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Article: The incidence of ophthalmopathy after radioiodine therapy for Graves' disease: Prognostic factors and the role of methimazole

TitleThe incidence of ophthalmopathy after radioiodine therapy for Graves' disease: Prognostic factors and the role of methimazole
Authors
Issue Date1994
PublisherThe Endocrine Society. The Journal's web site is located at http://jcem.endojournals.org
Citation
Journal Of Clinical Endocrinology And Metabolism, 1994, v. 79 n. 2, p. 542-546 How to Cite?
AbstractRadioactive iodine-131 (RAI) has been reported to be associated with a high incidence of development or exacerbation of Graves' ophthalmopathy (GO). This is thought to be associated with a surge of autoantibodies after RAI therapy. The role of methimazole (MMI), which possesses immunomodulatory action, in the prevention of GO was explored by studying 114 patients with Graves' disease. They were assigned randomly to receive either RAI alone or adjunctive antithyroid drugs, which consisted of MMI and L-T4 as a block- replacement therapy for 12 months and were followed for 2 yr. Thirty-five patients (30.7%) had GO at presentation. Twenty-one (18%) patients developed new GO, and six had worsening of preexisting GO. The development of hypothyroidism (P < 0.01) and an elevation of TSH (P < 0.05) were associated with increased risk of development or exacerbation of GO. The chance of development or exacerbation of GO is higher in those with no ophthalmopathy than in those with preexisting GO at presentation (P = 0.002). The incidence of development or exacerbation of GO was similar in the two treatment groups (RAI, 22.8%; adjunctive antithyroid drugs, 23.7%; P = NS). MMI was able to suppress the surge of TSH receptor antibody (TRAB) after RAI, but a surge in TRAB was not of prognostic significance for the development of GO after RAI. Patients who developed or had exacerbation of GO actually had lower TRAB at presentation (P = 0.02). We conclude that hypothyroidism with elevated TSH is an important adverse factor for the development or exacerbation of GO, and MMI was unable to prevent the development or exacerbation of GO after RAI.
Persistent Identifierhttp://hdl.handle.net/10722/49101
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.940
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKung, AWCen_HK
dc.contributor.authorYau, CCen_HK
dc.contributor.authorCheng, Aen_HK
dc.date.accessioned2008-06-12T06:34:26Z-
dc.date.available2008-06-12T06:34:26Z-
dc.date.issued1994en_HK
dc.identifier.citationJournal Of Clinical Endocrinology And Metabolism, 1994, v. 79 n. 2, p. 542-546en_HK
dc.identifier.issn0021-972Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/49101-
dc.description.abstractRadioactive iodine-131 (RAI) has been reported to be associated with a high incidence of development or exacerbation of Graves' ophthalmopathy (GO). This is thought to be associated with a surge of autoantibodies after RAI therapy. The role of methimazole (MMI), which possesses immunomodulatory action, in the prevention of GO was explored by studying 114 patients with Graves' disease. They were assigned randomly to receive either RAI alone or adjunctive antithyroid drugs, which consisted of MMI and L-T4 as a block- replacement therapy for 12 months and were followed for 2 yr. Thirty-five patients (30.7%) had GO at presentation. Twenty-one (18%) patients developed new GO, and six had worsening of preexisting GO. The development of hypothyroidism (P < 0.01) and an elevation of TSH (P < 0.05) were associated with increased risk of development or exacerbation of GO. The chance of development or exacerbation of GO is higher in those with no ophthalmopathy than in those with preexisting GO at presentation (P = 0.002). The incidence of development or exacerbation of GO was similar in the two treatment groups (RAI, 22.8%; adjunctive antithyroid drugs, 23.7%; P = NS). MMI was able to suppress the surge of TSH receptor antibody (TRAB) after RAI, but a surge in TRAB was not of prognostic significance for the development of GO after RAI. Patients who developed or had exacerbation of GO actually had lower TRAB at presentation (P = 0.02). We conclude that hypothyroidism with elevated TSH is an important adverse factor for the development or exacerbation of GO, and MMI was unable to prevent the development or exacerbation of GO after RAI.en_HK
dc.format.extent418 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherThe Endocrine Society. The Journal's web site is located at http://jcem.endojournals.orgen_HK
dc.relation.ispartofJournal of Clinical Endocrinology and Metabolismen_HK
dc.rightsJournal of Clinical Endocrinology and Metabolism. Copyright © The Endocrine Society.en_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshEye diseases - etiology - immunology - prevention & controlen_HK
dc.subject.meshGraves disease - complications - radiotherapyen_HK
dc.subject.meshIodine radioisotopes - adverse effects - therapeutic useen_HK
dc.subject.meshMethimazole - therapeutic useen_HK
dc.subject.meshAutoantibodies - blooden_HK
dc.titleThe incidence of ophthalmopathy after radioiodine therapy for Graves' disease: Prognostic factors and the role of methimazoleen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0021-972X&volume=79&issue=2&spage=542&epage=546&date=1994&atitle=The+incidence+of+ophthalmopathy+after+radioiodine+therapy+for+Graves%27+disease:+prognostic+factors+and+the+role+of+methimazoleen_HK
dc.identifier.emailKung, AWC:awckung@hku.hken_HK
dc.identifier.authorityKung, AWC=rp00368en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1210/jc.79.2.542en_HK
dc.identifier.pmid7913934-
dc.identifier.scopuseid_2-s2.0-0028030856en_HK
dc.identifier.hkuros4748-
dc.identifier.volume79en_HK
dc.identifier.issue2en_HK
dc.identifier.spage542en_HK
dc.identifier.epage546en_HK
dc.identifier.isiWOS:A1994PB50500038-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridKung, AWC=7102322339en_HK
dc.identifier.scopusauthoridYau, CC=7007038422en_HK
dc.identifier.scopusauthoridCheng, A=36055097300en_HK

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