Non-Suppressible TSH in a Patient Thyroidectomized Due to Follicular Thyroid Carcinoma

Introduction

Postoperative TSH-suppressive levothyroxine therapy is generally accepted as an effective therapy in patients with differentiated thyroid carcinoma ([Pujol et al., 1996]). Pseudomalabsorption (poor compliance of the patient with the therapy regimen) is the most common cause of failure with levothyroxine therapy ([Osterberg and Blaschke, 2005]; [Toft, 1994]; [Lips et al., 2004]). True failure to achieve TSH suppression may be caused by deficient absorption of thyroxine (e.g. due to concomitant medication such as iron, calcium supplements, cholestyramin, aluminum hydroxide, and raloxifene, foods such as fibre-enriched diets, grapefruit juice, soy protein supplements, or malabsorption due to gastrointestinal diseases) and by an increased thyroxine metabolism induced by estrogens ([Toft, 1994]; [Lips et al., 2004]; [Bell and Ovalle, 2001]; [Siraj et al., 2003]; [Liel et al., 1996]; [McDermott et al., 2005]). Additional, albeit extremely rare causes could be thyroxine resistance or a thyrotropin (TSH)-producing pituitary adenoma (TSH‐oma, accounting for about 0.5 % one percent of all functioning pituitary tumors). The usual characteristic biochemical abnormalities of TSH-omas are normal or high TSH concentrations and elevated (f)T4 and (f)T3 concentrations ([Refetoff et al., 1993]; [Beck-Peccoz et al., 1996]).

The case presented shows that it is not always noncompliance with medical advice or malabsorption when TSH-suppression cannot be achieved in a patient with differentiated thyroid carcinoma.

References

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