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DOI: 10.1055/s-2005-836535
© Georg Thieme Verlag Stuttgart · New York
Pathophysiologie der Knotenstruma: Konsequenzen für die Therapie und Rezidivprophylaxe
Pathophysiology of the Benigne Nodular Goitre: Consequences for Therapy and Prophylaxis of RecurrencyPublication History
Publication Date:
03 June 2005 (online)
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Zusammenfassung
Jodmangel ist die wesentlichste Ursache für die Entstehung von diffusen (hyperplastischen) und multinodösen Strumen (benignen Neoplasien). Die Schilddrüse gehört zu den Organen mit den häufigsten benignen Neoplasien, welche durch somatische Mutationen entstehen, wobei es offenbar auch eine familiäre genetische Prädisposition gibt, denn nicht alle Menschen in einem Jodmangelgebiet entwickeln Knotenstrumen. Diese treten familiär gehäuft auf. In Deutschland werden bei etwa 25-35 % aller Erwachsenen Knotenstrumen nachgewiesen. Angesichts der Häufigkeit von funktionell inaktiven, benignen Knotenstrumen gibt es nur sehr wenig kontrollierte Studien, die den klinisch wichtigen Effekt einer medikamentösen Therapie belegen, nämlich nicht nur die Verhinderung bzw. Verzögerung des Wachstums, sondern vor allem eine Verhinderung der malignen Entartung und die Prävention der Entstehung weitere Knoten, bzw. Rezidivknoten nach Strumaoperation. Eine TSH-suppressive Therapie kann eine Rezidivstruma nicht sicher verhindern. Aus pathophysiologischer Sicht sollte die Jodidsubstitution bevorzugt eingesetzt werden, denn wir wissen, dass sie keine negativen Wirkungen hat, wenn eine Autonomie ausgeschlossen ist. Prospektive, kontrollierte und langjährige Studien sind dringend notwendig, um zu zeigen, welche der konservativen Therapiemöglichkeiten am effektivsten ist, die oben angeführten, wichtigsten Therapieziele zu erreichen.
Abstract
Iodine deficiency is the main cause of the development of diffuse (hyperplastic) and multinodular goitre (benign neoplasia). The thyroid is one of the organs with the highest prevalence of benign neoplasias, probably because it has the potential for growth even in adulthood. Somatic mutations are responsible for the development of thyroid nodules, but there also seems to be a familiar genetic background, facilitating the development of benign thyroid neoplasia. In Germany 25-35 % of adult people are suffering from nodular goitre. There are limited controlled studies, which show the effect of a TSH suppressive therapy or iodine supplementation or both on the main goals of a conservative therapy, which are: prevention of malignant dedifferentiation, development of new nodules and growth inhibition or involution. But we know from meta-analyses that a TSH-suppressive therapy does not prevent recurrence of nodular goitre after surgery. From pathophysiological point of view, iodine supplementation, probably in combination with antioxidants should prevent the development of new nodules and probably malignant dedifferentiation. Prospective, controlled studies are still necessary to evaluate the best treatment of nodular goitre and prevention of recurrence after thyroid surgery.
Schlüsselwörter
Knotenstruma - Schilddrüsen-Neoplasie - Jodmangel - TSH-suppressive Therapie
Key words
multinodular goitre - thyroid neoplasia - iodine deficiency - TSH-suppressive therapy
Literatur
- 1 Studer H, Derwahl M. Mechanisms of nonneoplastic endocrine hyperplasia - a changing concept: a review focused on the thyroid gland. Endocr Rev. 1995; 16 411-426
- 2 Tomimori E, Pedrinola F, Cavaliere H, Knobel M, Medeiros-Neto G. Prevalence of incidental thyroid diseases in a relatively low iodine intake area. Thyroid. 1995; 5 273-276
- 3 Krohn K, Fuhrer D, Bayer Y. et al . Molecular pathogenesis of euthyroid and toxic multinodular goiter. Endocr Rev. 2004; [Epub ahead of print]
- 4 Reiners C, Wegscheider K, Schicha H. et al . Prevalence of thyroid disorders in the working population of Germany: ultrasonography screening in 96 278 unselected employees. Thyroid. 2004; 14 926-932
- 5 Rago T, Chiovato L, Aghini-Lombardi F, Grasso L, Pinchera A, Vitti P. Non-palpable thyroid nodules in a borderline iodine-deficient area: detection by ultrasonography and follow-up. J Endocrinol Invest. 2001; 24 770-776
- 6 Alexander E K, Marqusee E, Orcutt J, Benson C B, Frates M C, Doubilet P M, Cibas E S, Atri A. Thyroid nodule shape and prediction of malignancy. Thyroid. 2004; 14 953-958
- 7 Hegedus L. Clinical practice. The thyroid nodule. N Engl J Med. 2004; 351 1764-1771
- 8 Leenhardt L, Menegaux F, Franc B. et al . Selection of patients with solitary thyroid nodules for operation. Eur J Surg. 2002; 168 236-241
- 9 Frates M C, Benson C B, Doubilet P M, Cibas E S, Marqusee E. Can color Doppler sonography aid in the prediction of malignancy of thyroid nodules?. J Ultrasound Med. 2003; 22 127-131
- 10 Krohn K, Paschke R. Somatic mutations in thyroid nodular disease. Mol Genet Metab. 2002; 75 202-208
- 11 Stübner D, Gärtner R, Greil W, Gropper K, Brabant G, Permanetter W, Horn K, Pickardt C R. Hypertrophy and hyperplasia during goiter growth and involution in rats. Separate bioeffect of TSH and iodine. Acta Endocrinol. 1987; 116 537-548
- 12 Gärtner R, Pisarev M A. Thyroid Autoregulation. In: Braverman LE, Utiger RD (eds). Werner & Ingbar's The Thyroid. 8th ed. Lippincott Williams & Wilkins, Baltimore 2000; 85-90
- 13 Dugrillon A, Gärtner R. Delta-Iodolactone decrease epidermal growth factor-induced inositol - 1,4,5-triphosphate generation in porcine thyroid follicles - a possible mechanism of growth inhibition by iodide. Eur J Endocrinol. 1995; 132 735-743
- 14 Paschke R, Neumann S. Sodium/iodine symporter mRNA expression in cold thyroid nodules. Exp Clin Endocrinol Diabetes. 2001; 109 45-46
- 15 Bayer Y, Neumann S, Meyer B. et al . Genome-wide linkage analysis reveals evidence for four new susceptibility loci for familial euthyroid goiter. J Clin Endocrinol Metab. 2004; 89 4044-4052
- 16 Kuma K, Matsuzuka F, Kobayashi A. et al . Outcome of long standing solitary thyroid nodules. World J Surg. 1992; 16 583-588
- 17 Kuma K, Matsuzuka F, Yokozawa T, Miyauchi A, Sugawara M. Fate of untreated benigne thyroid nodules: Results of long-term follow-up. World J Surg. 1994; 18 495-499
- 18 Alexander E K, Hurwitz S, Heering J P. et al . Natural history of benigne solid and cystic thyroid nodules. Ann Intern Med. 2003; 138 315-318
- 19 Asanuma K, Kobayashi S, Shingu K. et al . The rate of tumour growth does not distinguish between malignant and benigne thyroid nodules. Eur J Surg. 2001; 167 102-105
- 20 Hoermann R, Quadbeck B. Course of thyroid nodules. Exp Clin Endocrinol Diabetes. 1998; 106 (Suppl 4) 27-28
- 21 Quadbeck B, Pruellage J, Roggenbruck U, Hirche H, Janssen O, Hoermann R. Long-term follow-up of thyroid nodule growth. Exp Clin Endocrinol Diabetes. 2002; 110 348-354
- 22 Kung A W, Chau M T, Lao T T, Tam S C, Low L C. The effect of pregnancy on thyroid nodule formation. J Clin Endocrinol Metab. 2002; 87 1010-1014
- 23 Cooper D S. Clinical review 66: Thyroxine suppression therapy for benign nodular disease. J Clin Endocrinol Metab. 1995; 80 331-334
- 24 Castro M R, Caraballo P J, Morris J C. Effectiveness of thyroid hormone suppressive therapy in benign solitary thyroid nodules: a meta-analysis. J Clin Endocrinol Metab. 2002; 87 4154-4159
- 25 Wemeau J L, Caron P, Schvartz C. et al . Effects of thyroid-stimulating hormone suppression with levothyroxine in reducing the volume of solitary thyroid nodules and improving extranodular nonpalpable changes: a randomized, double-blind, placebo-controlled trial by the French Thyroid Research Group. J Clin Endocrinol Metab. 2002; 87 4928-4934
- 26 La Rosa G L, Lupo L, Giufrida D, Gullo D, Vigneri R, Belfiore A. Levothyroxine and potassium iodide are both effective in treating benign solid cold nodules of the thyroid. Ann Intern Med. 1995; 122 1-8
- 27 Gharib H, Mazzaferri E L. Thyroxine suppressive therapy in patients with nodular thyroid disease. Ann Intern Med. 1998; 128 386-394
- 28 Glattre E, Thomassen Y, Thoresen S O. et al . Prediagnostic serum selenium in a case-control study of thyroid cancer. Int J Epidemiol. 1989; 18 45-49
Prof. Dr. R Gärtner
Medizinische Klinik Innenstadt der Universität München
Ziemssenstr. 1
80336 München
Phone: 0 89/51 60 23 32
Fax: 0 89/51 60 44 30
Email: roland.gaertner@med.uni-muenchen.de