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Journal articles on the topic 'Thiamazol'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Allelein, Stephanie, and Matthias Schott. "Update Morbus Basedow." DMW - Deutsche Medizinische Wochenschrift 144, no. 03 (January 31, 2019): 152–55. http://dx.doi.org/10.1055/a-0660-6046.

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Was ist neu? Diagnostik Die europäischen Leitlinien von 2018 beurteilen die Messung der TRAK durch die – meistens in der Routine verwendeten – Kompetitionsassays als hochsensitiv und spezifisch. Hierdurch ist es in der Regel möglich, einen Morbus Basedow sicher zu diagnostizieren und von einer Freisetzungshyperthyreose im Rahmen einer Autoimmunthyreoiditis zu unterscheiden. Zur Unterscheidung von blockierenden und stimulierenden Antikörpern kommen unter wissenschaftlichen Aspekten Bioassays zur Anwendung. Therapie Entsprechend der aktuellen Empfehlungen sollte wegen des etwas günstigeren Nebenwirkungsprofils – mit Ausnahme von Schwangeren – der Einsatz von Thiamazol/ Carbimazol gegenüber Propylthiouracil (PTU) vorgezogen werden. Bei einem Rezidiv oder bei fehlender Remission innerhalb von 12 bis 18 Monaten mit adäquater thyreostatischer Therapie ist eine ablative Therapie indiziert. Prognose Zur Einschätzung des Krankheitsverlaufs ist die Bestimmung der TRAK hilfreich. Schwangerschaft Die kürzlich erschienene Leitlinie zur Behandlung von Schwangeren mit Schilddrüsenerkrankungen gibt neue internationale Empfehlungen zur Therapie der manifesten Hyperthyreose bei Morbus Basedow. In den ersten 16 Schwangerschaftswochen (Phase der Organogenese) wird die Therapie mit PTU und im Falle einer vorbestehenden Behandlung mit Thiamazol eine zügige Umstellung auf PTU empfohlen. In der Schwangerschaft nach der 16. Woche wird nun keine klare Empfehlung bzgl. des einzusetzenden Thyreostatikums ausgesprochen. Es wird ein supprimierter TSH-Wert bei gleichzeitig (hoch-) normalem bzw. leichtgradig erhöhtem fT4-Wert angestrebt. Endokrine Orbitopathie Eine aktuelle Studie zeigt eine signifikante Besserung der endokrinen Orbitopathie mit Behandlung durch den in Deutschland noch nicht zugelassenen monoklonalen IGF-1-Rezeptor-Antikörper Teprotumumab.

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2

Cașorte, Mara, Simona Elena Albu, R. Iorgulescu, Anda Dumitrașcu, Dana Terzea, A. Golstein, and Cătălina Poiană. "FROM VASOMOTOR SYMPTOMS TO SOLID AND INSULAR PAPILLARY THYROID CANCER WITH OXYPHIL VARIANT AREAS." Journal of Surgical Sciences 2, no. 2 (April 1, 2015): 87–91. http://dx.doi.org/10.33695/jss.v2i2.113.

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The thyroid cancer had an increasing frequency during the last decades mostly related to better and accessible detection methods. The papillary type has the major epidemiologic impact. We present a case with mixed symptoms before surgery, a rare combination of both thyrotoxicosis and thyroid malignancy and an unusual pathologic report in a 56-year-old female known with total hysterectomy at age of 42, diagnosed with toxic goiter 2 years ago and under intermittent therapy with thiamazol. She presented for unspecific hot flashes and palpitation at gynaecology and she was referred for endocrine evaluation that revealed unspecific cervical compression complains, and a large goiter. The Thyroid-Stimulating Hormone was normal under thiamazol and so were the thyroid antibodies and calcitonin. The computed tomography pointed an isthmus and left lobe nodule of maximum 7.28 cm with mass effect on trachea. Total thyroidectomy was performed without any significant complications. The patient was hospitalised for 4 days (less than 48 hours postoperatively). The pathological report showed a papillary thyroid cancer (stage III) with oxyphil variant and an insular and solid pattern component. A high proliferative index is detected by vessels invasion and a ki-67 of 15 %. She received radioiodine therapy and then she started suppression levothyroxine treatment. The insular and oxyphilic pattern as well as the large tumour size of 6 cm suggest a severe prognosis. On the other hand, it is still a matter of debate whether non-autoimmune hyperthyroidism and solid pathologic features subscribe to the hypothesis of an aggressive cancer phenotype. Lifelong follow up is needed.

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3

Lok, C. A. R., A. F. ZüRCHER, and J. Van Der Velden. "A case of a hydatidiform mole in a 56-year-old woman." International Journal of Gynecologic Cancer 15, no. 1 (January 2005): 163–66. http://dx.doi.org/10.1136/ijgc-00009577-200501000-00024.

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A case of a 56-year-old woman with a mole pregnancy and a human chorionic gonadotropin (HCG)-induced thyreotoxicosis is presented. A proper diagnosis was only made after a period of patient and doctor's delay. After performing a hysterectomy, the HCG quickly normalized. Thyroid function normalized with thiamazol treatment. It is well known that older women have a higher risk to develop gestational trophoblastic disease (GTD). Furthermore, the chance of persistent trophoblastic disease is increased in this population. The literature on risk factors for developing persistent GTD and the possibilities for treatment in older patients is reviewed.

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4

Ciric, S. "SPMP 8103 Color-flow Doppler sonography in the therapy of graves' disease with thiamazol." Ultrasound in Medicine & Biology 23 (January 1997): S156. http://dx.doi.org/10.1016/s0301-5629(97)80873-3.

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5

Burggraaf, J., S. Lalezari, J. J. Emeis, U. M. Vischer, P. H. E. M. de Meyer, H. Pijl, and A. F. Cohen. "Endothelial Function in Patients with Hyperthyroidism Before and After Treatment with Propranolol and Thiamazol." Thyroid 11, no. 2 (February 2001): 153–60. http://dx.doi.org/10.1089/105072501300042820.

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6

Sviridenko, N. Y., E. F. Tugeeva, M. A. Aripov, and Yu I. Buziashvili. "Cardiac functional reserve and left ventricular parameters in patients with diffuse toxic goiter after drug correction of euthyroidism with thiamazol." Problems of Endocrinology 55, no. 3 (June 15, 2009): 21–24. http://dx.doi.org/10.14341/probl200955321-24.

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The aim of the investigation was to assess the time course of structural-and-functional and spatiogeometric changes following drug correction of euthyroidism in patients with diffuse toxic goiter and to determine prospects for restoring the cardiac functional reserve after elimination of thyrotoxicosis. The geometric parameters of the left ventricle (LV) and the readings of tissue Doppler echocardiography and exercise tests were compared in 27 female patients (mean age 53.3±9.2 years) who had thyrotoxicosis and 6 months after thyrosole-induced normalization of thyroid-stimulating and thyroid hormone. There were significant increases in myocardial mass and peak systolic and diastolic mitral ring motion rates and an increasing trend for LV linear sizes after correction of euthyroidism. Despite the fact that there were no significant differences in the majority of LV geometric parameters, with euthyroidism achievement, the cardiac functional reserve doubled as compared with the baseline values (105.7±11.4 and 57.8±14.7 W, respectively; p < 0.001), but remained below the control level (148.7±11.7 W; p < 0.05), which may contribute to the development of heart failure in future under certain conditions.

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7

Müller-Gärtner, Hans-Wilhelm, Claus Schneider, and Sören Schröder. "Autoimmune-resistance in Graves' disease tissues indication of a structural and functional heterogenicity." Acta Endocrinologica 113, no. 2 (October 1986): 233–41. http://dx.doi.org/10.1530/acta.0.1130233.

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Abstract. Out of 256 patients with Graves' disease and a characteristically low echogenic ultrasound appearance of the thyroid gland, 12 patients (4.7%) showed additionally one single or several intrathyroidal focal alterations with high echogenicity. Their volume was 0.2 to 7.0 cm (x̄ ± sd: 1.75 ± 2.24 cm). A common characteristic of the 12 patients was a longstanding history of Graves' disease and antithyroid treatment with thiamazol or carbimazol and a mean age of 55 ± 9 (sd) years (range 42–75 years). The foci with high echogenicity had a normal or macrofollicular histological structure (mean follicle lumen diameter 119.7 μm, as proven by histology in 4 cases) which was significantly higher than follicle lumina of the surrounding Graves' disease tissue (mean follicular lumen diameter 38.3 μm; P < 0.001). The height of follicle epithelium and the nuclei cross-section area of such foci was similar to corresponding normal tissue parameter in 5 out of 7 foci. The 99mTc-uptake of the foci amounted to 40 to 80% in comparison with Graves' disease tissue. 131-iodine autoradiography, thyroglobulin immunochemistry and 125-iodine-TSH binding analysis performed in selected cases confirmed the heterogenicity of these foci. The data provided evidence that the foci were unresponsive to TSH-receptor mediated stimulation through Graves' immunoglobulins. It is concluded that longstanding Graves' disease can be associated with tissue foci which are in a functional sense resistant to immunogenic stimulation by TSH-receptor autoantibodies.

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8

Theiler-Schwetz, Verena, Christian Trummer, and Stefan Pilz. "Hyperthyreose – Fokus Immunthyreopathie Basedow." Journal für Klinische Endokrinologie und Stoffwechsel 13, no. 3 (August 28, 2020): 96–105. http://dx.doi.org/10.1007/s41969-020-00112-x.

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Zusammenfassung Die häufigsten Ursachen für die Entstehung einer Hyperthyreose sind die Immunthyreopathie Basedow sowie die Schilddrüsenautonomie. Für die Diagnosestellung sind die Bestimmung der TSH-Rezeptor-Antikörper (TRAK) nebst Thyroidea-stimulierendem Hormon (TSH), freiem Thyroxin (fT4) und freiem Trijodthyronin (fT3) wichtig. Die Bestimmung der T3/T4-Ratio kann in der Abgrenzeng einer Immunthyreopathie Basedow zu einer destruktiven Thyreoiditis hilfreich sein. Bei der Immunthyreopathie Basedow sind das typische sonographische Bild einer hypoechogenen Schilddrüse mit erhöhter Vaskularisation und zunehmend auch die quantitative Bestimmung der Durchblutung in Form der „peak systolic velocity“ (PSV) weitere diagnostische Hilfsmittel. Die Szintigraphie hat bei der Diagnosestellung der Schilddrüsenautonomie nach wie vor ihren Stellenwert. Therapeutisch steht bei der Immunthyreopathie Basedow die medikamentöse, thyreostatische Therapie vorrangig mit Thiamazol in Form des Titrationsschemas im Vordergrund, die für 12–18 Monate durchgeführt wird. Liegen die TRAK dann im Normbereich, kann ein Absetzversuch unternommen werden. Wenn nicht, oder wenn es zum Auftreten eines Rezidivs kommt, sollte eine definitive Therapie mittels Radiojodtherapie oder Thyreoidektomie erwogen werden. Zur symptomatischen Behandlung können Betablocker wie Propranolol eingesetzt werden. Es gibt Hinweise, dass die lange praktizierte Jodrestriktion im Management der Immunthyreopathie Basedow vermieden werden sollte. Zum Einsatz von Selen liegen positive, aber noch großteils inkonsistente Daten vor, sodass eine Therapieempfehlung derzeit nicht ausgesprochen werden kann. In der Therapie der Schilddrüsenautonomie stehen Radiojodtherapie und die Operation im Vordergrund. Die Diagnose einer thyreotoxischen Krise ist eine klinische und wird anhand des Burch-Wartofsky-Scores gestellt – das Management erfordert meist intensivmedizinische Betreuung.

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9

Perger, Ludwig, Ulrich Bürgi, and Karin Fattinger. "Pharmakotherapie bei Hyperthyreose - unerwünschte Arzneimittelwirkungen." Therapeutische Umschau 68, no. 6 (June 1, 2011): 303–8. http://dx.doi.org/10.1024/0040-5930/a000169.

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Als Thyreostatika werden heute Thioimidazole (Carbimazol, Methimazol = Thiamazol) und Propylthiouracil eingesetzt. Carbimazol wird im Körper in Methimazol umgewandelt; ein Wechsel zwischen diesen Substanzen bringt bei Nebenwirkungen nichts. Des Weiteren kommt es bei Nebenwirkungen zwischen Thioimidazolen und Propylthiouracil manchmal zu Kreuzreaktionen. Zu den häufigen und typische Nebenwirkungen der Thyreostatika gehört eine dosisabhängige Hypothyreose, die Schilddrüsenfunktion soll deshalb regelmäßig überwacht werden. Weiter kann es zu Juckreiz und Hautausschlag kommen; hier kann man einen Wechsel der Substanz versuchen. Neben einer milden, dosisabhängigen Neutropenie, kann es vor allem in den ersten drei Monaten auch zu einer schweren Agranulozytose (3 per 10'000 Patienten, Kreuzreaktionen möglich) und sehr selten zu aplastischer Anämie kommen. Vor allem unter Propylthiouracil, aber selten auch unter Methimazol können ein asymptomatischer, transienter Leberenzymanstieg, aber auch schwere, ja tödlich verlaufende cholestatische oder hepatozelluläre Leberschäden auftreten. Wegen der Häufung von Propylthiouracil-bedingtem Leberversagen bei Kindern und Jugendlichen, sollte man hier präferentiell Thioimidazole einsetzen. Wegen dieser schweren Nebenwirkungen sollen Patienten unter Thyreostatika angewiesen werden, sich bei Auftreten von Fieber oder Halsschmerzen bzw. Malaise, Oberbauchbeschwerden und Ikterus umgehend beim Arzt zu melden. Des Weiteren kann es unter beiden Substanzen bei 1 - 5 % zu Arthralgien kommen. Da sich daraus schwere immunologische Nebenwirkungen entwickeln können, sollen die Thyreostatika dann abgesetzt werden. Eine Polyarthritis tritt vor allem in den ersten Monaten der Therapie auf, während ANCA-positive Vasculitiden oft erst nach langer Therapiedauer mit Propylthiouracil oder sehr selten unter Methimazol auftreten können. Das teratogene Risiko ist bei den Thioimidazolen höher (Aplasia cutis congenita), weswegen in der Schwangerschaft Propylthiouracil bevorzugt werden soll. In der Stillzeit können sowohl Thioimidazole als auch Propylthiouracil verabreicht werden. Perchlorat wir heute kaum mehr verwendet. Deswegen sind die früher unter längerer Therapie mit Perchlorat beobachteten Nebenwirkungen heute kaum mehr ein Thema.

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10

Hoylaerts, Marc F., Chantal Thys, Jef Arnout, and Jos Vermylen. "Recurrent Arterial Thrombosis Linked to Autoimmune Antibodies Enhancing von Willebrand Factor Binding to Platelets and Inducing FcγRII Receptor-Mediated Platelet Activation." Blood 91, no. 8 (April 15, 1998): 2810–17. http://dx.doi.org/10.1182/blood.v91.8.2810.2810_2810_2817.

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A patient with a history of recurrent late fetal loss associated with multiple placental infarcts and cerebrovascular ischemia at the age of 36, followed a year later by a myocardial infarction, was referred for further investigation. Coronary angiography was normal. Antinuclear factor, lupus anticoagulant, anticardiolipin antibodies, and other thrombophilia parameters were negative, but there was moderate hyperthyroidism with positive thyroid peroxidase antibodies. Platelet numbers and von Willebrand factor (vWF) were normal. Her platelets showed spontaneous aggregation that disappeared with aspirin intake. However, aggregation still was induced by low levels of ristocetin (0.3 to 0.5 mg/mL). The low-dose ristocetin aggregation in patient platelet-rich plasma (PRP) was completely blocked by neutralizing antiglycoprotein Ib (GPIb) and anti-vWF antibodies. The monoclonal anti-FcγRII receptor antibody IV.3 inhibited partly, which suggests that PRP aggregation by low-dose ristocetin was elicited by vWF-immunoglobulin (Ig) complexes. Upon addition to washed human platelets, with vWF (10 μg/mL), purified patient Igs dose-dependently enhanced ristocetin (0.15 mg/mL)-induced aggregation between 0 and 500 μg/mL, an effect that disappeared again above 1 mg/mL. Aggregation was dependent on the vWF concentration and was blocked by IV.3 or neutralizing anti-GPIb or anti-vWF antibodies. The spontaneous aggregation of normal platelets resuspended in patient plasma could be inhibited totally by IV.3 and partially by neutralizing anti-GPIb or anti-vWF antibodies. Perfusion with normal anticoagulated blood, enriched with 10% of control or patient plasma, over surfaces coated with vWF showed increased platelet adhesion and activation in the presence of patient antibodies. Treatment of the patient with the antithyroid drug thiamazol and temporary corticosteroids, aspirin, and ticlopidine did not correct the platelet hypersensitivity to ristocetin. These observations suggest that some autoantibodies to vWF may both enhance vWF binding to platelets and cause platelet activation through binding to the FcγRII receptor, and thereby may be responsible for a new form of antibody-mediated thrombosis.

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11

&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1198 (April 2008): 42. http://dx.doi.org/10.2165/00128415-200811980-00131.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1206 (June 2008): 29. http://dx.doi.org/10.2165/00128415-200812060-00094.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1320 (September 2010): 43–44. http://dx.doi.org/10.2165/00128415-201013200-00152.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1320 (September 2010): 43. http://dx.doi.org/10.2165/00128415-201013200-00153.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1321 (October 2010): 30. http://dx.doi.org/10.2165/00128415-201013210-00098.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1283 (January 2010): 86. http://dx.doi.org/10.2165/00128415-201012830-00274.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1277 (November 2009): 39–40. http://dx.doi.org/10.2165/00128415-200912770-00117.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1279 (November 2009): 32. http://dx.doi.org/10.2165/00128415-200912790-00094.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1308 (July 2010): 32. http://dx.doi.org/10.2165/00128415-201013080-00095.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1311 (July 2010): 40. http://dx.doi.org/10.2165/00128415-201013110-00141.

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21

&NA;. "Thiamazole." Reactions Weekly &NA;, no. 471 (October 1993): 12. http://dx.doi.org/10.2165/00128415-199304710-00060.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 431 (December 1992): 12. http://dx.doi.org/10.2165/00128415-199204310-00055.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1084 (January 2006): 25. http://dx.doi.org/10.2165/00128415-200610840-00082.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1093 (March 2006): 33. http://dx.doi.org/10.2165/00128415-200610930-00114.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1115 (August 2006): 21. http://dx.doi.org/10.2165/00128415-200611150-00069.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 859 (July 2001): 11–12. http://dx.doi.org/10.2165/00128415-200108590-00035.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1028 (November 2004): 14. http://dx.doi.org/10.2165/00128415-200410280-00052.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 326 (November 1990): 11. http://dx.doi.org/10.2165/00128415-199003260-00055.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 358 (July 1991): 12. http://dx.doi.org/10.2165/00128415-199103580-00068.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 552 (May 1995): 12. http://dx.doi.org/10.2165/00128415-199505520-00039.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 557 (July 1995): 12. http://dx.doi.org/10.2165/00128415-199505570-00037.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 564 (August 1995): 12. http://dx.doi.org/10.2165/00128415-199505640-00033.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 585 (January 1996): 12. http://dx.doi.org/10.2165/00128415-199605850-00041.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 607 (June 1996): 12. http://dx.doi.org/10.2165/00128415-199606070-00040.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 483 (January 1994): 12. http://dx.doi.org/10.2165/00128415-199404830-00054.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 485 (January 1994): 16. http://dx.doi.org/10.2165/00128415-199404850-00078.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 514 (August 1994): 11. http://dx.doi.org/10.2165/00128415-199405140-00042.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1286 (January 2010): 30. http://dx.doi.org/10.2165/00128415-201012860-00098.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1300 (May 2010): 51. http://dx.doi.org/10.2165/00128415-201013000-00177.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1302 (May 2010): 43–44. http://dx.doi.org/10.2165/00128415-201013020-00137.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 996-997 (April 2004): 13. http://dx.doi.org/10.2165/00128415-200409960-00039.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1004 (June 2004): 14. http://dx.doi.org/10.2165/00128415-200410040-00041.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1228 (November 2008): 33. http://dx.doi.org/10.2165/00128415-200812280-00090.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1229 (November 2008): 28. http://dx.doi.org/10.2165/00128415-200812290-00079.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1249 (April 2009): 43. http://dx.doi.org/10.2165/00128415-200912490-00134.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 914 (August 2002): 11. http://dx.doi.org/10.2165/00128415-200209140-00039.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 634 (January 1997): 12. http://dx.doi.org/10.2165/00128415-199706340-00043.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 679 (November 1997): 12. http://dx.doi.org/10.2165/00128415-199706790-00037.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1356 (June 2011): 33. http://dx.doi.org/10.2165/00128415-201113560-00115.

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&NA;. "Thiamazole." Reactions Weekly &NA;, no. 1358 (July 2011): 32. http://dx.doi.org/10.2165/00128415-201113580-00121.

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