Amiodarone-Induced Thyrotoxic Thyroiditis: A Diagnostic and Therapeutic Challenge

Abstract

Amiodarone is an iodine-based, potent antiarrhythmic drug bearing a structural resemblance to thyroxine (T4). It is known to produce thyroid abnormalities ranging from abnormal thyroid function testing to overt hypothyroidism or hyperthyroidism. These adverse effects may occur in patients with or without preexisting thyroid disease. Amiodarone-induced thyrotoxicosis (AIT) is a clinically recognized condition commonly due to iodine-induced excessive synthesis of thyroid, also known as type 1 AIT. In rare instances, AIT is caused by amiodarone-induced inflammation of thyroid tissue, resulting in release of preformed thyroid hormones and a hyperthyroid state, known as type 2 AIT. Distinguishing between the two states is important, as both conditions have different treatment implications; however, a mixed presentation is not uncommon, posing diagnostic and treatment challenges. We describe a case of a patient with amiodarone-induced type 2 hyperthyroidism and review the current literature on the best practices for diagnostic and treatment approaches.

Hyperthyroidism secondary to hysterosalpingography

“…[3,6,9] In severely ill patients, treating both AIT1 and AIT2 with anti-thyroid drugs and glucocorticoids with or without perchlorate reduces thyroid inflammation and also reduces the peripheral conversion of T4 to T3. [5,9,10] …”

The clinical value of regular thyroid function tests during amiodarone treatment

“…One study showed that thyroid surgery is a valid therapeutic option in a small subgroup (7% out of 394 patients) of AIT patients with severe left ventricular dysfunction (20). In general, subtotal or total thyroidectomy should be considered only in patients with progressive AIT when patients are resistant to a highdose prednisolone and watchful medical management could have negative effects (22,23). In general, subtotal or total thyroidectomy should be considered only in patients with progressive AIT when patients are resistant to a highdose prednisolone and watchful medical management could have negative effects (22,23).…”

Vpliv amiodarona na delovanje ščitnice – Prikaz primera

“…Pri tipu 2, ki je redkejši in se pojavlja pri osebah brez predhodnih ščitničnih bolezni, amiodaron sproži destruktivno vnetje ščitnice, kar vodi v sproščanje prej sintetiziranih ščitničnih hormonov v krvni obtok. Možna je tudi kombinacija obeh tipov (4,5). Pojav z amiodaronom povzročene hipertiroze je običaj-no nenaden, pri čemer se tip 1 pogosto pojavi v prvih mesecih uporabe amiodarona, medtem ko je srednji čas pojavljanja tipa 2 okoli 30 mesecev po pričetku zdravljenja (5).…”

“…Možna je tudi kombinacija obeh tipov (4,5). Pojav z amiodaronom povzročene hipertiroze je običaj-no nenaden, pri čemer se tip 1 pogosto pojavi v prvih mesecih uporabe amiodarona, medtem ko je srednji čas pojavljanja tipa 2 okoli 30 mesecev po pričetku zdravljenja (5). Amiodaron preko inhibicije 5'-dejodaze zavira periferno pretvorbo tiroksina (T4) v trijodtironin (T3) ter tako poviša serumsko koncen- tracijo T4, zniža koncentracijo T3 in poviša koncentracijo reverzne oblike T3, ki fiziološko ni aktivna (1,2,5).…”

“…Ob tem je potrebno upoštevati, da je metoda prve izbire pri zdravljenju z amiodaronom povzročene hipertiroze tipa 2 medikamentno zdravljenje s peroralnimi glukokortikoidi, ne pa totalna tiroidektomija, saj je pri bolnikih s hipertirozo povečano tveganje za pojav zapletov ob posegu, kot so na primer prekatne aritmije (4). Po drugi strani pa je totalna tiroidektomija učinkovita in varna metoda zdravljenja pri tisti izbrani skupini bolnikov z amiodaronom povzročene hipertiroze tipa 2, pri katerih glukokortikoidi v visokih odmerkih niso uspešni in ko je nujno neprekinjeno zdravljenje z amiodaronom, saj bi z ukinitvijo lahko prišlo do življenje ogrožu-jočih zapletov (4,5).…”