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SAT490 Graves’ Disease In Remission Aggravated By Himalayan Salt Consumption
Disclosure: M.K. Shakir: None. K.F. Brown: None. J.S. Hatfield: None. N.O. Vietor: None. T.D. Hoang: None. Introduction: In iodine-replete countries, iodine-induced thyrotoxicosis may occasionally develop after ingestion or therapy with high doses of iodine. Recently, Himalayan salt has become very...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10554723/ http://dx.doi.org/10.1210/jendso/bvad114.1963 |
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author | Shakir, Mohamed K M Brown, Kevin F Hatfield, Jennifer S Vietor, Nicole O Hoang, Thanh Duc |
author_facet | Shakir, Mohamed K M Brown, Kevin F Hatfield, Jennifer S Vietor, Nicole O Hoang, Thanh Duc |
author_sort | Shakir, Mohamed K M |
collection | PubMed |
description | Disclosure: M.K. Shakir: None. K.F. Brown: None. J.S. Hatfield: None. N.O. Vietor: None. T.D. Hoang: None. Introduction: In iodine-replete countries, iodine-induced thyrotoxicosis may occasionally develop after ingestion or therapy with high doses of iodine. Recently, Himalayan salt has become very popular to bridge iodine deficiency, control hypothyroidism, and improve thyroid function. We report a patient with a history of treated Graves’ disease (GD) who developed acute thyrotoxicosis following the use of Himalayan salt. Case report: A 58-year-old woman presented with symptoms of heat intolerance, and unexpected 18-lbs weight loss over 3 months. Physical examination: HR 108 bpm, BP 110/70 mm Hg, normal eye examination, thyroid 45 gms, diffusely enlarged. Examinations of the heart, lungs and abdomen were normal. Lab tests: TSH 0.01 IU/mL, free T(4) 3.8 ng/dL, T(3) 308 pg/dL, thyrotropin receptor Ab 4.2 IU/L (<1.0), and thyroid stimulating immunoglobulin 1.89 1U/L (0.06-0.55). The I(131) uptake was 60% at 4 hours and the thyroid scan revealed diffuse homogenous uptake confirming GD. She was treated with methimazole (MMI) for 2 years and remission was achieved. MMI was stopped and she remained euthyroid. Twelve months later, she developed hyperthyroid symptoms with a 15-lb weight loss, palpitations, and anxiety. Examination confirmed a 50-gram diffuse goiter and other physical findings consistent with hyperthyroidism. She admitted that she had been taking Himalayan salt (approximately 10 grams daily) in place of regular salt for the past 6 months. Lab tests confirmed recurrent GD: TSH <0.01 IU/mL, FT4 4.1 ng/dL, total T(3) 278 pg/dL, and I(131) uptake was 55% at 24 hours. A 24-hours urine iodine was 898 mcg (normal 100-199) and plasma iodine level was 484 mcg/L (normal 52-109). A diagnosis of iodine-induced recurrence of GD was made, and she was treated with MMI and low iodine diet. After 3 months, she improved significantly and was able to discontinue the MMI by 6 months. A follow- up urine iodine was 189 mcg/L with a plasma iodine level of 78 mcg/L. Subsequently she remained euthyroid for an additional 18 months of follow-up without any treatment. Conclusion: The recommended daily dietary allowance for iodine in adults is 150mcg. Himalayan rock salt may provide a rich source of iodine and consumption of large amounts can lead to iodine excess. However, the available studies do not provide the iodine content in commercially available Himalayan salt preparations. Although the Himalayan salt is advertised to have beneficial effects in patients with thyroid disorders, this food supplement may have deleterious effects in susceptible patients who do not have iodine deficiency, have GD, or are at risk for thyrotoxicosis. Indeed, Himalayan salt use exacerbated GD in our patient, as evidenced by iodine overdose during acute exacerbation and resolution of GD with iodine normalization and low dose MMI. We recommend that patients with thyroid disorders be educated regarding Himalayan salt use. Presentation Date: Saturday, June 17, 2023 |
format | Online Article Text |
id | pubmed-10554723 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-105547232023-10-06 SAT490 Graves’ Disease In Remission Aggravated By Himalayan Salt Consumption Shakir, Mohamed K M Brown, Kevin F Hatfield, Jennifer S Vietor, Nicole O Hoang, Thanh Duc J Endocr Soc Thyroid Disclosure: M.K. Shakir: None. K.F. Brown: None. J.S. Hatfield: None. N.O. Vietor: None. T.D. Hoang: None. Introduction: In iodine-replete countries, iodine-induced thyrotoxicosis may occasionally develop after ingestion or therapy with high doses of iodine. Recently, Himalayan salt has become very popular to bridge iodine deficiency, control hypothyroidism, and improve thyroid function. We report a patient with a history of treated Graves’ disease (GD) who developed acute thyrotoxicosis following the use of Himalayan salt. Case report: A 58-year-old woman presented with symptoms of heat intolerance, and unexpected 18-lbs weight loss over 3 months. Physical examination: HR 108 bpm, BP 110/70 mm Hg, normal eye examination, thyroid 45 gms, diffusely enlarged. Examinations of the heart, lungs and abdomen were normal. Lab tests: TSH 0.01 IU/mL, free T(4) 3.8 ng/dL, T(3) 308 pg/dL, thyrotropin receptor Ab 4.2 IU/L (<1.0), and thyroid stimulating immunoglobulin 1.89 1U/L (0.06-0.55). The I(131) uptake was 60% at 4 hours and the thyroid scan revealed diffuse homogenous uptake confirming GD. She was treated with methimazole (MMI) for 2 years and remission was achieved. MMI was stopped and she remained euthyroid. Twelve months later, she developed hyperthyroid symptoms with a 15-lb weight loss, palpitations, and anxiety. Examination confirmed a 50-gram diffuse goiter and other physical findings consistent with hyperthyroidism. She admitted that she had been taking Himalayan salt (approximately 10 grams daily) in place of regular salt for the past 6 months. Lab tests confirmed recurrent GD: TSH <0.01 IU/mL, FT4 4.1 ng/dL, total T(3) 278 pg/dL, and I(131) uptake was 55% at 24 hours. A 24-hours urine iodine was 898 mcg (normal 100-199) and plasma iodine level was 484 mcg/L (normal 52-109). A diagnosis of iodine-induced recurrence of GD was made, and she was treated with MMI and low iodine diet. After 3 months, she improved significantly and was able to discontinue the MMI by 6 months. A follow- up urine iodine was 189 mcg/L with a plasma iodine level of 78 mcg/L. Subsequently she remained euthyroid for an additional 18 months of follow-up without any treatment. Conclusion: The recommended daily dietary allowance for iodine in adults is 150mcg. Himalayan rock salt may provide a rich source of iodine and consumption of large amounts can lead to iodine excess. However, the available studies do not provide the iodine content in commercially available Himalayan salt preparations. Although the Himalayan salt is advertised to have beneficial effects in patients with thyroid disorders, this food supplement may have deleterious effects in susceptible patients who do not have iodine deficiency, have GD, or are at risk for thyrotoxicosis. Indeed, Himalayan salt use exacerbated GD in our patient, as evidenced by iodine overdose during acute exacerbation and resolution of GD with iodine normalization and low dose MMI. We recommend that patients with thyroid disorders be educated regarding Himalayan salt use. Presentation Date: Saturday, June 17, 2023 Oxford University Press 2023-10-05 /pmc/articles/PMC10554723/ http://dx.doi.org/10.1210/jendso/bvad114.1963 Text en © The Author(s) 2023. Published by Oxford University Press on behalf of the Endocrine Society. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs licence (https://creativecommons.org/licenses/by-nc-nd/4.0/), which permits non-commercial reproduction and distribution of the work, in any medium, provided the original work is not altered or transformed in any way, and that the work is properly cited. For commercial re-use, please contact journals.permissions@oup.com |
spellingShingle | Thyroid Shakir, Mohamed K M Brown, Kevin F Hatfield, Jennifer S Vietor, Nicole O Hoang, Thanh Duc SAT490 Graves’ Disease In Remission Aggravated By Himalayan Salt Consumption |
title | SAT490 Graves’ Disease In Remission Aggravated By Himalayan Salt Consumption |
title_full | SAT490 Graves’ Disease In Remission Aggravated By Himalayan Salt Consumption |
title_fullStr | SAT490 Graves’ Disease In Remission Aggravated By Himalayan Salt Consumption |
title_full_unstemmed | SAT490 Graves’ Disease In Remission Aggravated By Himalayan Salt Consumption |
title_short | SAT490 Graves’ Disease In Remission Aggravated By Himalayan Salt Consumption |
title_sort | sat490 graves’ disease in remission aggravated by himalayan salt consumption |
topic | Thyroid |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10554723/ http://dx.doi.org/10.1210/jendso/bvad114.1963 |
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