METHODS: A total of 757 patients treated with PD-(L)1-Ab or PD-(L)1-Ab/TKI were evaluated for anti-thyroid antibodies (ATAs) at baseline and for thyroid function for 48 weeks after treatment initiation and then observed until the last visit.
RESULTS: The cumulative incidences of destructive thyroiditis [4/23 (17.4%) vs. 45/734 (6.1%) patients, p < 0.001], isolated hypothyroidism [10/23 (43.5%) vs. 29/734 (4.0%) patients, p < 0.001], and all thyroid dysfunction [14/23 (60.9%) vs. 74/734 (10.1%) patients, p < 0.001] were significantly higher in the PD-(L)1-Ab/TKI group than PD-(L)1-Ab group, respectively. All patients positive for ATAs at baseline developed thyroid dysfunction after PD-(L)1-Ab/TKI treatment, a significantly higher incidence than that in those negative for ATAs at baseline [4/4 (100%) vs. 10/19 (52.6%) patients, p = 0.026].
CONCLUSIONS: The addition of TKIs increased the risk of thyroid dysfunction induced by PD-(L)1-Ab, with the risk being higher in patients positive for baseline ATAs.
方法:总共757例接受PD-(L)1-Ab或PD-(L)1-Ab/TKI治疗的患者在基线时评估抗甲状腺抗体(ATAs),并在治疗开始后48周评估甲状腺功能,然后观察直至最后一次就诊。
结果:破坏性甲状腺炎的累积发病率[4/23(17.4%)与45/734(6.1%)患者,p<0.001],孤立性甲状腺功能减退症[10/23(43.5%)vs.29/734(4.0%)患者,p<0.001],和所有甲状腺功能障碍[14/23(60.9%)vs.74/734(10.1%)患者,p<0.001]在PD-(L)1-Ab/TKI组中显著高于PD-(L)1-Ab组,分别。基线时ATAs阳性的所有患者在PD-(L)1-Ab/TKI治疗后出现甲状腺功能障碍,在基线时,发病率明显高于ATAs阴性者[4/4(100%)与10/19(52.6%)患者,p=0.026]。
结论:添加TKI会增加PD-(L)1-Ab引起的甲状腺功能障碍的风险,基线ATAs阳性患者的风险更高。