Author:
Kobayashi Tomoko,Iwama Shintaro,Yamagami Ayana,Izuchi Tetsushi,Suzuki Koji,Otake Koki,Yasuda Yoshinori,Ando Masahiko,Onoue Takeshi,Miyata Takashi,Sugiyama Mariko,Hagiwara Daisuke,Suga Hidetaka,Banno Ryoichi,Hase Tetsunari,Nishio Naoki,Mori Shoichiro,Shimokata Tomoya,Sano Tomoyasu,Niimi Kaoru,Yoshikawa Nobuhisa,Akamatsu Shusuke,Ando Yuichi,Akiyama Masashi,Sone Michihiko,Ishii Makoto,Arima Hiroshi
Abstract
Abstract
Background
Anti-programmed cell death-1 (ligand-1) antibody [PD-(L)1-Ab] can cause destructive thyroiditis and/or hypothyroidism. In addition, tyrosine kinase inhibitors (TKIs) frequently induce hypothyroidism. The aim of this prospective study is to examine the incidence and clinical characteristics of thyroid dysfunction induced by combination therapy of a PD-(L)1-Ab and TKI [PD-(L)1-Ab/TKI].
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.
Publisher
Springer Science and Business Media LLC
Cited by
1 articles.
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