Amiodarone
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Drug-induced thyrotoxicosis: 2 case reports A study conducted at the Mordovia Pediatric Republic Clinical Hospital, Russia, between 2015 and 2018 and involving 45 children (aged 1–17 years) receiving amiodarone for heart rhythm disturbance, described two children [including one girl; ages not stated; not all sexes stated], who developed amiodarone-induced thyrotoxicosis during treatment with amiodarone for heart rhythm disturbance [routes and duration of treatment to reaction onsets not stated; not all dosages and outcomes stated]. The child, who had unspecified heart rhythm disturbance, started receiving amiodarone, a daily loading dose in three administrations followed by a reduced daily maintenance dose in two administrations. Thereafter, the child developed a decrease in TSH levels upto the lower end of the norm, increase in the level of free T4 (tetraiodothyronine) and increase in the level of antithyroid antibodies above the norm. Based on these finding the child was diagnosed with type II amiodarone-induced thyrotoxicosis. The girl (birth year 2004) started receiving amiodarone 8 mg/kg/day in three administrations since the age of 6 years for frequent and poorly tolerated bouts of paroxysmal supraventricular tachycardia. She also had Wolff-Parkinson-White (WPW) syndrome. One year following the initiation of amiodarone, an ultrasound revealed an increased thyroid volume with a normal structure and normal level of thyroid hormones. Stage 1 diffuse euthyroid goiter was diagnosed. She was considered at risk of developing an amiodarone thyropathy. Amiodarone discontinuation and a radiofrequency ablation (RFA) was recommended, but her parents refused. One and half year following the initiation of amiodarone, the thyroid volume increased to 7.5 cm3 (stage I) with a normal structure. The concentration of free T4 increased to 24.2 pmol/L. She was referred to the Federal Center for Diagnostics and Treatment of Dysrhythmias, where she underwent RFA of an additional atrioventricular connection. Amiodarone was discontinued. Two months following discharge from the center, a bout of paroxysmal tachycardia with syncope developed. She independently re-started amiodarone. A paediatric endocrinologist clinically diagnosed euthyroidism and advised discontinuation of amiodarone. At that time, she had TSH of 0.19 µIU/mL, free T4 of 29.16 pmol/L and free T3 of 6.28 pmol/L. She was again sent to the Federal Center, where RFA was repeated. However, the bouts of palpations recurred. After discharge from the center, during evaluation by a pediatric endocrinologist, clinical signs of thyrotoxicosis were not noted. The thyroid was enlarged to stage 1, elastic, homogenous and painless. She had TSH of 0.05 µIU/mL, free T4 of 32.25 pmol/L, free T3 of 9.31 pmol/L (N), and anti-thyroid antibodies were not detected. Amiodarone-induced thyrotoxicosis was diagnosed. Amiodarone was switched to atenolol. Subsequently, the palpitations did not recur. She was in a sinus rhythm, and the levels of TSH and free T3 normalised. She had free T4 leve
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