Thyrotropin hyperresponsiveness to TRH despite hyperthyroxinemia in amiodarone-treated subjects.

Abstract

Pituitary responsiveness to TRH was assessed prospectively over 24 weeks, in 15 patients receiving 300 mg amiodarone a day. All developed significant hyperthyroxinemia (both total and free), and marked elevations in reverse T3 compared to pretreatment levels. Although basal TSH levels were unchanged in all of them, TSH increased by greater than 50% when compared to pretreatment responses, in eight patients, while they remained unchanged (+/- 15%) in the remaining seven. All eight with exaggerated responses also showed significant reductions (P less than .001) in plasma levels of total and free T3, whereas in the seven who did not show any increase in TSH responses, T3 levels were unchanged. The increase in TSH response to TRH was strongly correlated (r = -.82, P less than .001) with T3 levels. Total and free T4 levels were equally elevated in both groups. These observations indicate that amiodarone effectively blocks the suppressive effect of hyperthyroxinemia on TSH secretion, and that T3 is the mediator of thyroid feedback control in amiodarone treated patients.

• Authors: R H Rao, H M Buckell, V P Rege, G S Spathis
• Journal: Metabolism: clinical and experimental (Metabolism) Vol. 36 Issue 11 Pg. 1086-90 (Nov 1987) ISSN: 0026-0495 [Print] United States
• PMID: 3118137 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Triiodothyronine
• Triiodothyronine, Reverse
• Thyrotropin-Releasing Hormone
• Thyrotropin
• Amiodarone
• Thyroxine

Topics

• Amiodarone (blood, pharmacokinetics, therapeutic use)
• Female
• Humans
• Male
• Tachycardia (blood, drug therapy)
• Thyrotropin (blood, metabolism)
• Thyrotropin-Releasing Hormone
• Thyroxine (blood)
• Triiodothyronine (blood)
• Triiodothyronine, Reverse (blood)