Please use this identifier to cite or link to this item: https://doi.org/10.1080/15384047.2016.1178427
Title: Bortezomib-related neuropathy may mask CNS relapse in multiple myeloma: A call for diligence
Authors: Abid, Muhammad Bilal
De Mel, Sanjay
Abid, Muhammad Abbas
Tan, Kong Bing
Chng, Wee Joo 
Keywords: Science & Technology
Life Sciences & Biomedicine
Oncology
Autologous stem cell transplantation (ASCT)
bortezomib (velcade)
bortezomib-induced peripheral neuropathy (BIPN)
immunomodulator (IMID)
multiple myeloma (MM)
proteasome inhibitors (PI)
CENTRAL-NERVOUS-SYSTEM
STEM-CELL TRANSPLANTATION
LONG-TERM SURVIVAL
PERIPHERAL NEUROPATHY
CHROMOSOMAL-ABNORMALITIES
INVOLVEMENT
POMALIDOMIDE
ASSOCIATION
IMPROVEMENT
THERAPY
Issue Date: 1-Jan-2016
Publisher: TAYLOR & FRANCIS INC
Citation: Abid, Muhammad Bilal, De Mel, Sanjay, Abid, Muhammad Abbas, Tan, Kong Bing, Chng, Wee Joo (2016-01-01). Bortezomib-related neuropathy may mask CNS relapse in multiple myeloma: A call for diligence. CANCER BIOLOGY & THERAPY 17 (7) : 723-726. ScholarBank@NUS Repository. https://doi.org/10.1080/15384047.2016.1178427
Abstract: Neuropathy is a common adverse effect of bortezomib. Isolated central nervous system (CNS) relapse in MM remains exceedingly rare and carries a dismal prognosis. We present an unusual case of bortezomib related neuropathy masking a CNS relapse of MM. Case presentation: A 57-year-old female was diagnosed with standard-risk MM with clinical and cytogenetic features not typically associated with CNS involvement. She was treated with 4 cycles of bortezomib/cyclophosphamide/dexamethasone (VCD) and achieved a VGPR, after which she underwent an autologous stem cell transplant (ASCT) followed by bortezomib maintenance. Six months after ASCT she developed symptoms suggestive of peripheral neuropathy which was attributed to bortezomib. However the symptoms persisted despite discontinuation of bortezomib. Imaging and cerebrospinal fluid analysis subsequently confirmed a CNS relapse. Discussion: CNS involvement in MM (CNS-MM) is uncommon and is considered an aggressive disease. Recently published literature has reported biomarkers with prognostic potential. However, isolated CNS relapse is even less common; an event which carries a very poor prognosis. Given the heterogeneous neurologic manifestations associated with MM, clinical suspicion may be masked by confounding factors such as bortezomib-based therapy. The disease may further remain incognito if the patient does not exhibit any of the high risk features and biomarkers associated with CNS involvement. Conclusion: In the era of proteasome inhibitor (PtdIns)/immunomodulator (IMID)-based therapy for MM which carries neurologic adverse effects, it is prudent to consider CNS relapse early. This case further highlights the need for more robust biomarkers to predict CNS relapse and use of newer novel agents which demonstrate potential for CNS penetration.
Source Title: CANCER BIOLOGY & THERAPY
URI: https://scholarbank.nus.edu.sg/handle/10635/229037
ISSN: 15384047
15558576
DOI: 10.1080/15384047.2016.1178427
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