Vitamin D supplementation increases objective response rate and prolongs progression‐free time in patients with advanced melanoma undergoing anti–PD‐1 therapy

医学 维生素 内科学 黑色素瘤 彭布罗利珠单抗 无容量 胃肠病学 维生素D与神经学 免疫疗法 免疫系统 CD8型 癌症 肿瘤科 免疫学 癌症研究
作者
Łukasz Galus,Michał Michalak,Mateusz Lorenz,Renata Stoińska‐Swiniarek,Daria Tusień Małecka,Agnieszka Galus,Tomasz Kolenda,Ewa Leporowska,Jacek Mackiewicz
出处
期刊:Cancer [Wiley]
卷期号:129 (13): 2047-2055 被引量:24
标识
DOI:10.1002/cncr.34718
摘要

Vitamin D3 is a prohormone with pleiotropic effects, including modulating the functions of the immune system and may affect the effectiveness of anti-PD-1 treatment in patients with cancer. According to the literature, the potential mechanism of vitamin D's influence on the effectiveness of therapy is most likely related to the amount and activity of tumor-infiltrating lymphocytes. There are data showing the effect of vitamin D on cells regulating the activity of CD8 lymphocytes.A total of 200 patients with advanced melanoma were included in the study. All patients received anti-PD-1 immunotherapy (nivolumab or pembrolizumab) as first-line treatment. Serum vitamin D levels were measured in patients both before and every 12 weeks during treatment. Part of the group had vitamin D measured retrospectively from the preserved serum. The other part of the supplementation group was tested prospectively.The response rate in the group with low vitamin D levels and not supplemented was 36.2%, whereas in the group with normal baseline levels or a normal level obtained with supplementation was 56.0% (p = .01). Moreover, progression-free survival in these groups was 5.75 and 11.25 months, respectively (p = .03). In terms of overall survival, there was also a difference in favor of the group with normal vitamin D levels (27 vs. 31.5 months, respectively; p = .39).In our opinion, maintaining the vitamin D level within the normal range during anti-PD-1 immunotherapy in advanced melanoma patients should be a standard procedure allowing the improvement of treatment outcomes.
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