ETA2023 Poster Presentations Treatment 2 (9 abstracts)
TKIS for advanced thyroid cancer increase tsh levels in thyroidectomized patients: A meta-analysis
Tommaso Piticchio 1 , Antonino Belfiore 2 , Pasqualino Malandrino 3 , Pierpaolo Trimboli 4 , Federica Gambero 5 , Andrea Scuto 5 , Salvatore Volpe 5 , Guenda Di Benedetto 5 , Tumino Dario 5 , Rosario Le Moli 5 , Grete Privitera 5 , Alfredo Pulvirenti 5 & Francesco Frasca 6
1University of Catania, Endocrinology Unit - Garibaldi-Nesima Hospital, Department of Clinical and Experimental Medicine, Catania, Italy; 2University of Catania, Endocrinology Section - Department of Clinical and Experimental Medicine, Catania, Italy; 3Endocrinology Unit - Garibaldi Nesima Hospital, Catania, Italy; 4Università Della Svizzera Italiana (Usi), Servizio DI Endocrinologia e Diabetologia, Ospedale Regionale DI Lugano, Ente Ospedaliero Cantonale (Eoc), Facoltà DI Scienze Biomediche, Lugano, Switzerland; 5University of Catania, Department of Clinical and Experimental Medicine, Catania, Italy; 6Universita DI Catania, University of Catania, Endocrinologia, Garibaldi Nesima, Catania, Italy
Background: Tyrosine kinase inhibitors (TKIs) are modern antineoplastic molecules widely used in the medical treatment of many cancers including iodine refractory differentiated thyroid carcer (DTC) and advanced medullary thyroid cancer (MTC). In patients with thyroid gland, TKIs frequently cause a destructive and/or autoimmune thyroiditis with consequent hypothyroidism. However, authors have reported unexpected TSH increase or hypothyroidism even in patients with total thyroidectomy on levothyroxine replacement therapy during treatment with TKIs. There is still no agreement in the literature on the real frequency and mechanisms underlying this phenomenon.
Objectives: Aim of this meta-analysis is to evaluate the risk of TSH increase in thyroidectomized patients treated with TKI and identify potential influencing factors.
Methods: The study was conducted according to MOOSE. The search was performed on online databases Medline and ClinicalTrials.gov. No language or time restriction were used. Article type restriction was applied with filters “Clinical Trial” and “Randomized Controlled Trial”. Molecules considered in the search were those proposed by the last update of ESMO guidelines on the use of systemic therapy in advanced thyroid cancer (July 2022). The last search was performed on December 17th, 2022. Quality assessment was performed, when appropriate. Proportion meta-analyses were performed using random-effect model. Statistical analyses were performed using StataSE 17.
Results: The online search retrieved 2037 studies and 19 of which with total 1747 patients were finally included for quantitative analysis. The risk of bias was generally low. The pooled absolute risk of TSH increase was 32% (95%CI: 22–42%; I²=95.44%). The heterogeneity was explored according to several covariates, including sample size, kind of drug and mean time of drug treatment, and was solved by severity of TSH increase reported (increase within normal range vs hypothyroidism) (P = 0.04). Drugs used for MTC showed a pooled risk of TSH increase of 43% (95%CI: 26–60%; I²=97.2%) and those used for DTC 25% (95%CI: 13–37%; I²=93.9%). This difference almost reaches statistical significance (P = 0.08). Lenvatinib 24 mg/die (pooled risk 29%; 95%CI: 8-50%; I²=96.6%) and Cabozantinib 140 mg/die (pooled risk 65%; 95%CI: 40-89%; I²=86.21%) are respectively the drugs with higher risk of TSH increase in DTC drug subgroup and in MTC ones. There are no statistically significant differences between the various drugs of each subgroup.
Conclusions: This is the first meta-analysis to estimate the risk of TSH increase in thyroidectomized patients during treatment with TKIs for advanced thyroid cancer. The absolute risk seems to be very important, especially for patients treated with drugs used for MCT. Therefore, physicians and in particular endocrinologists must pay attention to this insidious side effect.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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