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Clinical Characteristics of Amiodarone-Induced Thyrotoxicosis and Hypothyroidism in Japan
Since amiodarone was introduced in Japan in 1992, the incidence of the drug-induced thyroid dysfunction has been increasing. We studied the thyroid function of 13 patients with amiodarone-induced thyrotoxicosis (AIT) and 11 patients with amiodarone-associated hypothyroidism (AAH) who had been referr...
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| Published in: | ENDOCRINE JOURNAL 1999, Vol.46(3), pp.443-451 |
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| container_title | ENDOCRINE JOURNAL |
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| creator | SATO, KANJI MIYAKAWA, MEGUMI ETO, MIYUKI INABA, TAKAKO MATSUDA, NAOKI SHIGA, TSUYOSHI OHNISHI, SATOSHI KASANUKI, HIROSHI |
| description | Since amiodarone was introduced in Japan in 1992, the incidence of the drug-induced thyroid dysfunction has been increasing. We studied the thyroid function of 13 patients with amiodarone-induced thyrotoxicosis (AIT) and 11 patients with amiodarone-associated hypothyroidism (AAH) who had been referred to our Institute in the last 6years. AIT and AAH developed after 39±21 and 20±16 months of amiodarone treatment, respectively. One patient developed AAH followed by AIT. The AIT ranged from subclinical to overt thyrotoxicosis. Four patients with moderate to marked AIT were treated with methimazole. Their thyrotoxicosis persisted for 3 to 9months, despite administration of antithyroid agents. One patient with mild thyrotoxicosis was treated with prednisolone, resulting in a euthyroid state in a few months. Eight patients with asymptomatic to moderate thyrotoxicosis resolved spontaneously without any treatment. In four asymptomatic patients with AIT, serum levels of T3 and T4 were in the upper normal range or slightly high ( |
| doi_str_mv | 10.1507/endocrj.46.443 |
| format | article |
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We studied the thyroid function of 13 patients with amiodarone-induced thyrotoxicosis (AIT) and 11 patients with amiodarone-associated hypothyroidism (AAH) who had been referred to our Institute in the last 6years. AIT and AAH developed after 39±21 and 20±16 months of amiodarone treatment, respectively. One patient developed AAH followed by AIT. The AIT ranged from subclinical to overt thyrotoxicosis. Four patients with moderate to marked AIT were treated with methimazole. Their thyrotoxicosis persisted for 3 to 9months, despite administration of antithyroid agents. One patient with mild thyrotoxicosis was treated with prednisolone, resulting in a euthyroid state in a few months. Eight patients with asymptomatic to moderate thyrotoxicosis resolved spontaneously without any treatment. In four asymptomatic patients with AIT, serum levels of T3 and T4 were in the upper normal range or slightly high (<12μg/dl), accompanied by suppressed TSH (<0.1 μU/ml) and high thyroglobulin levels, suggesting destruction-induced thyrotoxicosis. Such a subclinical thyrotoxicosis developed repeatedly in one patient. Ultrasonographic studies revealed no nodular lesion in the thyroid, and color flow Doppler sonography demonstrated no hypervascularity in the thyroid gland in any AIT patient. Although it is postulated in Europe that there are two types of AIT, namely type I, which develops in patients with latent Graves' disease or toxic multinodular goiter, and type II, which develops in an apparently normal thyroid as destructive thyroiditis, all AIT patients we have seen so far had developed destructive type AIT. Sufficient intake of iodide and a very low incidence of toxic multinodular goiter may account for the rare incidence of type I AIT in our country. Mild to moderate AIT resolved spontaneously without discontinuing amiodarone, but it was discontinuedin two of 13 AIT patients because of extrathyroidal adverse reactions.</description><identifier>ISSN: 0918-8959</identifier><identifier>EISSN: 1348-4540</identifier><identifier>DOI: 10.1507/endocrj.46.443</identifier><identifier>PMID: 10503998</identifier><language>eng</language><publisher>Japan: The Japan Endocrine Society</publisher><subject>Adult ; Aged ; Amiodarone ; Amiodarone - adverse effects ; Anti-Arrhythmia Agents - adverse effects ; Antithyroid Agents - therapeutic use ; Color flow Doppler sonography ; Female ; Humans ; Hypothyroidism ; Hypothyroidism - chemically induced ; Hypothyroidism - drug therapy ; Iodide ; Japan ; Male ; Methimazole - therapeutic use ; Middle Aged ; Prednisolone - therapeutic use ; Thyrotoxicosis ; Thyrotoxicosis - blood ; Thyrotoxicosis - chemically induced ; Thyrotoxicosis - drug therapy ; Thyrotropin - blood ; Thyroxine - blood ; Time Factors ; Triiodothyronine - blood</subject><ispartof>Endocrine Journal, 1999, Vol.46(3), pp.443-451</ispartof><rights>The Japan Endocrine Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c655t-8bc11398903212fa32f31748fd3290e8be9ddb47f27d90e62787ee9cdda1aaa93</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,1882,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10503998$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SATO, KANJI</creatorcontrib><creatorcontrib>MIYAKAWA, MEGUMI</creatorcontrib><creatorcontrib>ETO, MIYUKI</creatorcontrib><creatorcontrib>INABA, TAKAKO</creatorcontrib><creatorcontrib>MATSUDA, NAOKI</creatorcontrib><creatorcontrib>SHIGA, TSUYOSHI</creatorcontrib><creatorcontrib>OHNISHI, SATOSHI</creatorcontrib><creatorcontrib>KASANUKI, HIROSHI</creatorcontrib><creatorcontrib>Department of Cardiology</creatorcontrib><creatorcontrib>Department of Medicine</creatorcontrib><creatorcontrib>The Heart Institute of Japan</creatorcontrib><creatorcontrib>Institute of Clinical Endocrinotogy</creatorcontrib><creatorcontrib>Tokyo Women's Medical University</creatorcontrib><title>Clinical Characteristics of Amiodarone-Induced Thyrotoxicosis and Hypothyroidism in Japan</title><title>ENDOCRINE JOURNAL</title><addtitle>Endocr J</addtitle><description>Since amiodarone was introduced in Japan in 1992, the incidence of the drug-induced thyroid dysfunction has been increasing. We studied the thyroid function of 13 patients with amiodarone-induced thyrotoxicosis (AIT) and 11 patients with amiodarone-associated hypothyroidism (AAH) who had been referred to our Institute in the last 6years. AIT and AAH developed after 39±21 and 20±16 months of amiodarone treatment, respectively. One patient developed AAH followed by AIT. The AIT ranged from subclinical to overt thyrotoxicosis. Four patients with moderate to marked AIT were treated with methimazole. Their thyrotoxicosis persisted for 3 to 9months, despite administration of antithyroid agents. One patient with mild thyrotoxicosis was treated with prednisolone, resulting in a euthyroid state in a few months. Eight patients with asymptomatic to moderate thyrotoxicosis resolved spontaneously without any treatment. In four asymptomatic patients with AIT, serum levels of T3 and T4 were in the upper normal range or slightly high (<12μg/dl), accompanied by suppressed TSH (<0.1 μU/ml) and high thyroglobulin levels, suggesting destruction-induced thyrotoxicosis. Such a subclinical thyrotoxicosis developed repeatedly in one patient. Ultrasonographic studies revealed no nodular lesion in the thyroid, and color flow Doppler sonography demonstrated no hypervascularity in the thyroid gland in any AIT patient. Although it is postulated in Europe that there are two types of AIT, namely type I, which develops in patients with latent Graves' disease or toxic multinodular goiter, and type II, which develops in an apparently normal thyroid as destructive thyroiditis, all AIT patients we have seen so far had developed destructive type AIT. Sufficient intake of iodide and a very low incidence of toxic multinodular goiter may account for the rare incidence of type I AIT in our country. Mild to moderate AIT resolved spontaneously without discontinuing amiodarone, but it was discontinuedin two of 13 AIT patients because of extrathyroidal adverse reactions.</description><subject>Adult</subject><subject>Aged</subject><subject>Amiodarone</subject><subject>Amiodarone - adverse effects</subject><subject>Anti-Arrhythmia Agents - adverse effects</subject><subject>Antithyroid Agents - therapeutic use</subject><subject>Color flow Doppler sonography</subject><subject>Female</subject><subject>Humans</subject><subject>Hypothyroidism</subject><subject>Hypothyroidism - chemically induced</subject><subject>Hypothyroidism - drug therapy</subject><subject>Iodide</subject><subject>Japan</subject><subject>Male</subject><subject>Methimazole - therapeutic use</subject><subject>Middle Aged</subject><subject>Prednisolone - therapeutic use</subject><subject>Thyrotoxicosis</subject><subject>Thyrotoxicosis - blood</subject><subject>Thyrotoxicosis - chemically induced</subject><subject>Thyrotoxicosis - drug therapy</subject><subject>Thyrotropin - blood</subject><subject>Thyroxine - blood</subject><subject>Time Factors</subject><subject>Triiodothyronine - blood</subject><issn>0918-8959</issn><issn>1348-4540</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><recordid>eNpNkUFPwyAUx4nRuDm9ejT9Ap1QaAvHpdFtZomXefBEGFDH0kKFLnHfXuo29cAjPP7vz3s_ALhHcIpyWD5qq5z0uykppoTgCzBGmNCU5ARegjFkiKaU5WwEbkLYQYhxTvA1GCGYQ8wYHYP3qjHWSNEk1VZ4IXvtTeiNDImrk1lrnBLeWZ0urdpLrZL19uBd776MdMGERFiVLA6d64e0USa0ibHJi-iEvQVXtWiCvjvtE_D2_LSuFunqdb6sZqtUFnnep3QjEcKMMogzlNUCZzVGJaG1whmDmm40U2pDyjorVTwXWUlLrZlUSiAhBMMTMD36Su9C8LrmnTet8AeOIB8Y8RMjTgoeGcWCh2NBt9-0Wv2TH6FEwfwoiLcDGmcjI813bu9tnITLz-LHkiPGGIeQFBBziOKK9jHkCMHImqE_p13oxYf-fUr4iLjR586iDx66O4foclbI-CtRhr8BfSiVbw</recordid><startdate>1999</startdate><enddate>1999</enddate><creator>SATO, KANJI</creator><creator>MIYAKAWA, MEGUMI</creator><creator>ETO, MIYUKI</creator><creator>INABA, TAKAKO</creator><creator>MATSUDA, NAOKI</creator><creator>SHIGA, TSUYOSHI</creator><creator>OHNISHI, SATOSHI</creator><creator>KASANUKI, HIROSHI</creator><general>The Japan Endocrine Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>1999</creationdate><title>Clinical Characteristics of Amiodarone-Induced Thyrotoxicosis and Hypothyroidism in Japan</title><author>SATO, KANJI ; MIYAKAWA, MEGUMI ; ETO, MIYUKI ; INABA, TAKAKO ; MATSUDA, NAOKI ; SHIGA, TSUYOSHI ; OHNISHI, SATOSHI ; KASANUKI, HIROSHI</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c655t-8bc11398903212fa32f31748fd3290e8be9ddb47f27d90e62787ee9cdda1aaa93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Amiodarone</topic><topic>Amiodarone - adverse effects</topic><topic>Anti-Arrhythmia Agents - adverse effects</topic><topic>Antithyroid Agents - therapeutic use</topic><topic>Color flow Doppler sonography</topic><topic>Female</topic><topic>Humans</topic><topic>Hypothyroidism</topic><topic>Hypothyroidism - chemically induced</topic><topic>Hypothyroidism - drug therapy</topic><topic>Iodide</topic><topic>Japan</topic><topic>Male</topic><topic>Methimazole - therapeutic use</topic><topic>Middle Aged</topic><topic>Prednisolone - therapeutic use</topic><topic>Thyrotoxicosis</topic><topic>Thyrotoxicosis - blood</topic><topic>Thyrotoxicosis - chemically induced</topic><topic>Thyrotoxicosis - drug therapy</topic><topic>Thyrotropin - blood</topic><topic>Thyroxine - blood</topic><topic>Time Factors</topic><topic>Triiodothyronine - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SATO, KANJI</creatorcontrib><creatorcontrib>MIYAKAWA, MEGUMI</creatorcontrib><creatorcontrib>ETO, MIYUKI</creatorcontrib><creatorcontrib>INABA, TAKAKO</creatorcontrib><creatorcontrib>MATSUDA, NAOKI</creatorcontrib><creatorcontrib>SHIGA, TSUYOSHI</creatorcontrib><creatorcontrib>OHNISHI, SATOSHI</creatorcontrib><creatorcontrib>KASANUKI, HIROSHI</creatorcontrib><creatorcontrib>Department of Cardiology</creatorcontrib><creatorcontrib>Department of Medicine</creatorcontrib><creatorcontrib>The Heart Institute of Japan</creatorcontrib><creatorcontrib>Institute of Clinical Endocrinotogy</creatorcontrib><creatorcontrib>Tokyo Women's Medical University</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>ENDOCRINE JOURNAL</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SATO, KANJI</au><au>MIYAKAWA, MEGUMI</au><au>ETO, MIYUKI</au><au>INABA, TAKAKO</au><au>MATSUDA, NAOKI</au><au>SHIGA, TSUYOSHI</au><au>OHNISHI, SATOSHI</au><au>KASANUKI, HIROSHI</au><aucorp>Department of Cardiology</aucorp><aucorp>Department of Medicine</aucorp><aucorp>The Heart Institute of Japan</aucorp><aucorp>Institute of Clinical Endocrinotogy</aucorp><aucorp>Tokyo Women's Medical University</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clinical Characteristics of Amiodarone-Induced Thyrotoxicosis and Hypothyroidism in Japan</atitle><jtitle>ENDOCRINE JOURNAL</jtitle><addtitle>Endocr J</addtitle><date>1999</date><risdate>1999</risdate><volume>46</volume><issue>3</issue><spage>443</spage><epage>451</epage><pages>443-451</pages><issn>0918-8959</issn><eissn>1348-4540</eissn><abstract>Since amiodarone was introduced in Japan in 1992, the incidence of the drug-induced thyroid dysfunction has been increasing. We studied the thyroid function of 13 patients with amiodarone-induced thyrotoxicosis (AIT) and 11 patients with amiodarone-associated hypothyroidism (AAH) who had been referred to our Institute in the last 6years. AIT and AAH developed after 39±21 and 20±16 months of amiodarone treatment, respectively. One patient developed AAH followed by AIT. The AIT ranged from subclinical to overt thyrotoxicosis. Four patients with moderate to marked AIT were treated with methimazole. Their thyrotoxicosis persisted for 3 to 9months, despite administration of antithyroid agents. One patient with mild thyrotoxicosis was treated with prednisolone, resulting in a euthyroid state in a few months. Eight patients with asymptomatic to moderate thyrotoxicosis resolved spontaneously without any treatment. In four asymptomatic patients with AIT, serum levels of T3 and T4 were in the upper normal range or slightly high (<12μg/dl), accompanied by suppressed TSH (<0.1 μU/ml) and high thyroglobulin levels, suggesting destruction-induced thyrotoxicosis. Such a subclinical thyrotoxicosis developed repeatedly in one patient. Ultrasonographic studies revealed no nodular lesion in the thyroid, and color flow Doppler sonography demonstrated no hypervascularity in the thyroid gland in any AIT patient. Although it is postulated in Europe that there are two types of AIT, namely type I, which develops in patients with latent Graves' disease or toxic multinodular goiter, and type II, which develops in an apparently normal thyroid as destructive thyroiditis, all AIT patients we have seen so far had developed destructive type AIT. Sufficient intake of iodide and a very low incidence of toxic multinodular goiter may account for the rare incidence of type I AIT in our country. Mild to moderate AIT resolved spontaneously without discontinuing amiodarone, but it was discontinuedin two of 13 AIT patients because of extrathyroidal adverse reactions.</abstract><cop>Japan</cop><pub>The Japan Endocrine Society</pub><pmid>10503998</pmid><doi>10.1507/endocrj.46.443</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Endocrine Journal, 1999, Vol.46(3), pp.443-451 |
| issn | 0918-8959 1348-4540 |
| language | eng |
| recordid | cdi_crossref_primary_10_1507_endocrj_46_443 |
| source | J-STAGE (Japan Science & Technology Information Aggregator, Electronic) - Open Access English articles |
| subjects | Adult Aged Amiodarone Amiodarone - adverse effects Anti-Arrhythmia Agents - adverse effects Antithyroid Agents - therapeutic use Color flow Doppler sonography Female Humans Hypothyroidism Hypothyroidism - chemically induced Hypothyroidism - drug therapy Iodide Japan Male Methimazole - therapeutic use Middle Aged Prednisolone - therapeutic use Thyrotoxicosis Thyrotoxicosis - blood Thyrotoxicosis - chemically induced Thyrotoxicosis - drug therapy Thyrotropin - blood Thyroxine - blood Time Factors Triiodothyronine - blood |
| title | Clinical Characteristics of Amiodarone-Induced Thyrotoxicosis and Hypothyroidism in Japan |
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