Nilotinib-Induced Dystonia and Cognitive Deficits in a Neurologically Normal Patient with Chronic Myeloid Leukemia
Justine Chan1, Paarth Shah1, Guillermo Moguel-Cobos1
1Department of Neurology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ, USA.
Abstract:
Nilotinib is a tyrosine kinase inhibitor used to treat patients with chronic myeloid leukemia (CML). This agent is also being studied in neurodegenerative disorders including Parkinson disease. Studies have shown that nilotinib may decrease the accumulation of parkin substrates and decrease the loss of dopaminergic cells. The use of nilotinib in neurologic disorders is relatively new, and little information about this use has been published. We report on a patient receiving nilotinib for CML. The patient had no previous neurologic deficits, and developed intermittent dystonic posturing of the left upper extremity and cognitive impairment after she began nilotinib treatment. The mechanisms behind this adverse effect are not clear; however, her symptoms began after nilotinib was introduced, decreased with dose reduction, stopped with its cessation, and re-emerged when the medication was restarted. To our knowledge, this is the first reported patient with neurologic symptoms secondary to nilotinib use.
Insights
Nilotinib, used for chronic myeloid leukemia (CML), may cause new neurologic symptoms like dystonia and cognitive issues. This report details the first patient experiencing these adverse effects, which resolved upon medication cessation.
Area of Science:
- Pharmacology
- Neurology
- Oncology
Background:
- Nilotinib is a tyrosine kinase inhibitor approved for chronic myeloid leukemia (CML).
- Emerging research suggests nilotinib's potential in neurodegenerative disorders like Parkinson's disease.
- Its use in neurological conditions is novel, with limited published data.
Observation:
- A patient with CML on nilotinib treatment developed new-onset neurological symptoms.
- The patient experienced intermittent dystonic posturing in the left upper extremity and cognitive impairment.
- These symptoms emerged after initiating nilotinib, improved with dose reduction, and reappeared upon re-administration.
Findings:
- This case report details the first instance of neurological symptoms potentially secondary to nilotinib use.
- The temporal relationship between nilotinib administration and symptom onset/resolution suggests a causal link.
- The underlying mechanisms for these nilotinib-induced neurological adverse effects remain unclear.
Implications:
- This case highlights the need for vigilance regarding potential neurological adverse effects of nilotinib, even in patients treated for CML.
- Further research is warranted to elucidate the mechanisms of nilotinib-induced neurotoxicity.
- Clinicians should consider nilotinib as a potential cause of new-onset neurological symptoms in patients.
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