Eur J Endocrinol
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DOI: 10.1530/EJE-07-0345
European Journal of Endocrinology, Vol 157, Issue 3, 367
Copyright © 2007 by European Society of Endocrinology
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LETTER TO THE EDITOR

Recombinant human TSH acutely impairs endothelium-dependent vasodilation

Angela Dardano and Fabio Monzani

Department of Internal Medicine, University of Pisa, via Roma 67, 56126 Pisa, Italy

(Correspondence should be addressed to F Monzani; Email: fmonzani{at}med.unipi.it)

We read with interest the review article by Duntas & Biondi dealing with clinical and quality of life consequences induced by short-term hypothyroidism (1). Withdrawal of levothyroxine therapy exacerbates neuropsychiatric symptoms and increases cardiovascular risk, although these effects are usually reversible restoring a condition of stable euthyroidism (1). Short-term hypothyroidism is associated with cardiac abnormalities, increased peripheral vascular resistance, and endothelium dysfunction. In this setting, the recent use of recombinant human thyrotropin (rhTSH) in the clinical practice of thyroid carcinoma represents a valid alternative to levothyroxine withdrawal. The authors state that rhTSH administration is not accompanied by significant cardiac alterations and induces beneficial effects on the vascular system by increasing circulating nitric oxide (2). In this regard, we have recently assessed the acute effects of TSH on endothelial function in patients monitored for differentiated thyroid carcinoma (DTC) (3). Our data demonstrate that acutely raising serum TSH into the supraphysiological range leads to an acute impairment of endothelium-dependent vasodilation along with a significant increase in blood interleukin (IL)-6, tumour necrosis factor {alpha} (TNF{alpha}), and lipoperoxide levels. These observations are in keeping with the in vitro evidence of functional TSH receptors in several extra-thyroidal tissues, such as cardiomyocytes (4), aortic endothelium (5), and bone marrow cells (6), in which TSH is able to directly induce IL-6 and TNF{alpha} production (7). TNF{alpha} is a pivotal NO-controlling cytokine and may promote the expression of inducible NO synthase, leading to increased oxidative stress (8). This mechanism may explain the increased NO metabolites previously described in patients receiving rhTSH for the follow-up of DTC (2). Therefore, while agreeing with the authors that rhTSH administration is generally safe and able to avoid most signs and symptoms of short-term hypothyroidism, we underline that rhTSH per se may acutely induce low-grade inflammation and endothelial function impairment.

References

    1. Duntas LH & Biondi B. Short-term hypothyroidism after Levothyroxine-withdrawal in patients with differentiated thyroid cancer: clinical and quality of life consequences. European Journal of Endocrinology 2007 156 13–19.[Abstract/Free Full Text]

    2. Giusti M, Valenti S, Guazzini B, Molinari E, Cavallero D, Augeri C & Minuto F. Circulating nitric oxide is modulated by recombinant human TSH administration during monitoring of thyroid cancer remnant. Journal of Endocrinological Investigation 2003 26 1192–1197.[ISI][Medline]

    3. Dardano A, Ghiadoni L, Plantinga Y, Caraccio N, Bemi A, Duranti E, Taddei S, Ferrannini E, Salvetti A & Monzani F. Recombinant human thyrotropin reduces endothelium-dependent vasodilation in patients monitored for differentiated thyroid carcinoma. Journal of Clinical Endocrinology and Metabolism 2006 91 4175–4178.[Abstract/Free Full Text]

    4. Drvota V, Janson A, Norman C, Sylven C, Haggblad J, Bronnegard M & Marcus C. Evidence for the presence of functional thyrotropin receptor in cardiac muscle. Biochemical and Biophysical Research Communications 1995 211 426–431.[CrossRef][ISI][Medline]

    5. Donnini D, Ambesi-Impiombato FS & Curcio F. Thyrotropin stimulates production of procoagulant and vasodilative factors in human aortic endothelial cells. Thyroid 2003 13 517–521.[CrossRef][ISI][Medline]

    6. Whetsell M, Bagriacik EU, Seetharamaiah GS, Prabhakar BS & Klein JR. Neuroendocrine-induced synthesis of bone marrow-derived cytokines with inflammatory immunomodulating properties. Cellular Immunology 1999 192 159–166.[CrossRef][ISI][Medline]

    7. Wang HC, Dragoo J, Zhou Q & Klein JR. An intrinsic thyrotropin-mediated pathway of TNF-alpha production by bone marrow cells. Blood 2003 101 119–123.[Abstract/Free Full Text]

    8. Licinio J, Prolo P, McCann SM & Wong ML. Brain iNOS: current understanding and clinical implications. Molecular Medicine Today 1999 5 225–232.[CrossRef][ISI][Medline]

Received 23 May 2007
Accepted 30 May 2007





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