A 67-year-old male, moderate drinker, with a history of hypertensive heart disease, moderate pulmonary hypertension, heart failure due to transient left ventricular systolic failure and paroxysmal atrial fibrillation treated with amiodarone since 2013.
The usual treatment was torasemide 10 mg QD, acenocoumarol 4 mg QD, enalapril 10 mg QD, bisoprol 2.5 mg QD and 20 mg QD.
In April 2015 she presented primary hyperthyroidism in a control laboratory: free T4 25.5 pg/ml and thyroid stimulating hormone (TSH) 0.002 Ul/ml.
Thyroid scintigraphy showed an image compatible with diffuse hyperuptake goiter.
Thyroid autoimmunity showed antithyroglobulin antibodies, antiperoxidase antibodies and TSH receptor antibodies in normal ranges.
She was referred for hyperthyroidism due to amiodarone type 5; therefore, this treatment was suspended and thiamazol 5 mg every 8 hours was administered.
The dose of bisoprolol increased from 2.5 mg to 5 mg QD for the control of atrial fibrillation.
After two months of treatment with thiamazol in endocrinology consultations, elevation of hepatic enzymes was observed in laboratory tests: glutamate-oxalacetate transaminase (GOT) total bilirubin (UGT) 109 mg / L
The patient was admitted to Internal Medicine to study the possible causes of internal stasis and cytolysis.
Autoimmune and infectious causes were ruled out.
Hepatotropic virus serology was negative.
These results associated with the use of tyrosidazole; consequently, it was removed and progressive improvement of enzyme levels was observed until complete normalization two months later.
Thyroid hormone levels returned to normal, so monitoring was recommended every 6-12 months without requiring treatment.
