Key result
Long-term amiodarone therapy triggers late-onset thyrotoxicosis in a pediatric congenital heart disease case.
Why the study?
Amiodarone-induced thyrotoxicosis (AIT) presents a heterogeneous and challenging clinical entity, especially in pediatric patients, with difficulties in subtype differentiation and treatment.
Case Report (n=1)
Highlights the challenges of managing amiodarone-induced thyrotoxicosis in pediatric patients with congenital heart disease.
Differentiation of AIT subtypes may guide therapy in children; leaves open need for prospective validation.
Thyroid dysfunction is one of the most common adverse effects of amiodarone therapy, ranging from subclinical changes to overt clinical thyrotoxicosis (AIT) and/or hypothyroidism. Due to its heterogeneity, AIT lasts as a defiant entity, leading to a thorny treatment course, particularly in pediatrics. AIT can be classified as either type 1, type 2 or mixed form based on its pathophysiology. Differentiating between the main AIT subtypes is quite relevant, since there is specific treatment for both, however, this distinction may be difficult in clinical practice. We describe a rare case of AIT in a pediatric patient, with an uncommon congenital cardiac malformation, that started amiodarone therapy due to paroxysmal supraventricular tachycardia. AIT was reported 26 months after drug onset, with a sudden and explosive emerging. This case highlights the current AIT management challenges on the highdemanding pediatric field pursuing, ultimately, an enhanced patient´s care.
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Oliveira et al. (2019) conducted a case report in Amiodarone-Induced Thyrotoxicosis (n=1). Amiodarone was evaluated on Amiodarone-Induced Thyrotoxicosis (AIT). Amiodarone therapy in a pediatric patient with a congenital cardiac malformation resulted in the sudden emergence of amiodarone-induced thyrotoxicosis 26 months after drug onset.
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