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Clinical Thyroidology November 2002 Volume 14 Issue 3

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Clinical Thyroidology November 2002 Volume 14 Issue 3 CLINICAL THYROIDOLOGY VOLUME XIV ● ISSUE 3 NOVEMBER 2002 HYPERTHYROIDISM NODULAR GOITER The Dietary Supplement Tiratricol (3,3,5′-Triiodothy- Thyroxine Therapy Does Not Reduce the Size of Benign roacetic Acid) Can Cause Symptoms of Solitary Thyroid Nodules: Systematic Analysis of Hyperthyroidism ..................................................................41 Multiple Studies ....................................................................51 The Serum Free Triiodothyronine to Free Thyroxine THYROID CANCER Ratio and the Peripheral Blood Eosinophil to Monocyte Ratio Help to Distinguish between Graves’ Disease and Completion Thyroidectomy Can Be Done Safely after Thyroiditis as a Cause of Thyrotoxicosis ........................42 Thyroid Lobectomy in Patients with Thyroid Carcinoma..............................................................................52 GRAVES’ DISEASE Changes in Surgical Practice and Use of Postoperative Concordance of Graves’ Disease Is Greater in Monozy- Radioiodine Therapy Have Had Limited Effect on Out- gotic than Dizygotic Twins ................................................43 come in Patients with Papillary Thyroid Carcinoma ......53 Shedding of Part of the Thyrotropin Receptor May Be Fertility Is Not Impaired after Radioiodine Therapy in Important in the Pathogenesis of Hyperthyroidism in Men with Thyroid Carcinoma............................................54 Graves’ Disease ....................................................................44 High Serum Antithyroglobulin Concentrations after Neonatal Hyperthyroidism Occurs Only in Infants Initial Therapy Are Associated with Recurrence in Whose Mothers Have Very High Serum Thyrotropin Patients with Thyroid Carcinoma ......................................55 Receptor-Stimulating Antibody Concentrations ............45 THYROID FUNCTION IN PREGNANCY GRAVES’ OPHTHALMOPATHY Some Women with Hyperemesis Gravidarum Have Patients with Graves’ Ophthalmopathy May Have Long- Transient Hyperthyroidism ................................................56 Term Impairment in Vision and Quality of Life............46 CONGENITAL HYPOTHYROIDISM HYPOTHYROIDISM Discordance of Thyroid Dysgenesis in Monozygotic Germline Loss-of-Function Mutations of the Twins ......................................................................................57 Thyrotropin-Receptor Gene Are a Cause of Subclinical Hypothyroidism ....................................................................47 NONTHYROIDAL ILLNESS Progression from Subclinical to Overt Hypothyroidism Thyroid Abnormalities in Recipients of Bone Marrow Is Most Likely in Women with Higher Serum TSH Transplants Are Usually Associated with Chronic Graft- Concentrations and High Serum Antithyroid Antibody versus-Host Disease ............................................................58 Titers ......................................................................................48 3,5-Diiodothyropropionic Acid Has Favorable Short- Serum Concentrations of Multiple Enzymes May Be Term Effects on Cardiac Hemodynamics in Patients with High in Patients with Hypothyroidism ............................49 Congestive Heart Failure ....................................................59 Thyroxine Inhibits Thyrotropin Secretion in Patients IODINE METABOLISM with Central Hypothyroidism ............................................50 Recurrence of Mild Iodine Deficiency in Tasmania ......60 A publication of the American Thyroid Association CLINICAL THYROIDOLOGY VOLUME XIV ● ISSUE 3 NOVEMBER 2002 Editor-in-Chief ATA News Robert D. Utiger, M.D. Thyroid Division Department of Medicine Future Meetings Brigham & Women’s Hospital 77 Avenue Louis Pasteur Boston, MA 02115 75th Annual Meeting (617) 525-5171 Telephone September 16 to 21, 2003 (617) 731-4718 Fax [email protected] The Breakers Palm Beach, FL President 76th Annual Meeting Carole A. Spencer, Ph.D. September 29 to October 3, 2004 Secretary Westin Bayshore Resort and Marina Paul W. Ladenson, M.D. Vancouver, British Columbia, Canada President Elect Peter A. Singer, M.D. 13th International Thyroid Congress Treasurer David S. Cooper, M.D. October 30 to November 4, 2005 Buenos Aires, Argentina Publications Committee Chair Martin I. Surks, M.D. Director of Public Affairs Edie Stern Executive Director Barbara R. Smith, C.A.E. American Thyroid Association 6066 Leesburg Pike, Suite 650 Falls Church, VA 22041 Telephone: 703-998-8890 Fax: 703-998-8893 Email: [email protected] Designed By Saratoga Graphics 7 Kaatskill Way Ballston Spa, NY 12020 Clinical Thyroidology is now available Telephone: (518) 583-0243 Kandra L. Files, Art Director on the ATA web site (www.thyroid.org). Email: [email protected] Clinical Thyroidology Copyright © 2002 American Thyroid Association, Inc. Printed in the USA. All rights reserved. HYPERTHYROIDISM The dietary supplement tiratricol (3,5,3′-triiodothyroacetic acid) can cause symptoms of hyperthyroidism Bauer BA, Elkin PL, Erickson D, Klee GG, Brennan MD. Symptomatic hyperthyroidism in a patient taking the dietary supplement tiratricol. Mayo Clin Proc 2002;77:587-90. SUMMARY centration was 0.015 mU/L (normal, 0.3 to 5.0), her serum free T4 concentration was low (0.6 ng/dL [7.7 pmol/L]), Background Tiratricol (3,5,3′-triiodothyroacetic acid, or and her serum triiodothyronine (T3) concentration was high triac) is a metabolite of thyroxine (T4) that has some intrin- (293 ng/dL [4.5 nmol/L]). Tiratricol was not tested, but sic thyromimetic activity. It is marketed in health food stores 3,5,3′-triiodothyropropionic acid had 33 percent cross-reac- and on the Internet as a substance that accelerates metab- tivity in the serum T3 assay. (Six months earlier her serum olism and burns fat. This paper describes a patient in whom TSH concentration had been 2.9 mU/L and her serum total tiratricol caused symptoms of hyperthyroidism. T4 concentration 6.2 µg/dL ([80 nmol/L]). Case Report The patient was an 87-year-old woman who The patient was advised to stop taking all the dietary sup- was referred to the Mayo Clinic in May 2001. Four months plements. Her symptoms disappeared, and four weeks later earlier she was told by a chiropractor that she had a mild her serum TSH concentration was 5.9 mU/L and her serum anemia, and she had been advised to take multiple dietary free T4 and T3 concentrations were normal. She then supplements (Osteo-Genics, Hemagenics, Serenagen, Bio resumed taking all the supplements except tiratricol. Her Pure Protein, Acida-Zyme, Therazyme, Ginkgo biloba, multi- symptoms did not recur, and six weeks later the tests of thy- vitamins, and tiratricol). The dose of tiratricol was three roid function were normal. 1000-µg tablets daily. Two months later, she noted the onset of persistent nervousness, insomnia, tremor, fatigue, and Conclusion Tiratricol is a thyroid hormone analogue that weight loss. Physical examination, including examination of can be purchased as a dietary supplement and can cause the thyroid, was normal. Her serum thyrotropin (TSH) con- symptoms of hyperthyroidism. COMMENTARY cause hyperthyroidism, if taken in suffi- it remains available at at least one Web cient quantities (1), but they can hardly site (www.muscleshop.net/TriCuts.htm). There is a long list of natural prod- be called dietary or nutritional supple- There, ninety 1000-µg tablets of tiratricol ucts euphemistically called dietary or ments, and there is no evidence that they can be purchased for $79.99. The sug- nutritional supplements that affect thy- stimulate fat catabolism, as they are gested dose is 3000 µg daily. This is roid hormone production or action, and advertised to do. enough to provide a 62.5-kg person with that therefore can cause hypothyroidism Tiratricol binds well to thyroid hor- the 48 µg/kg/day needed to cause at or hyperthyroidism. One group of prod- mone receptors in vitro, but has about 5 least mild hyperthyroidism. There is no ucts are those that contain large amounts to 10 percent of the calorigenic activity reason to think that tiratricol has unique of iodine, such as kelp, that can increase of T3 in vivo. In studies in patients with properties as a “fat burner”; it is just or decrease thyroid hormone production thyroid carcinoma and severe hypothy- another way of selling thyroid hormone in patients with different thyroid disor- roidism, the mean doses of T4 and tira- and at the same time evading regulation ders. A second consists of products rich tricol needed to reduce serum TSH con- by the Food and Drug Administration. in tyrosine. These are marketed on the centrations to just below 0.1 mU/L were grounds that tyrosine is an essential sub- 2.2 µg/kg/day and 48 µg/kg/day (ratio, Robert D. Utiger, M.D. strate for thyroid hormone production, 1:22), respectively (2). As compared with and therefore an increase in tyrosine T4, tiratricol had similar effects on a thy- References intake will increase thyroid hormone pro- rotoxicosis symptom score, body weight, duction. This is a classic half-truth; tyro- resting metabolic rate, fat oxidation, and 1. Eliason BC, Doenier JA, Nuhlicek sine is of course needed for thyroid hor- urinary nitrogen excretion, but it had rel- DN. Desiccated thyroid in a nutritional mone production, but there is no evi- atively greater effects on the liver and supplement. J Fam Pract 1994;38:287-8. dence that feeding tyrosine increases thy- skeleton (2). The patients given tiratricol roid hormone production in anybody. A had undetectable serum free T4 concen- 2. Sherman SI, Ringel MD, Smith MJ, et third consists of
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