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Conversion to Graves disease from Hashimoto thyroiditis: a study of 24 patients

OBJECTIVE: The conversion of Hashimoto's thyroiditis (HT) to hyperthyroidism due to thyrotropin receptor antibodies is intriguing and considered rare. The contribution of TSH receptor blocking antibodies (TRAb), which may be stimulators (TSAb) or blockers (TBAb), is suspected. We describe clini...

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Autores principales: Gonzalez-Aguilera, Beatriz, Betea, Daniela, Lutteri, Laurence, Cavalier, Etienne, Geenen, Vincent, Beckers, Albert, Valdes-Socin, Hernan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Sociedade Brasileira de Endocrinologia e Metabologia 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10118676/
https://www.ncbi.nlm.nih.gov/pubmed/30624501
http://dx.doi.org/10.20945/2359-3997000000086
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author Gonzalez-Aguilera, Beatriz
Betea, Daniela
Lutteri, Laurence
Cavalier, Etienne
Geenen, Vincent
Beckers, Albert
Valdes-Socin, Hernan
author_facet Gonzalez-Aguilera, Beatriz
Betea, Daniela
Lutteri, Laurence
Cavalier, Etienne
Geenen, Vincent
Beckers, Albert
Valdes-Socin, Hernan
author_sort Gonzalez-Aguilera, Beatriz
collection PubMed
description OBJECTIVE: The conversion of Hashimoto's thyroiditis (HT) to hyperthyroidism due to thyrotropin receptor antibodies is intriguing and considered rare. The contribution of TSH receptor blocking antibodies (TRAb), which may be stimulators (TSAb) or blockers (TBAb), is suspected. We describe clinical and biological variables in a series of patients switching from Hashimoto's thyroiditis to Grave's disease. SUBJECTS AND METHODS: Retrospective case study of 24 patients with Hashimoto's thyroiditis followed during 48 ± 36 months that developed later Graves’ disease (GD). These variables were analysed in the hypo and hyperthyroid phase: age, sex, initial TSH, free triiodothyronine (fT3), free thyroxine (fT4), anti-TPO, TBII antibodies, parietal cell autoantibodies, time between hypo and hyperthyroidism, thyroid volume and levothyroxine doses (LT). RESULTS: In HT, mean TSH was 9.4 ± 26.1 UI/L and levothyroxine treatment was 66.2 ± 30.8 µg/day. The switch to GD was observed 38 ± 45 months after HT diagnosis. As expected, we found significant differences on TSH, FT3, FT4 and TBAb levels. Three out of 14 patients had parietal cell autoantibodies. In two of these three cases there was an Helicobacter pylori infection. There were no significant differences between HT and GD groups with respect to thyroid volume. CONCLUSIONS: To our knowledge, large series documenting the conversion of HT to GD are scarce. Although rare, this phenomenon should not be misdiagnosed. Suspicion should be raised whenever thyroxine posology must be tapered down during the follow-up of HT patients. Further immunological and genetic studies are needed to explain this unusual autoimmune change.
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spelling pubmed-101186762023-04-21 Conversion to Graves disease from Hashimoto thyroiditis: a study of 24 patients Gonzalez-Aguilera, Beatriz Betea, Daniela Lutteri, Laurence Cavalier, Etienne Geenen, Vincent Beckers, Albert Valdes-Socin, Hernan Arch Endocrinol Metab Original Article OBJECTIVE: The conversion of Hashimoto's thyroiditis (HT) to hyperthyroidism due to thyrotropin receptor antibodies is intriguing and considered rare. The contribution of TSH receptor blocking antibodies (TRAb), which may be stimulators (TSAb) or blockers (TBAb), is suspected. We describe clinical and biological variables in a series of patients switching from Hashimoto's thyroiditis to Grave's disease. SUBJECTS AND METHODS: Retrospective case study of 24 patients with Hashimoto's thyroiditis followed during 48 ± 36 months that developed later Graves’ disease (GD). These variables were analysed in the hypo and hyperthyroid phase: age, sex, initial TSH, free triiodothyronine (fT3), free thyroxine (fT4), anti-TPO, TBII antibodies, parietal cell autoantibodies, time between hypo and hyperthyroidism, thyroid volume and levothyroxine doses (LT). RESULTS: In HT, mean TSH was 9.4 ± 26.1 UI/L and levothyroxine treatment was 66.2 ± 30.8 µg/day. The switch to GD was observed 38 ± 45 months after HT diagnosis. As expected, we found significant differences on TSH, FT3, FT4 and TBAb levels. Three out of 14 patients had parietal cell autoantibodies. In two of these three cases there was an Helicobacter pylori infection. There were no significant differences between HT and GD groups with respect to thyroid volume. CONCLUSIONS: To our knowledge, large series documenting the conversion of HT to GD are scarce. Although rare, this phenomenon should not be misdiagnosed. Suspicion should be raised whenever thyroxine posology must be tapered down during the follow-up of HT patients. Further immunological and genetic studies are needed to explain this unusual autoimmune change. Sociedade Brasileira de Endocrinologia e Metabologia 2018-10-01 /pmc/articles/PMC10118676/ /pubmed/30624501 http://dx.doi.org/10.20945/2359-3997000000086 Text en https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Gonzalez-Aguilera, Beatriz
Betea, Daniela
Lutteri, Laurence
Cavalier, Etienne
Geenen, Vincent
Beckers, Albert
Valdes-Socin, Hernan
Conversion to Graves disease from Hashimoto thyroiditis: a study of 24 patients
title Conversion to Graves disease from Hashimoto thyroiditis: a study of 24 patients
title_full Conversion to Graves disease from Hashimoto thyroiditis: a study of 24 patients
title_fullStr Conversion to Graves disease from Hashimoto thyroiditis: a study of 24 patients
title_full_unstemmed Conversion to Graves disease from Hashimoto thyroiditis: a study of 24 patients
title_short Conversion to Graves disease from Hashimoto thyroiditis: a study of 24 patients
title_sort conversion to graves disease from hashimoto thyroiditis: a study of 24 patients
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10118676/
https://www.ncbi.nlm.nih.gov/pubmed/30624501
http://dx.doi.org/10.20945/2359-3997000000086
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