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Thyroid hormone metabolism in heart failure: iodothyronine deiodinases in focus

Olivares, Emerson La; Carvalho, Denise Pb

Current Opinion in Endocrinology, Diabetes and Obesity: October 2010 - Volume 17 - Issue 5 - p 414–417
doi: 10.1097/MED.0b013e32833d9196
Thyroid: Edited by Paul J. Davis
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Purpose of review Heart disease is the leading cause of death worldwide and no efficient treatment against this threatening condition exists. Based on their recognized regulatory action on cardiovascular system, thyroid hormones emerged as a good alternative for patients with heart disease. Although many studies have shown beneficial effects of thyroid hormone replacement in patients with heart failure, many questions are still unsolved. Thus, the purpose of this review was to discuss changes in thyroid hormone economy with special emphasis on thyroid hormone metabolism in models of heart failure.

Recent findings Severe illness, such as heart failure, is characterized by changes in thyroid hormone economy, characterized by decreased serum T3 and increased serum rT3, a condition called the ‘low T3-syndrome’. Unlike other animal models of thyroid status derangement during systemic illness, some clinical and experimental studies have observed compensatory stimulation of the hypothalamus–pituitary–thyroid axis in patients and models of heart failure. In this context, induction of type 3 deiodinase is the main cause of decreased T3. This is uniquely reminiscent of the pathophysiology of the ‘consumptive hypothyroidism’, which has previously been described in patients with large D3-expressing tumors.

Summary Tight regulation of cardiac T3 levels occurs in heart failure and understanding the pathophysiology of this phenomenon might support future researches to find new efficient strategies to treat heart failure.

aCardiovascular Physiology and Pharmacology Laboratory, Departamento de Ciências Fisiológicas, Instituto de Biologia, Universidade Federal Rural do Rio de Janeiro

bEndocrine Physiology Laboratory, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, CCS – Bloco G – Cidade Universitária – Ilha do Fundão/Rio de Janeiro, Brazil

Correspondence to Dr Denise Pires de Carvalho, MD, PhD, Endocrine Physiology Laboratory, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, CCS – Bloco G – Cidade Universitária – Ilha do Fundão/Rio de Janeiro 21941902, Brazil Tel: +55 21 25626552; fax: +55 21 22808193; e-mail: dencarv@biof.ufrj.br

© 2010 Lippincott Williams & Wilkins, Inc.