<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.2d1 20170631//EN" "JATS-journalpublishing1.dtd">
<article xlink="http://www.w3.org/1999/xlink" dtd-version="1.0" article-type="healthcare" lang="en"><front><journal-meta><journal-id journal-id-type="publisher">IJCRR</journal-id><journal-id journal-id-type="nlm-ta">I Journ Cur Res Re</journal-id><journal-title-group><journal-title>International Journal of Current Research and Review</journal-title><abbrev-journal-title abbrev-type="pubmed">I Journ Cur Res Re</abbrev-journal-title></journal-title-group><issn pub-type="ppub">2231-2196</issn><issn pub-type="opub">0975-5241</issn><publisher><publisher-name>Radiance Research Academy</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="publisher-id">4916</article-id><article-id pub-id-type="doi"/><article-id pub-id-type="doi-url">https://doi.org/10.31782/IJCRR.2026.181302</article-id><article-categories><subj-group subj-group-type="heading"><subject>Healthcare</subject></subj-group></article-categories><title-group><article-title>&#13;
	Amiodarone-Induced Thyrotoxicosis in a Patient Undergoing Long-Term Treatment with a Fixed Dose of Amiodarone&#13;
&#13;
&#13;
&#13;
	 &#13;
&#13;
&#13;
&#13;
	 &#13;
&#13;
&#13;
&#13;
	 &#13;
&#13;
</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Stolarczyk</surname><given-names>Dominika</given-names></name></contrib><contrib contrib-type="author"><name><surname>MaSitkoria</surname><given-names/></name></contrib></contrib-group><pub-date pub-type="ppub"><day>15</day><month>07</month><year>2026</year></pub-date><volume>3)</volume><issue/><fpage>10</fpage><lpage>15</lpage><permissions><copyright-statement>This article is copyright of Popeye Publishing, 2009</copyright-statement><copyright-year>2009</copyright-year><license license-type="open-access" href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY 4.0) Licence. You may share and adapt the material, but must give appropriate credit to the source, provide a link to the licence, and indicate if changes were made.</license-p></license></permissions><abstract><p>&#13;
	Introduction: This clinical case demonstrates the importance of vigilance, strict control, and monitoring of pharmacological treatment administered consistently over several years with the same drug at a fixed dose. Case presentation: The clinical case concerns a 65-year-old female patient admitted to the Internal Medicine Ward with diar rhoea and progressive weakness lasting for about 3 weeks. Her medical history included weight loss of approximately 5.5 kg in a week and subfebrile conditions up to 38.3 °C. The patient had been under the constant care of a cardiologist for several years due to non-persistent ventricular arrhythmias. She was taking a daily dose of 100 mg of Amiodarone. A Burch–Wartofsky Point Scale score of 35 indicated impending thyroid storm. Given the severity of thyrotoxicosis, the absence of a previously document ed thyroid disorder, the long duration of amiodarone exposure, and the ultrasound findings, amiodarone-induced thyrotoxicosis with a possible mixed/indeterminate phenotype was considered. Results: Amiodarone was discontinued and treatment with thiamazole 20 mg three times daily, sodium perchlorate 300 mg three times daily, and prednisone 40 mg once daily was initiated. Sodium perchlorate was stopped after 7 days because of a fall in platelet count from 351,000/µL to 162,000/µL. During hospitalization, fT3 progressively decreased and reached 7.90 pmol/L at discharge, whereas fT4 remained markedly elevated. After discharge, thyroid hormone concentrations continued to improve; 14 days later, TSH was 0.21 µIU/mL, fT3 6.9 pmol/L and fT4 75.12 pmol/L. The more than 50% reduction in fT3 and subsequent clinical improvement were considered supportive of a predominant destructive component of AIT. Thiamazole was subsequently tapered and discontinued, while prednisone was continued with gradual dose reduction. Conclusion: This case illustrates that severe AIT may occur during apparently stable long-term amiodarone therapy. The clini cal, biochemical and ultrasonographic findings suggested a mixed/indeterminate phenotype, although the subsequent biochemi cal response was more consistent with a predominant destructive component. The case also demonstrates the importance of early recognition and individualized treatment of severe AIT. Because long-term follow-up was unavailable, the subsequent thyroid status and risk of recurrence could not be established.&#13;
&#13;
</p></abstract><kwd-group><kwd>Hyperthyroidism</kwd><kwd> Thyrotoxicosis</kwd><kwd> Amiodarone</kwd><kwd> Diarrhoea</kwd><kwd> Side effects</kwd><kwd> Long-term therapy</kwd></kwd-group></article-meta></front></article>
