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Thyrotropin hyperresponsiveness to TRH despite hyperthyroxinemia in amiodarone-treated subjects
R H Rao1, H M Buckell, V P Rege
1Department of Medicine, St Helier Hospital, Carshalton, United Kingdom.
Metabolism: Clinical and Experimental
|November 1, 1987
Summary
Amiodarone causes hyperthyroxinemia by blocking thyroid hormone feedback. Triiodothyronine (T3) is the key mediator of this feedback control in patients treated with amiodarone.
Area of Science:
- Endocrinology
- Pharmacology
Background:
- Amiodarone is an antiarrhythmic drug known to affect thyroid hormone levels.
- Hyperthyroxinemia, characterized by elevated thyroxine (T4) and triiodothyronine (T3), can occur during amiodarone treatment.
Purpose of the Study:
- To investigate pituitary responsiveness to thyrotropin-releasing hormone (TRH) in patients receiving amiodarone.
- To determine the role of thyroid hormones, particularly T3, in feedback regulation during amiodarone therapy.
Main Methods:
- Prospective assessment of pituitary responsiveness to TRH over 24 weeks in 15 patients on amiodarone.
- Measurement of total and free T4, reverse T3, T3, and TSH levels before and during amiodarone treatment.
- Categorization of patients based on TSH response to TRH.
Main Results:
- All patients developed hyperthyroxinemia and elevated reverse T3.
- Eight patients showed an exaggerated TSH response to TRH, accompanied by decreased T3 levels.
- Seven patients had unchanged TSH response, with stable T3 levels.
- A strong negative correlation was observed between TSH response and T3 levels (r = -.82).
Conclusions:
- Amiodarone blocks the suppressive effect of hyperthyroxinemia on TSH secretion.
- Triiodothyronine (T3) is the primary mediator of thyroid hormone feedback control in amiodarone-treated patients.
- This suggests a unique mechanism of thyroid hormone regulation influenced by amiodarone.