Background: Vitiligo-like leukoderma is being increasingly reported in patients with breast cancer treated with cyclin-dependent kinase 4 and 6 (CDK4/6) inhibitors.
Objective: The aim of the study was to systematically review the characteristics of CDK4/6 inhibitor-induced vitiligo-like leukoderma.
Methods: A comprehensive literature search was conducted to identify published cases of vitiligo-like leukoderma following CDK4/6 inhibitor therapy administered for advanced breast cancer. Three additional cases from our tertiary vitiligo clinic are reported.
Results: Thirteen publications met the inclusion criteria, for a study population of 62 patients, including the 3 newly reported patients attending our vitiligo clinic. All patients were female; median age was 61 years (range 39 to 87 years). Ribociclib was the CDK4/6 inhibitor most frequently associated with vitiligo-like leukoderma, in 75.8% of cases. The condition predominantly affected sun-exposed areas (87.8%) and caused symptoms such as intense pruritus in 63.6% of cases. Despite multiple treatment methods, 55.7% of the patients showed no repigmentation. CDK4/6 inhibitor therapy was discontinued in 13 patients (20.1%) for various reasons, including vitiligo-like leukoderma; however, cessation did not improve the outcome. Most studies lacked data on progression-free survival.
Conclusion: CDK4/6-inhibitor-induced vitiligo-like leukoderma has distinct clinical characteristics compared to classic vitiligo and is mostly recalcitrant to treatment. Stopping CDK4/6 inhibitors does not alleviate or improve the condition. Further research is essential to elucidate its prognostic significance.
© The Author(s) 2025. Published by Oxford University Press on behalf of British Association of Dermatologists. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.