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SAT489 Grave’s Disease Secondary To Alemtuzumabuse
Disclosure: M.S. Gong: None. D. Lee: None. R. Arceo-Mendoza: None. Introduction: We present a case of alemtuzumab-induced autoimmune thyroid disease in a patient with Multiple Sclerosis (MS). Clinical Case: A 42/F was evaluated by endocrine inpatient service for hyperthyroidism. She presented with t...
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/PMC10554499/ http://dx.doi.org/10.1210/jendso/bvad114.1962 |
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author | Gong, Michael Shifeng Lee, David Arceo-Mendoza, Rod Marianne |
author_facet | Gong, Michael Shifeng Lee, David Arceo-Mendoza, Rod Marianne |
author_sort | Gong, Michael Shifeng |
collection | PubMed |
description | Disclosure: M.S. Gong: None. D. Lee: None. R. Arceo-Mendoza: None. Introduction: We present a case of alemtuzumab-induced autoimmune thyroid disease in a patient with Multiple Sclerosis (MS). Clinical Case: A 42/F was evaluated by endocrine inpatient service for hyperthyroidism. She presented with tremors, dyspnea, and ataxic gait. She has known MS and was treated with Alemtuzumab (ALZ) in 2018 and in 2019, with her initial infusion being 4 years prior to this admission. Lab tests on admission showed TSH of <0.01 uIU/mL with elevated Free T3 and Free T4 of 1987 pg/dL (NV:171-371 pg/dL) and 3.9 ng/dL (NV:0.7-1.5 ng/dL) respectively. Her Thyroid Stimulating Immunoglobulin and TSH receptor binding antibody were elevated. Baseline TSH prior to starting ALZ and a follow up TSH in 2020 were in the normal range. She denies personal or family history of thyroid disease. Hospital course was further compounded by ongoing leukopenia, with a WBC of 2.3 and ANC of 1.1. Initiation of thionamide therapy was discussed however patient declined to start methimazole when risk of agranulocytosis, albeit low, was explained. She had opted to proceed with RAI therapy for definitive management but then changed her mind. We were just initially able to treat her with prednisone, beta blocker and cholestyramine with close biochemical monitoring as an outpatient. Her Grave’s hyperthyroidism was refractory to medical management hence she was eventually admitted again for medical optimization and surgical evaluation. Her hospital course upon readmission was complicated by worsening hemoptysis and a diagnosis of pulmonary embolism. At this point, it was decided she is not a good surgical candidate for thyroid surgery given comorbidities. She eventually agreed to start methimazole after undergoing bone marrow biopsy for worsening leukopenia and cleared by hematology to start the antithyroid drug. At this time, she remains to be on methimazole as an outpatient. Clinical course however, is unfortunately complicated by patient’s ongoing poor compliance to clinic follow up. Clinical Lesson: ALZ is an anti-CD52 monoclonal Ab which induces depletion of B and T lymphocytes causing lymphopenia and immunosuppression. It is an effective treatment for MS but is linked to a number of autoimmune adverse event. Thyroid autoimmune dysfunction may occur in 20-30% of patients, and Grave’s disease accounts for 60-70% of cases. The ALZ product label recommends TFT monitoring every 3 months for at least 48 months after the last infusion. Our patient presented with Grave’s disease in 4 years following initial ALZ administration. To our knowledge, there is no published case with reported ALZ-induced Grave’s disease with this length of interval since infusion. Our case highlights not only the importance of pretreatment screening but continued vigilance and close thyroid function monitoring in patients treated with ALZ even several years after therapy. Presentation Date: Saturday, June 17, 2023 |
format | Online Article Text |
id | pubmed-10554499 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-105544992023-10-06 SAT489 Grave’s Disease Secondary To Alemtuzumabuse Gong, Michael Shifeng Lee, David Arceo-Mendoza, Rod Marianne J Endocr Soc Thyroid Disclosure: M.S. Gong: None. D. Lee: None. R. Arceo-Mendoza: None. Introduction: We present a case of alemtuzumab-induced autoimmune thyroid disease in a patient with Multiple Sclerosis (MS). Clinical Case: A 42/F was evaluated by endocrine inpatient service for hyperthyroidism. She presented with tremors, dyspnea, and ataxic gait. She has known MS and was treated with Alemtuzumab (ALZ) in 2018 and in 2019, with her initial infusion being 4 years prior to this admission. Lab tests on admission showed TSH of <0.01 uIU/mL with elevated Free T3 and Free T4 of 1987 pg/dL (NV:171-371 pg/dL) and 3.9 ng/dL (NV:0.7-1.5 ng/dL) respectively. Her Thyroid Stimulating Immunoglobulin and TSH receptor binding antibody were elevated. Baseline TSH prior to starting ALZ and a follow up TSH in 2020 were in the normal range. She denies personal or family history of thyroid disease. Hospital course was further compounded by ongoing leukopenia, with a WBC of 2.3 and ANC of 1.1. Initiation of thionamide therapy was discussed however patient declined to start methimazole when risk of agranulocytosis, albeit low, was explained. She had opted to proceed with RAI therapy for definitive management but then changed her mind. We were just initially able to treat her with prednisone, beta blocker and cholestyramine with close biochemical monitoring as an outpatient. Her Grave’s hyperthyroidism was refractory to medical management hence she was eventually admitted again for medical optimization and surgical evaluation. Her hospital course upon readmission was complicated by worsening hemoptysis and a diagnosis of pulmonary embolism. At this point, it was decided she is not a good surgical candidate for thyroid surgery given comorbidities. She eventually agreed to start methimazole after undergoing bone marrow biopsy for worsening leukopenia and cleared by hematology to start the antithyroid drug. At this time, she remains to be on methimazole as an outpatient. Clinical course however, is unfortunately complicated by patient’s ongoing poor compliance to clinic follow up. Clinical Lesson: ALZ is an anti-CD52 monoclonal Ab which induces depletion of B and T lymphocytes causing lymphopenia and immunosuppression. It is an effective treatment for MS but is linked to a number of autoimmune adverse event. Thyroid autoimmune dysfunction may occur in 20-30% of patients, and Grave’s disease accounts for 60-70% of cases. The ALZ product label recommends TFT monitoring every 3 months for at least 48 months after the last infusion. Our patient presented with Grave’s disease in 4 years following initial ALZ administration. To our knowledge, there is no published case with reported ALZ-induced Grave’s disease with this length of interval since infusion. Our case highlights not only the importance of pretreatment screening but continued vigilance and close thyroid function monitoring in patients treated with ALZ even several years after therapy. Presentation Date: Saturday, June 17, 2023 Oxford University Press 2023-10-05 /pmc/articles/PMC10554499/ http://dx.doi.org/10.1210/jendso/bvad114.1962 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 Gong, Michael Shifeng Lee, David Arceo-Mendoza, Rod Marianne SAT489 Grave’s Disease Secondary To Alemtuzumabuse |
title | SAT489 Grave’s Disease Secondary To Alemtuzumabuse |
title_full | SAT489 Grave’s Disease Secondary To Alemtuzumabuse |
title_fullStr | SAT489 Grave’s Disease Secondary To Alemtuzumabuse |
title_full_unstemmed | SAT489 Grave’s Disease Secondary To Alemtuzumabuse |
title_short | SAT489 Grave’s Disease Secondary To Alemtuzumabuse |
title_sort | sat489 grave’s disease secondary to alemtuzumabuse |
topic | Thyroid |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10554499/ http://dx.doi.org/10.1210/jendso/bvad114.1962 |
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