CLINICAL STUDY Selenium and goiter prevalence in borderline iodine sufficiency Volker F H Brauer, Ulrich Schweizer 1 , Josef Ko ¨hrle 1 and Ralf Paschke Third Department of Medicine, University of Leipzig, Ph-Rosenthal-Street, 27, 04103 Leipzig, Germany and 1 Institute for Experimental Endocrinology, Charite ´ Universita ¨tsmedizin Berlin, Berlin, Germany (Correspondence should be addressed to R Paschke; Email: ralf.paschke@medizin.uni-leipzig.de) Abstract Design: Selenium (Se) is required for the biosynthesis of selenocysteine-containing proteins. Several selenoenzymes, e.g. glutathione peroxidases and thioredoxin reductases, are expressed in the thyroid. Selenoenzymes of the deiodinase family regulate the levels of thyroid hormones. For clinical investigators, it is difficult to determine the role of Se in the etiology of (nodular-)goiter, because there are considerable variations of Se concentrations in different populations as reflected by dietary habits, bioavailability of Se compounds, and racial differences. Moreover, most previous clinical trials which investigated the influence of Se on thyroid volume harbored a bias due to the coexistence of severe iodine deficiency in the study populations. Methods: Therefore, we investigated the influence of Se on thyroid volume in an area with borderline iodine sufficiency. First, we investigated randomly selected probands for urinary iodine (UI) and creatinine excretion in spot urine samples and determined the prevalence of goiter and thyroid nodules by high-resolution ultrasonography. After this, we determined urinary Se excretion (USe) in probands with goiter as well as in matched probands without goiter. Adjustments between the two compared groups were made for age, gender, history of thyroid disorders, smoking, and UI excretion. Results: The mean USe and UI rates of all 172 probands were 24 mg Se/l or 27 mg Se/g creatinine and 96 mg I/l or 113 mg I/g creatinine indicating borderline selenium (20–200 mg/l) and iodine (100– 200 mg/l) sufficiency of the study population. Probands with goiter (nZ89) showed significantly higher USe levels than probands with normal thyroid volume (nZ83; P!0.05). USe rates were not influenced by present smoking or pregnancy. Conclusions: In our investigation, USe was not an independent risk factor for the development of goiter. The higher USe in probands with goiter in comparison with probands with normal thyroid volume is most likely a coincidence. Se does not significantly influence thyroid volume in borderline iodine sufficiency because the iodine status is most likely the more important determinant. European Journal of Endocrinology 155 807–812 Introduction Selenium (Se) is an essential micronutrient and as a component of selenocysteine, Se is involved in the catalysis of all known selenoenzymes e.g., iodothyr- onine deiodinases. The iodothyronine deiodinases are required for the activation and the inactivation of the thyroid hormones T4 and T3 respectively (1–5). Since the human thyroid contains the highest concentration of Se in comparison with all other organs (3) even in the case of Se-deficient nutrition (6), an important role of Se for thyroid function was suggested. For clinical investigators, it is difficult to determine the role of Se in the etiology of (nodular-)goiter, because there are considerable variations of Se concentrations in different populations as reflected by dietary habits, bioavailability of Se compounds, and racial differences (4, 7–12). Moreover, previous clinical trials investigated popu- lations with concurrent moderate to severe Se and iodine deficiency (7, 10, 13, 14) or failed to describe the iodine status of the investigated population (15). For these reasons, heterogeneous results with no differences for thyroid volume and Se concentration have been described for 140 males with goiter in comparison with 140 healthy probands (10), whereas other investigators (7) found a significantly negative relationship between thyroid volume and Se concentration in 73 school children. Many previous clinical trials (7, 10, 13, 16) which investigated the influence of Se on thyroid volume harbored a bias due to the coexistence of severe iodine deficiency in their study populations. Since the iodine status is likely to be the key factor in the maintenance of normal thyroid volume and function (17–20), trials in severely iodine-deficient areas could not clearly evaluate the role of Se deficiency in the etiology of goiter. Clinical investigators suggested that a coexistent Se deficiency increases thyroid-stimulating hormone (TSH) levels in severely iodine-deficient areas thereby subsequently contributing to the development of goiter (13, 16). Up to now, there is only sparse data European Journal of Endocrinology (2006) 155 807–812 ISSN 0804-4643 q 2006 Society of the European Journal of Endocrinology DOI: 10.1530/eje.1.02302 Online version via www.eje-online.org