BMC neurology · 2026
Tyrosine kinase inhibitor-associated cerebral vasculopathy with a distinct non-enhancing vessel wall phenotype: a case report.
СтатьяНазвание и аннотация: Перевод в очереди
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Yang Jeong Eun, Jeon Jae Ho, Do Young Rok, Yun Jaeseob
Аннотация
BACKGROUND: Tyrosine kinase inhibitors (TKIs) are associated with adverse vascular events, including cerebrovascular stenosis. However, most reported cases rely on luminal imaging, and the arterial wall characteristics of TKI-associated vasculopathy remain insufficiently characterized.
CASE PRESENTATION: A 47-year-old man with chronic myeloid leukemia developed recurrent transient ischemic attacks during long-term exposure to multiple tyrosine kinase inhibitors, including sequential treatment with nilotinib and ponatinib. Neurovascular imaging revealed extensive multifocal steno-occlusive lesions involving both intracranial and extracranial arteries, accompanied by severe hemodynamic compromise. High-resolution vessel wall MRI demonstrated diffuse circumferential wall thickening with negative remodeling in both distal internal carotid arteries and eccentric thickening along the anterior walls of the bilateral M1 segments of the middle cerebral artery. Notably, no definite mural enhancement was observed. Following discontinuation of ponatinib and transition to alternative therapy, cerebral perfusion improved at two months, and the patient remained clinically stable without recurrent ischemic events.
CONCLUSIONS: This case illustrates a potentially distinct vessel wall thickening pattern in TKI-associated vasculopathy, providing information beyond luminal stenosis. The absence of definite mural enhancement and clinical and hemodynamic improvement after treatment modification suggest a drug-related vascular component. Vessel wall imaging may aid in the evaluation of this condition and inform management strategies.
CASE PRESENTATION: A 47-year-old man with chronic myeloid leukemia developed recurrent transient ischemic attacks during long-term exposure to multiple tyrosine kinase inhibitors, including sequential treatment with nilotinib and ponatinib. Neurovascular imaging revealed extensive multifocal steno-occlusive lesions involving both intracranial and extracranial arteries, accompanied by severe hemodynamic compromise. High-resolution vessel wall MRI demonstrated diffuse circumferential wall thickening with negative remodeling in both distal internal carotid arteries and eccentric thickening along the anterior walls of the bilateral M1 segments of the middle cerebral artery. Notably, no definite mural enhancement was observed. Following discontinuation of ponatinib and transition to alternative therapy, cerebral perfusion improved at two months, and the patient remained clinically stable without recurrent ischemic events.
CONCLUSIONS: This case illustrates a potentially distinct vessel wall thickening pattern in TKI-associated vasculopathy, providing information beyond luminal stenosis. The absence of definite mural enhancement and clinical and hemodynamic improvement after treatment modification suggest a drug-related vascular component. Vessel wall imaging may aid in the evaluation of this condition and inform management strategies.