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dc.contributor.authorCronin, C C
dc.contributor.authorHiggins, T M
dc.contributor.authorMurphy, D
dc.contributor.authorFerriss, J B
dc.date.accessioned2012-02-03T15:15:35Z
dc.date.available2012-02-03T15:15:35Z
dc.date.issued2012-02-03T15:15:35Z
dc.identifier.citationIr Med J. 1996 Jul-Aug;89(4):141-2.en_GB
dc.identifier.issn0332-3102 (Print)en_GB
dc.identifier.issn0332-3102 (Linking)en_GB
dc.identifier.pmid8824038en_GB
dc.identifier.urihttp://hdl.handle.net/10147/209225
dc.description.abstractHypothyroidism in patients with Graves' disease is usually the result of ablative treatment. We describe a 58 year old man with Graves' ophthalmopathy and pre-tibial myxoedema, who presented with spontaneous primary hypothyroidism. Circulating TSH receptor antibody activity was increased, while thyroid microsomal antibody was detectable in titres greater than one in one hundred thousand. It is likely that the TSH receptor antibody of Graves' disease was ineffective in stimulating hyperthyroidism because of concomitant thyroid destruction due to Hashimoto's disease. Alternatively, primary hypothyroidism could have resulted from the effects of a circulating TSH receptor blocking antibody.
dc.language.isoengen_GB
dc.subject.meshGraves Disease/*complications/diagnosisen_GB
dc.subject.meshHumansen_GB
dc.subject.meshHypothyroidism/*etiologyen_GB
dc.subject.meshLeg Dermatoses/etiologyen_GB
dc.subject.meshMaleen_GB
dc.subject.meshMiddle Ageden_GB
dc.subject.meshMyxedema/etiologyen_GB
dc.subject.meshThyroiditis, Autoimmune/*complications/diagnosisen_GB
dc.titleConcomitant Graves' disease and Hashimoto's thyroiditis, presenting as primary hypothyroidism.en_GB
dc.contributor.departmentDepartment of Medicine, Cork University Hospital.en_GB
dc.identifier.journalIrish medical journalen_GB
dc.description.provinceMunster
refterms.dateFOA2024-05-21T12:02:52Z
html.description.abstractHypothyroidism in patients with Graves' disease is usually the result of ablative treatment. We describe a 58 year old man with Graves' ophthalmopathy and pre-tibial myxoedema, who presented with spontaneous primary hypothyroidism. Circulating TSH receptor antibody activity was increased, while thyroid microsomal antibody was detectable in titres greater than one in one hundred thousand. It is likely that the TSH receptor antibody of Graves' disease was ineffective in stimulating hyperthyroidism because of concomitant thyroid destruction due to Hashimoto's disease. Alternatively, primary hypothyroidism could have resulted from the effects of a circulating TSH receptor blocking antibody.


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