Graves Disease Following Subacute Thyroiditis in a Chinese Man

Background/Objective: The development of Graves disease (GD) after subacute thyroiditis (SAT) is rare, with approximately 31 reported cases, of which only 5 occurred in men. We describe a case of GD diagnosed based on newly elevated thyroid-stimulating immunoglobulin (TSI) and thyroid-stimulating ho...

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Main Authors: Souad Al-Bacha, MD, Sharon Wu Lahiri, MD
Format: Article
Language:English
Published: Elsevier 2022-03-01
Series:AACE Clinical Case Reports
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2376060521001061
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author Souad Al-Bacha, MD
Sharon Wu Lahiri, MD
author_facet Souad Al-Bacha, MD
Sharon Wu Lahiri, MD
author_sort Souad Al-Bacha, MD
collection DOAJ
description Background/Objective: The development of Graves disease (GD) after subacute thyroiditis (SAT) is rare, with approximately 31 reported cases, of which only 5 occurred in men. We describe a case of GD diagnosed based on newly elevated thyroid-stimulating immunoglobulin (TSI) and thyroid-stimulating hormone (TSH) receptor autoantibody (TRAb) levels after SAT. Case Report: A 32-year-old Chinese man presented with right anterior neck pain, swelling, sore throat, cough, and fever. He had a diffuse tender goiter but no proptosis, lid lag, or stare. His TSH level was 0.03 mIU/mL (normal range [NR] 0.45-5.33 mIU/mL), serum free thyroxine (FT4) level was 2.40 ng/dL (NR 0.61-1.44 ng/dL), total triiodothyronine (TT3) level was 113 ng/dL (NR 87-178 ng/dL), TSI level was <0.10 IU/L (NR < 0.10 IU/L), and erythrocyte sedimentation rate was 21 mm/h (NR < 15 mm/h). After 7 weeks of prednisone, the symptoms resolved, FT4 level was 0.95 ng/dL, and TT3 level was 91 ng/dL. At 11 weeks after SAT onset, the TSH level was <0.01 mIU/mL, TT3 level was 257 ng/dL, FT4 level was 3.03 ng/dL, TSI level was 1.94 IU/L, then 3.42 IU/L 2 weeks later, TRAb level was 8.72 IU/L (NR < 2 IU/L), and erythrocyte sedimentation rate was 4 mm/h. After 1 month of methimazole, the FT4 level was 1.32 ng/dL and TT3 level was 110 ng/dL. Genetic testing revealed human leukocyte antigen-B35 and DRB1∗15:01 positivity. Discussion: GD after SAT is thought to be due to the activation of thyroid autoimmunity induced by SAT in genetically susceptible individuals. Conclusions: This case illustrates the induction of thyroid autoimmunity after SAT, resulting in GD, supporting TSI and/or TRAb testing if hyperthyroidism recurs. The presence of HLA alleles associated with SAT and GD suggests a genetic contribution to the development of thyroid autoimmunity.
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spelling doaj.art-223fd393913349df914cdfab0f5a6aa62022-12-21T21:10:38ZengElsevierAACE Clinical Case Reports2376-06052022-03-01827377Graves Disease Following Subacute Thyroiditis in a Chinese ManSouad Al-Bacha, MD0Sharon Wu Lahiri, MD1Department of Internal Medicine, Division of Endocrinology, Diabetes, Bone and Mineral Disorders, Henry Ford Health System, Detroit, MichiganAddress correspondence to Dr Sharon Wu Lahiri, Department of Internal Medicine, Division of Endocrinology, Diabetes, Bone and Mineral Disorders, Henry Ford Health System, New Center One, 3031 W. Grand Blvd, 8th Floor, Detroit, MI 48202.; Department of Internal Medicine, Division of Endocrinology, Diabetes, Bone and Mineral Disorders, Henry Ford Health System, Detroit, MichiganBackground/Objective: The development of Graves disease (GD) after subacute thyroiditis (SAT) is rare, with approximately 31 reported cases, of which only 5 occurred in men. We describe a case of GD diagnosed based on newly elevated thyroid-stimulating immunoglobulin (TSI) and thyroid-stimulating hormone (TSH) receptor autoantibody (TRAb) levels after SAT. Case Report: A 32-year-old Chinese man presented with right anterior neck pain, swelling, sore throat, cough, and fever. He had a diffuse tender goiter but no proptosis, lid lag, or stare. His TSH level was 0.03 mIU/mL (normal range [NR] 0.45-5.33 mIU/mL), serum free thyroxine (FT4) level was 2.40 ng/dL (NR 0.61-1.44 ng/dL), total triiodothyronine (TT3) level was 113 ng/dL (NR 87-178 ng/dL), TSI level was <0.10 IU/L (NR < 0.10 IU/L), and erythrocyte sedimentation rate was 21 mm/h (NR < 15 mm/h). After 7 weeks of prednisone, the symptoms resolved, FT4 level was 0.95 ng/dL, and TT3 level was 91 ng/dL. At 11 weeks after SAT onset, the TSH level was <0.01 mIU/mL, TT3 level was 257 ng/dL, FT4 level was 3.03 ng/dL, TSI level was 1.94 IU/L, then 3.42 IU/L 2 weeks later, TRAb level was 8.72 IU/L (NR < 2 IU/L), and erythrocyte sedimentation rate was 4 mm/h. After 1 month of methimazole, the FT4 level was 1.32 ng/dL and TT3 level was 110 ng/dL. Genetic testing revealed human leukocyte antigen-B35 and DRB1∗15:01 positivity. Discussion: GD after SAT is thought to be due to the activation of thyroid autoimmunity induced by SAT in genetically susceptible individuals. Conclusions: This case illustrates the induction of thyroid autoimmunity after SAT, resulting in GD, supporting TSI and/or TRAb testing if hyperthyroidism recurs. The presence of HLA alleles associated with SAT and GD suggests a genetic contribution to the development of thyroid autoimmunity.http://www.sciencedirect.com/science/article/pii/S2376060521001061Graves diseasesubacute thyroiditisChineseHLA typingthyroid-stimulating immunoglobulinTSH receptor autoantibody
spellingShingle Souad Al-Bacha, MD
Sharon Wu Lahiri, MD
Graves Disease Following Subacute Thyroiditis in a Chinese Man
AACE Clinical Case Reports
Graves disease
subacute thyroiditis
Chinese
HLA typing
thyroid-stimulating immunoglobulin
TSH receptor autoantibody
title Graves Disease Following Subacute Thyroiditis in a Chinese Man
title_full Graves Disease Following Subacute Thyroiditis in a Chinese Man
title_fullStr Graves Disease Following Subacute Thyroiditis in a Chinese Man
title_full_unstemmed Graves Disease Following Subacute Thyroiditis in a Chinese Man
title_short Graves Disease Following Subacute Thyroiditis in a Chinese Man
title_sort graves disease following subacute thyroiditis in a chinese man
topic Graves disease
subacute thyroiditis
Chinese
HLA typing
thyroid-stimulating immunoglobulin
TSH receptor autoantibody
url http://www.sciencedirect.com/science/article/pii/S2376060521001061
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