A rare neurological adverse event of palbociclib: a chronic inflammatory demyelinating polyneuropathy (CIDP) mimic
4 affiliations
- 1Department of Neurology, Henry Ford Health, Detroit, MI USA
- 2Wayne State University School of Medicine, Detroit, MI USA
- 3Department of Hematology/Oncology, Henry Ford Health, Detroit, MI USA
- 4Michigan State University, East Lansing, MI USA
Abstract
Purpose: Hormone receptor-positive (HR+)/human epidermal growth factor receptor 2-negative (HER2–) breast cancer accounts for approximately 65–70% of all breast cancer cases. First-line treatment for metastatic HR+/HER2– disease typically includes endocrine therapy combined with a CDK4/6 inhibitor, achieving progression-free survival (PFS) of 24–33 months with preserved quality of life. Although CDK4/6 inhibitors are generally well tolerated, they are associated with hematologic and gastrointestinal toxicities. We describe a patient who developed features of chronic immune-mediate polyradiculoneuropathy associated with neurofascin antibodies following initiation of palbociclib.
Methods: We conducted a detailed clinical review of a patient with metastatic HR+/HER2– breast cancer who developed progressive bilateral upper and lower extremity weakness after starting palbociclib. Clinical presentation, laboratory findings, imaging studies, electrodiagnostic testing, and treatment response were reviewed.
Results: A 43-year old female with metastatic HR+/HER2- breast cancer developed asymmetric progressive weakness and sensory symptoms approximately two weeks after initiating palbociclib. Electrodiagnostic testing demonstrated a mixed axonal and demyelinating sensorimotor polyneuropathy meeting EAN/PNS criteria for an acquired inflammatory demyelinating polyradiculoneuropathy. Initial diagnostic considerations included acute inflammatory demyelinating polyradiculoneuropathy (AIDP) and multifocal CIDP (formerly termed multifocal acquired demyelinating sensory and motor neuropathy [MADSAM]). Despite initial improvement following treatment with IVIG, the patient experienced continued neurologic progression requiring plasmapheresis, repeat IVIG, high-dose corticosteroids, and rituximab. Subsequent testing demonstrated anti-neurofascin-155 and anti-neurofascin-186 antibody positivity. Longitudinal follow-up demonstrated significant functional recovery following rituximab therapy.
Conclusion: This case suggests a possible association between palbociclib exposure and the development of chronic immune-mediate polyradiculoneuropathy associated with neurofascin antibodies. Clinicians should consider immune mediated neuropathies in patients receiving CDK4/6 inhibitor therapy who develop weakness, sensory deficits, and areflexia. Further investigation is warranted to better characterize potential immunologic effects of CDK4/6 inhibition and their relationship to autoimmune neurologic disease.
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BibTeX
@article{zeynoun2026rare,
title = {{A rare neurological adverse event of palbociclib: a chronic inflammatory demyelinating polyneuropathy (CIDP) mimic}},
author = {Joy Zeynoun and Madeline Evans and Kimberly Boldig and Haythem Ali},
journal = {Breast Cancer Research and Treatment},
year = {2026},
month = nov,
doi = {10.1007/s10549-026-08081-6},
url = {https://doi.org/10.1007/s10549-026-08081-6},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - A rare neurological adverse event of palbociclib: a chronic inflammatory demyelinating polyneuropathy (CIDP) mimic
AU - Joy Zeynoun
AU - Madeline Evans
AU - Kimberly Boldig
AU - Haythem Ali
PY - 2026
DA - 2026/11/04
JO - Breast Cancer Research and Treatment
DO - 10.1007/s10549-026-08081-6
UR - https://doi.org/10.1007/s10549-026-08081-6
AB - Purpose: Hormone receptor-positive (HR+)/human epidermal growth factor receptor 2-negative (HER2–) breast cancer accounts for approximately 65–70% of all breast cancer cases. First-line treatment for metastatic HR+/HER2– disease typically includes endocrine therapy combined with a CDK4/6 inhibitor, achieving progression-free survival (PFS) of 24–33 months with preserved quality of life. Although CDK4/6 inhibitors are generally well tolerated, they are associated with hematologic and gastrointestinal toxicities. We describe a patient who developed features of chronic immune-mediate polyradiculoneuropathy associated with neurofascin antibodies following initiation of palbociclib. Methods: We conducted a detailed clinical review of a patient with metastatic HR+/HER2– breast cancer who developed progressive bilateral upper and lower extremity weakness after starting palbociclib. Clinical presentation, laboratory findings, imaging studies, electrodiagnostic testing, and treatment response were reviewed. Results: A 43-year old female with metastatic HR+/HER2- breast cancer developed asymmetric progressive weakness and sensory symptoms approximately two weeks after initiating palbociclib. Electrodiagnostic testing demonstrated a mixed axonal and demyelinating sensorimotor polyneuropathy meeting EAN/PNS criteria for an acquired inflammatory demyelinating polyradiculoneuropathy. Initial diagnostic considerations included acute inflammatory demyelinating polyradiculoneuropathy (AIDP) and multifocal CIDP (formerly termed multifocal acquired demyelinating sensory and motor neuropathy [MADSAM]). Despite initial improvement following treatment with IVIG, the patient experienced continued neurologic progression requiring plasmapheresis, repeat IVIG, high-dose corticosteroids, and rituximab. Subsequent testing demonstrated anti-neurofascin-155 and anti-neurofascin-186 antibody positivity. Longitudinal follow-up demonstrated significant functional recovery following rituximab therapy. Conclusion: This case suggests a possible association between palbociclib exposure and the development of chronic immune-mediate polyradiculoneuropathy associated with neurofascin antibodies. Clinicians should consider immune mediated neuropathies in patients receiving CDK4/6 inhibitor therapy who develop weakness, sensory deficits, and areflexia. Further investigation is warranted to better characterize potential immunologic effects of CDK4/6 inhibition and their relationship to autoimmune neurologic disease.
SN - 0167-6806
SN - 1573-7217
ER -