worthington, Sarah; Hughes, Derralynn; Mehta, Atul; Kyriakou, Charalampian; Griffiths, Paul D.; Wechalekar, Ashutosh D.
• Is Part Of: European journal of haematology. Volume 104:Number 3(2020)
• Page Start: 230
• Page End: 235
• Publication Date: 2020-01-10
• Subjects: immunology and infectious diseases -- multiple myeloma; Hematology -- Periodicals; Blood -- Diseases -- Periodicals; Blood -- Periodicals; 616.15005
• DOI: 10.1111/ejh.13366
• Languages: English
• ISSNs: 0902-4441

Abstract

Abstract: Objective: Cytomegalovirus (CMV) is an opportunistic herpesvirus, and reactivation of infection is possible in immunocompromised patients. Historically, the risk for haematology patients is restricted to those treated with an allogeneic transplant or T‐cell depleting agents. Bortezomib is a highly efficacious proteasome inhibitor widely used to treat multiple myeloma and light chain (AL) amyloidosis patients. The objective of this small prospective study was to quantify the risk of CMV reactivation associated with bortezomib treatment. Methods: Fifty‐seven consecutive multiple myeloma or AL amyloidosis patients commencing bortezomib‐based therapy were included. Viral copy numbers were established at baseline and then at fortnightly intervals during treatment. Pre‐emptive anti‐viral treatment was initiated in patients with a viral load >7500 copies/mL. Results: Reactivation of CMV was detected in 39% (n = 12/31) of seropositive bortezomib treated patients compared with 0% of CMV seronegative patients. Detectable DNAemia developed during the first two cycles of treatment in 83% (n = 10/12) patients. Anti‐viral treatment was initiated in 42% (n = 5/12), but no cases of active CMV disease were seen. Conclusion: This study suggests that there is a substantial risk of CMV reactivation in CMV‐seropositive plasma cell dyscrasia patients treated with bortezomib.