Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2007) 14 P317

ECE2007 Poster Presentations (1) (659 abstracts)

Different prevalence of type 1 and type 2 amiodarone-induced thyrotoxicosis over a 30-year period

Luca Tomisti 1 , Enrica Dell’Unto 1 , Chiara Cosci 1 , Chiara Sardella 1 , Luigi Bartalena 2 , Fausto Bogazzi 1 & Enio Martino 1

1University of Pisa, Pisa, Italy; 2University of Insubria, Varese, Italy.

Amiodarone induced thyrotoxicosis (AIT) may develop in patients with either underlying thyroid disorders (type 1) or normal gland (type 2). The latter is considered a drug-induced destructive thyroditis, usually responding to glucocorticoids. Further treatments after restoring euthyroidism are often not necessary. The former is a true form of iodine-induced hyperthyroidism the management of which includes thionamides, potassium perchlorate and thyrodectomy. The prevalence of the two forms of AIT is unknown.

Objective: To study the prevalence of type 1 and type 2 AIT.

Patients: Two hundred and fifteen consecutive patients with AIT referred to our Department over a 30-year period.

Results: Type 1 AIT was more prevalent at the beginning of the study(67%). During the middle 80’s the prevalence of the two AIT forms crossed each other. Thereafter prevalence of type 2 AIT progressively increased (up to 88% in 2006; P<0.0001) while that of type 1 AIT decreased. Type 2 AIT patients had a male preponderance, higher serum FT4/FT3 ratio (P<0.002), lower thyroidal 3 °h and 24 °h RAIU values(P<0.0001) and received a higher cumulative dose of amiodarone than type 1 AIT patients (P<0.0001).

Conclusions: Over a 30-year period, the prevalence of type 2 AIT progressively increased and that of type 1 decreased. Thus, endocrinologist will face mostly with type 2 AIT patients, who will have a potentially self-limiting destructive thyroiditis, often successfully treated with glucocorticoids. On the other hand, a more aggressive (total thyrodectomy) therapeutic option might be necessary in patients unresponsive to glucocorticoids. Finally, after restoring euthyroidism, patients should be followed for late-developing hypothyroidism.

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