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Suspected liraglutide (glucagon-like peptide-1 receptor agonist)-induced hyperthyroidism: A case report
Siti Nur Syakinah Md Sabudin1, Lili Husniati Yaacob2, Muhammad Rahmat Che Omar3
1MBBS, MMed (Family Medicine), Medical and Basic Dental Sciences Unit, School of Dental Sciences, Health Campus, Universiti Sains Malaysia, Kubang Kerian, Kelantan, Malaysia.
Abstract:
Liraglutide, a glucagon-like peptide-1 receptor agonist (GLP-1 RA), is widely used for weight management and glycaemic control. While generally well-tolerated, various adverse effects have been reported. Thyroid dysfunction, particularly hyperthyroidism, is rare. This report describes the case of a 34-year-old woman with new-onset hyperthyroidism following liraglutide use for weight loss. The patient presented with worsening palpitations and insomnia after 3 weeks of liraglutide use. She had no prior thyroid disease or significant family history. Examination revealed sinus tachycardia with no goitre or tremors. Laboratory findings confirmed hyperthyroidism with a suppressed TSH level (0.03 mlU/L) and an elevated free T4 level (20.8 pmol/L). Thyrotropin receptor antibody was negative, ruling out Graves' disease. Liraglutide was discontinued, and the patient was treated with carbimazole and propranolol, resulting in symptom resolution and normalisation of thyroid function within weeks. Liraglutide-induced thyroid dysfunction is poorly understood. Possible mechanisms include GLP-1 receptor activity in thyroid tissue, disruption of the hypothalamic-pituitary-thyroid axis or inflammation of thyroid follicular cells. This case demonstrates a strong temporal association between liraglutide use and hyperthyroidism, which resolved upon drug discontinuation. Although thyroid dysfunction with GLP-1 RAs has been noted in preclinical studies, human data remain limited. This case highlights a rare adverse effect of liraglutide and underscores the need for vigilance when monitoring patients on GLP-1 RAs. Monitoring of thyroid function should be considered in symptomatic patients. Further research is warranted to better understand the underlying mechanisms and prevalence of GLP-1 RA-induced thyroid abnormalities.
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