• Faro R Verelst, Michiel Marcel Jozef Beyens, Elke Vandenbroucke, Katheleen Forceville, and Th B TwicklerMarcelMhttps://orcid.org/0000-0001-8738-207XDepartment of Endocrinology, Diabetology and Metabolic Disease, AZ Monica, Deurne, Belgium.Faculty of Medicine and Health Sciences, University of Antwerp, Antwerp, Belgium..
• Internal Medicine, Antwerp University, Antwerp, Belgium.
• Eur. J. Clin. Invest. 2022 Jul 1; 52 (7): e13790.

AbstractHypothyroidism is a frequently occurring side effect in patients under treatment with immune checkpoint inhibitors (ICIs). Actually, the origin of hypothyroidism with ICI use is classified as a primary (thyroid) or as secondary/tertiary hypothyroidism (hypothalamus-pituitary). Treatment consists of levothyroxine (L-T4) substitution. Recently, we were rarely confronted with a clinically overt hypothyroidism in three patients under treatment with ICIs who were non-responsive to T4 therapy. As a therapeutical escape, liothyronine (L-T3) was started with a significant clinical and/or biochemical improvement suggesting an underlying functional defect in the peripheral free T4 (fT4) to free T3 (fT3) conversion (as supported by calculation of SPINA-GD). Against this background, we discussed our three patients along an extended review of this clinical topic.© 2022 Stichting European Society for Clinical Investigation Journal Foundation. Published by John Wiley & Sons Ltd.

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