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Recombinant Human Thyrotropin Reduces Endothelium-Dependent Vasodilation in Patients Monitored for Differentiated Thyroid Carcinoma

Department of Internal Medicine, University of Pisa, 56126 Pisa, Italy

Address all correspondence and requests for reprints to: Fabio Monzani, M.D., Department of Internal Medicine, University of Pisa, via Roma 67, 56126 Pisa, Italy. E-mail: fmonzani{at}med.unipi.it.

Aim: We evaluated endothelial-dependent vasodilation after administration of recombinant human TSH (rhTSH) in patients monitored for differentiated thyroid carcinoma. The role of inflammation and oxidative stress was also assessed.

Protocol: Twenty-four patients (21 women, mean age 40.5 ± 9.2 yr) received rhTSH (0.9 mg daily) on 2 consecutive days. At baseline and the day after the second rhTSH injection, endothelium-dependent vasodilation as flow-mediated dilation (FMD, induced by 5 min of forearm ischemia) and endothelium-independent vasodilation (glyceril trinitrate 25 µg, sublingual) were evaluated by high-resolution ultrasound in the brachial artery. At each experimental time, blood was drawn for the evaluation of thyroglobulin, TSH, free T₃, free T₄, as well as IL-6, C reactive protein, TNF, lipoperoxides, and ferric reducing antioxidant power levels as markers of inflammation and oxidative stress.

Results: At baseline, patients’ serum TSH values were below the normal range [0.12 mIU/liter (range 0.01–0.30)] in the face of normal free T₄ and free T₃ levels; FMD (8.9 ± 3.4 vs. 9.2 ± 3.1%, respectively) and response to glyceril trinitrate (11.0 ± 4.3 vs. 10.8 ± 4.7%, respectively) were similar in patients and controls. All the patients had serum thyroglobulin value less than 1 ng/ml, suggesting the absence of cancer recurrences. Besides the expected elevation of serum TSH, rhTSH induced a significant impairment of FMD (7.4 ± 3.0 vs. 8.9 ± 3.4%; P < 0.01) along with a significant elevation of blood IL-6 (P = 0.01), TNF (P < 0.001), and lipoperoxide levels (P = 0.01), as well as a reduction of ferric reducing antioxidant power (P = 0.01).

Conclusions: rhTSH administration acutely impaired endothelium-dependent vasodilation, possibly through the induction of low-grade inflammation and reduced nitric oxide availability by oxidative stress.

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