Der Internist

, Volume 46, Issue 12, pp 1318–1323

Therapie und Prävention der Hyperthyreose

Schwerpunkt: Was ist gesichert in der Therapie?

Zusammenfassung

TSH-Werte unterhalb des Referenzbereichs werden in Deutschland bei über 10% der Bevölkerung beobachtet. Nicht immer handelt es sich um therapiebedürftige Hyperthyreosen. Insbesondere bei älteren Patienten kann sich hierunter aber eine Schilddrüsenautonomie verbergen, die durch iatrogene Jodzufuhr zu schwer beherrschbaren Entgleisungen führen kann. Prophylaktisch und therapeutisch bietet sich neben den Thionamiden der Einsatz von Perchlorat an. Mittelfristig ist eine definitive Sanierung durch Operation oder Radiojodtherapie anzustreben. Bei jüngeren Patienten liegt der Hyperthyreose häufiger ein florider Morbus Basedow zugrunde. Zur medikamentösen Behandlung werden hier Thionamide eingesetzt, um zunächst eine Rekompensation und nach 12- bis 18-monatiger Therapie nach dem Niedrig-Dosis-Konzept eine Dauerremission zu erreichen. Gegenstand der klinischen Forschung ist die Charakterisierung von Risikofaktoren, die es erlauben, die Rezidivwahrscheinlichkeit schon frühzeitig abzuschätzen. Durch Studien bislang nicht abgesichert ist die z. T. schon weit verbreitete Selensubstitution mit dem Ziel, eine Verbesserung der antioxidativen Schutzsysteme zu erreichen.

Schlüsselwörter

Hyperthyreose M. Basedow Schilddrüsenautonomie Thionamide Perchlorat 

Therapy and prevention of hyperthyroidism

Abstract

A decreased serum TSH level can be observed in more than 10% of the German population. Although treatment is not mandatory in each of these cases patients with an unrecognized autonomous thyroid dysfunction have a substantial risk of developing thyrotoxicosis when exposed to large amounts of iodine. Thionamid drugs in combination with potassium perchlorate are given for preventive and therapeutic reasons until definitive thyroidectomy or radioiodine therapy is performed. In younger patients Graves’ disease is the main cause of hyperthyroidism. Medical treatment with antithyroid drugs is established to render patients euthyroid. Having decreased the dose as far as possible, drug therapy is continued for 12–18 months to achieve a maximum rate of permanent remission. Ongoing clinical research aims to characterize clinical or laboratory predictors associated with a high risk of relapse after medication is stopped. Selenium supplementation is proposed to be a new therapeutic approach for autoimmune thyroid disease. It is already used quite liberally although data of powerful randomized trials are not available.

Keywords

Hyperthyroidism Graves’ disease Thyroid autonomy Thionamides Perchlorate 

Literatur

  1. 1.
    Abraham P, Avenell A, Watson WA, Park CM, Bevan JS (2005) Antithyroid drug regimen for treating Graves‘ hyperthyroidism. Cochrane Database Syst Rev: CD003420Google Scholar
  2. 2.
    Benker G, Reinwein D, Kahaly G, Tegler L, Alexander WD, Fassbinder J, Hirche H (1998) Is there a methimazole dose effect on remission rate in Graves‘ disease? Results from a long-term prospective study. The European Multicentre Trial Group of the Treatment of Hyperthyroidism with Antithyroid Drugs. Clin Endocrinol (Oxf) 49: 451–457CrossRefGoogle Scholar
  3. 3.
    Benvenga S, Amato A, Calvani M, Trimarchi F (2004) Effects of carnitine on thyroid hormone action. Ann N Y Acad Sci 1033: 158–167CrossRefPubMedGoogle Scholar
  4. 4.
    Cheng W, Fu YX, Porres JM, Ross DA, Lei XG (1999) Selenium-dependent cellular glutathione peroxidase protects mice against a pro-oxidant-induced oxidation of NADPH, NADH, lipids, and protein. Faseb J 13: 1467–1475PubMedGoogle Scholar
  5. 5.
    Cooper DS (2005) Antithyroid drugs. N Engl J Med 352: 905–917CrossRefPubMedGoogle Scholar
  6. 6.
    Dietlein M, Dressler J, Grünwald F et al. (2004) Leitlinie zur Radioiodtherapie bei benignen Schilddrüsenerkrankungen (Version 3). Nuklearmedizin 43: 217–220PubMedGoogle Scholar
  7. 7.
    Fricke E, Fricke H, Esdorn E et al. (2004) Scintigraphy for risk stratification of iodine-induced thyrotoxicosis in patients receiving contrast agent for coronary angiography: a prospective study of patients with low thyrotropin. J Clin Endocrinol Metab 89: 6092–6096CrossRefPubMedGoogle Scholar
  8. 8.
    Gärtner R, Gasnier BC (2003) Selenium in the treatment of autoimmune thyroiditis. Biofactors 19: 165–170PubMedGoogle Scholar
  9. 9.
    Gärtner R, Gasnier BC, Dietrich JW, Krebs B, Angstwurm MW (2002) Selenium supplementation in patients with autoimmune thyroiditis decreases thyroid peroxidase antibodies concentrations. J Clin Endocrinol Metab 87: 1687–1691CrossRefPubMedGoogle Scholar
  10. 10.
    Heufelder AE, Wiersinga WM (1999) Störungen der Schilddrüsenfunktion durch Amiodaron. Dtsch Ärztebl 96: A853–A860Google Scholar
  11. 11.
    Hintze G, Blombach O, Fink H, Burkhardt U, Kobberling J (1999) Risk of iodine-induced thyrotoxicosis after coronary angiography: an investigation in 788 unselected subjects. Eur J Endocrinol 140: 264–267CrossRefPubMedGoogle Scholar
  12. 12.
    Hörmann R, Quadbeck B, Roggenbuck U et al. (2002) Relapse of Graves‘ disease after successful outcome of antithyroid drug therapy: results of a prospective randomized study on the use of levothyroxine. Thyroid 12: 1119–1128CrossRefPubMedGoogle Scholar
  13. 13.
    Kahaly GJ, Dietlein M (2002) Cost estimation of thyroid disorders in Germany. Thyroid 12: 909–914CrossRefPubMedGoogle Scholar
  14. 14.
    Mandel SJ, Brent GA, Larsen PR (1994) Review of antithyroid drug use during pregnancy and report of a case of aplasia cutis. Thyroid 4: 129–133PubMedGoogle Scholar
  15. 15.
    Manz F, Bohmer T, Gartner R, Grossklaus R, Klett M, Schneider R (2002) Quantification of iodine supply: representative data on intake and urinary excretion of iodine from the German population in 1996. Ann Nutr Metab 46: 128–138CrossRefPubMedGoogle Scholar
  16. 16.
    Martino E, Bartalena L, Bogazzi F, Braverman LE (2001) The effects of amiodarone on the thyroid. Endocr Rev 22: 240–254CrossRefPubMedGoogle Scholar
  17. 17.
    Maugendre D, Gatel A, Campion L, Massart C, Guilhem I, Lorcy Y, Lescouarch J, Herry JY, Allannic H (1999) Antithyroid drugs and Graves‘ disease — prospective randomized assessment of long-term treatment. Clin Endocrinol (Oxf) 50: 127–132CrossRefGoogle Scholar
  18. 18.
    Meng W, Scriba PC (2002) Jodversorgung in Deutschland. Dtsch Ärztebl 99: A2560–A2564Google Scholar
  19. 19.
    Quadbeck B, Janssen OE, Mann K (2004) Therapie des Morbus Basedow: Probleme und neue Entwicklungen: Medikamentöse Therapie. Z Arztl Fortbild Qualitatssich 98 [Suppl 5]: 37–44Google Scholar
  20. 20.
    Rayman MP (2000) The importance of selenium to human health. Lancet 356: 233–241CrossRefPubMedGoogle Scholar
  21. 21.
    Reinwein D, Benker G, Lazarus JH, Alexander WD (1993) A prospective randomized trial of antithyroid drug dose in Graves‘ disease therapy. European Multicenter Study Group on Antithyroid Drug Treatment. J Clin Endocrinol Metab 76: 1516–1521CrossRefPubMedGoogle Scholar
  22. 22.
    Rendl J, Saller B (2001) Schilddrüse und Röntgenkontrastmittel. Dtsch Ärztebl 98: B339–B343Google Scholar
  23. 23.
    Schott M, Morgenthaler NG, Fritzen R, Feldkamp J, Willenberg HS, Scherbaum WA, Seissler J (2004) Levels of autoantibodies against human TSH receptor predict relapse of hyperthyroidism in Graves‘ disease. Horm Metab Res 36: 92–96CrossRefPubMedGoogle Scholar
  24. 24.
    Umweltbundesamt (2002) Selen und Human-Biomonitoring. Bundesgesundhbl Gesundheitsforsch Gesundheitsschutz 45: 190–195CrossRefGoogle Scholar
  25. 25.
    Völzke H, Alte D, Kohlmann T, Ludemann J, Nauck M, John U, Meng W (2005) Reference intervals of serum thyroid function tests in a previously iodine-deficient area. Thyroid 15: 279–285CrossRefPubMedGoogle Scholar
  26. 26.
    Völzke H, Ludemann J, Robinson DM et al. (2003) The prevalence of undiagnosed thyroid disorders in a previously iodine-deficient area. Thyroid 13: 803–810CrossRefPubMedGoogle Scholar
  27. 27.
    Vrca VB, Skreb F, Cepelak I, Romic Z, Mayer L (2004) Supplementation with antioxidants in the treatment of Graves‘ disease; the effect on glutathione peroxidase activity and concentration of selenium. Clin Chim Acta 341: 55–63CrossRefPubMedGoogle Scholar
  28. 28.
    Wolff J (1998) Perchlorate and the thyroid gland. Pharmacol Rev 50: 89–105PubMedGoogle Scholar
  29. 29.
    Zimmermann MB, Köhrle J (2002) The impact of iron and selenium deficiencies on iodine and thyroid metabolism: biochemistry and relevance to public health. Thyroid 12: 867–878CrossRefPubMedGoogle Scholar

Copyright information

© Springer Medizin Verlag 2005

Authors and Affiliations

  1. 1.Klinik und Poliklinik für Innere Medizin IUniversitätsklinik Regensburg
  2. 2.Klinik und Poliklinik für Innere Medizin IKlinikum der UniversitätRegensburg

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