Abstract
Thyroid disorders have emerged as one of the most common immune-related adverse events (irAEs) associated with immune checkpoint inhibitors (ICI) therapy, yet optimum management and biomarkers to predict vulnerable individuals remain unknown. High dose glucocorticoid (HDG) therapy is routinely recommended for irAEs. However, systemic analysis of the impact of glucocorticoid therapy on the outcome of ICI-induced thyroid disorders is lacking. Our study analyzed presentation of thyroid disorders caused by different ICIs and examined the effects of systemic HDG treatment on the outcome of thyroid disorders. We analyzed 151 patients with or without ICI-related thyroid disorders. We divided the patients with ICI-related thyroid disorders into two subgroups: HDG and no HDG treatment. We evaluated the effects of HDG on the duration of thyrotoxicosis, the converting time from thyrotoxicosis to hypothyroidism, the onset time of hypothyroidism, and maintenance dose of levothyroxine. We explored the association of baseline TSH level with ICI-related thyroid disorders. Our results showed there were no significant differences between HDG and no HDG groups in terms of the median duration of thyrotoxicosis: 28 (range: 7-85) and 42 (range: 14-273) days, the median time to conversion from thyrotoxicosis to hypothyroidism: 39 days (range: 14-169) and 42 days (range: 14-315) days, the median time to onset of hypothyroidism: 63 (range: 21-190) and 63 (range: 14-489) days, and the median maintenance dose of levothyroxine: 1.5 (range: 0.4 - 2.3) μg/kg/day, and 1.3 (range: 0.3 - 2.5) μg/kg/day. The median pretreatment TSH levels were 2.3 (range: 0.3 - 5.2) mIU/L and 1.7 (range: 0.5 - 4.5) mIU/L in patients with and without ICPi-related thyroid disorders, respectively. The baseline TSH levels were significantly higher in patients who developed ICPi-related thyroid disorders (P = 0.05). Our results show that HDG treatment did not improve the outcome of ICPi-related thyroid disorders and higher baseline TSH increased the risk for the development of ICPi-related thyroid disorders.
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