Ultrasound arterial anomalies in patients exposed to nilotinib therapy for chronic myeloid leukemia.
Adult
Aged
Antineoplastic Agents
/ adverse effects
Female
France
/ epidemiology
Humans
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
/ drug therapy
Male
Middle Aged
Predictive Value of Tests
Prevalence
Protein Kinase Inhibitors
/ adverse effects
Pyrimidines
/ adverse effects
Retrospective Studies
Risk Assessment
Risk Factors
Treatment Outcome
Ultrasonography
Vascular Diseases
/ chemically induced
Chronic myeloid leukemia
Nilotinib
Ultrasound arterial anomalies
Journal
Journal de medecine vasculaire
ISSN: 2542-4513
Titre abrégé: J Med Vasc
Pays: France
ID NLM: 101709200
Informations de publication
Date de publication:
Apr 2021
Apr 2021
Historique:
received:
25
06
2020
accepted:
06
02
2021
entrez:
23
3
2021
pubmed:
24
3
2021
medline:
8
7
2021
Statut:
ppublish
Résumé
Patients exposed to nilotinib for chronic myeloid leukemia (CML) appear to be at risk of arterial complication. The prevalence and aspect of ultrasound asymptomatic arterial lesions are unknown. To describe prevalence and characteristics of ultrasound arterial anomalies in patients treated with nilotinib for CML. Patients treated with nilotinib from 2006 to 2015 in the department of the Paoli-Calmettes Institute, Marseille, were included retrospectively. A vascular ultrasound screening was carried out from 2010. The arterial lesions at the first examination were described: plaque and its echogenicity, stenosis or occlusion. A vascular arterial anomaly (VAA) was defined by the presence of a clinical and/or ultrasound anomaly. Patients with or without VAA at initial vascular examination were compared using bivariate and multivariate analysis. 74 patients were included (51.4% men, mean age 54.5 years); 25 patients had ultrasound arterial anomalies (33.8%). Carotid bulb was the most involved territory (44%). Arterial anomalies were: 88% plaques, 44%>50% stenosis and 12% occlusion. 72.7% plaques were echolucent or hypoechogenic. A VAA was present in 25 patients with initial vascular evaluation (33.8%). Patients with VAA at baseline were significantly older (64.9 vs 49.3, P<0.001), older at nilotinib initiation (60.8 vs 46.5, P<0.001), with more arterial hypertension (40% vs 12.2%, P=0.01), with more cardiovascular risk factors (P=0.03). In patient with no cardiovascular risk factor 12.5% had VAA (n=24). Nilotinib seems to be associated to arterial lesions of unstable lipid-like appearance. The most involved arterial territory was the carotid bulb and the most common lesion was echolucent or hypoechogenic plaque. VAA can occur in patients without cardiovascular risk factors. This result encourages us to systematically screen and follow all patients exposed to nilotinib even those without cardiovascular risk factors.
Identifiants
pubmed: 33752848
pii: S2542-4513(21)00026-2
doi: 10.1016/j.jdmv.2021.02.002
pii:
doi:
Substances chimiques
Antineoplastic Agents
0
Protein Kinase Inhibitors
0
Pyrimidines
0
nilotinib
F41401512X
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
66-71Informations de copyright
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