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抗甲状腺球蛋白抗体作为毒性结节性甲状腺肿放射性碘治疗后发生格雷夫斯病的潜在危险因素:病例报告

Anti-thyroglobulin Antibodies as a Possible Risk Factor for Graves' Disease After Radioiodine Treatment for Toxic Nodular Goiter: Case Report.

作者信息

Rouiller Nathalie, Nicod Lalonde Marie, Sykiotis Gerasimos P

机构信息

Service of Endocrinology, Diabetology and Metabolism, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.

Service of Nuclear Medicine and Molecular Imaging, Lausanne University Hospital and University of Lausanne, Lausanne, Switzerland.

出版信息

Front Nucl Med. 2022 Mar 15;2:858062. doi: 10.3389/fnume.2022.858062. eCollection 2022.

DOI:10.3389/fnume.2022.858062
PMID:39354980
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11440983/
Abstract

BACKGROUND

The manifestation of Graves' disease (GD) in patients treated with radioactive iodine (RAI) for hyperfunctioning thyroid nodules (RAI-induced GD or post-RAI GD) remains a long-standing challenge in radionuclide therapy. Known risk factors for post-RAI GD include preexisting subclinical hyperthyroidism, positive thyroid peroxidase autoantibodies (TPOAb), positive TSH receptor autoantibodies (TRAb) or otherwise undiagnosed GD. However, these risk factors are not present in all patients with post-RAI GD, and therefore it cannot always be predicted in a reliable manner if a given patient has a high risk for RAI-induced GD or not.

CASE PRESENTATION

We describe the case of a 64 year-old woman known for hyperthyroidism due to toxic nodular goiter; she was treated initially with carbimazole, and then, due to recurrence, underwent RAI treatment. Three months later, symptomatic hyperthyroidism persisted. Diagnosis of new-onset GD was made based on typical ultrasound findings and newly-positive TRAb. Our patient had only positive thyroglobulin antibodies (TgAb) before RAI treatment, whereas TPOAb were negative.

CONCLUSIONS

In the literature, TgAb have never been reported as a possible risk factor for RAI-induced GD. The present case suggests that the assessment for pre-existing autoimmunity in patients considering RAI for hyperfunctioning thyroid nodules should probably also include TgAb.

摘要

背景

对于因功能亢进性甲状腺结节接受放射性碘(RAI)治疗的患者,格雷夫斯病(GD)的表现(放射性碘诱导的GD或放射性碘治疗后GD)仍是放射性核素治疗中一个长期存在的挑战。放射性碘治疗后GD的已知风险因素包括既往存在的亚临床甲状腺功能亢进、甲状腺过氧化物酶自身抗体(TPOAb)阳性、促甲状腺激素受体自身抗体(TRAb)阳性或其他未诊断的GD。然而,并非所有放射性碘治疗后GD的患者都存在这些风险因素,因此,对于特定患者是否有放射性碘诱导GD的高风险,并不总能以可靠的方式进行预测。

病例介绍

我们描述了一名64岁女性的病例,该患者因毒性结节性甲状腺肿导致甲状腺功能亢进;她最初接受甲巯咪唑治疗,随后因复发接受放射性碘治疗。三个月后,症状性甲状腺功能亢进持续存在。基于典型的超声检查结果和新出现的TRAb阳性,诊断为新发GD。我们的患者在放射性碘治疗前仅甲状腺球蛋白抗体(TgAb)呈阳性,而TPOAb为阴性。

结论

在文献中,从未报道过TgAb是放射性碘诱导GD的可能风险因素。本病例表明,对于考虑因功能亢进性甲状腺结节接受放射性碘治疗的患者,对既往自身免疫的评估可能还应包括TgAb。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1697/11440983/48e10d66e62a/fnume-02-858062-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1697/11440983/48e10d66e62a/fnume-02-858062-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1697/11440983/48e10d66e62a/fnume-02-858062-g0001.jpg

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本文引用的文献

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Graves Disease Induced by Radioiodine Therapy for Toxic Nodular Goiter: A Case Report.放射性碘治疗毒性结节性甲状腺肿诱发格雷夫斯病:一例报告
Mol Imaging Radionucl Ther. 2015 Oct 5;24(3):135-7. doi: 10.4274/mirt.74046.
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Radioiodine therapy versus antithyroid medications for Graves' disease.
放射性碘治疗与抗甲状腺药物治疗Graves病的比较。
Cochrane Database Syst Rev. 2016 Feb 18;2(2):CD010094. doi: 10.1002/14651858.CD010094.pub2.
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Incidence of radioiodine induced Graves' disease in patients with multinodular toxic goiter.多结节毒性甲状腺肿患者中放射性碘诱发的格雷夫斯病的发病率。
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Incidence of postradioiodine immunogenic hyperthyroidism/Graves' disease in relation to a temporary increase in thyrotropin receptor antibodies after radioiodine therapy for autonomous thyroid disease.放射性碘治疗自主性甲状腺疾病后,促甲状腺素受体抗体暂时升高与放射性碘后免疫原性甲状腺功能亢进症/格雷夫斯病的发生率
Thyroid. 2006 Mar;16(3):281-8. doi: 10.1089/thy.2006.16.281.
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Incidence of radiation-induced Graves' disease in patients treated with radioiodine for thyroid autonomy before and after introduction of a high-sensitivity TSH receptor antibody assay.在引入高敏促甲状腺激素受体抗体检测前后,接受放射性碘治疗甲状腺自主性的患者中放射性碘诱发的格雷夫斯病的发病率。
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Transition of nodular toxic goiter to autoimmune hyperthyroidism triggered by 131I therapy.131I治疗引发结节性毒性甲状腺肿向自身免疫性甲状腺功能亢进的转变。
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