Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: The role of thyroid hormone therapy in acutely ill cardiac patients. | Available online http content 9 4 333 Commentary The role of thyroid hormone therapy in acutely ill cardiac patients Kathleen L Wyne Assistant Professor Division of Endocrinology and Metabolism Department of Internal Medicine University of Texas Southwestern Medical Center at Dallas Dallas TX USA Author for correspondence Kathleen L Wyne Published online 13 June 2005 This article is online at http content 9 4 333 2005 BioMed Central Ltd Critical Care 2005 9 333-334 DOI cc3738 See related research by Iltumur et al. in this issue http content 9 4 R416 Abstract The presence of a low T3 syndrome in the setting of nonthyroidal illness has long been recognized as the euthyroid sick syndrome with the recommendation to observe and not treat with thyroid hormone replacement therapy. That approach has recently been challenged in the setting of critical cardiac illness. Research demonstrating that thyroid hormone therapy may improve hemodynamic parameters has rekindled interest in the use of thyroid hormone therapy in critical illness. Continued improvements in survival after critical cardiac illness provokes the question of whether thyroid hormone therapy would provide further incremental benefit. The question of whether thyroid hormone supplementation should be provided to critically ill patients without a known history of thyroid disease is not a new debate 1 . Analysis of such patients led to the recognition of the euthyroid sick syndrome which is characterized by low normal thyroxine T4 levels low normal 3 5 3 -tri-iodothyronine T3 levels variable thyroid-stimulating hormone TSH levels and elevated 3 3 5 -tri-iodothyronine reverse T3 rT3 levels. The physiologic changes that lead to these alterations are the body s attempt to conserve metabolism during illness. T4 is normally metabolized through sequential deiodination to T3 then to 3 3 -di-iodothyronine T2 which is then rapidly degraded to .
