ETJ autoimmune thyroid diseases collection

 

Autoimmune thyroid diseases are the commonest autoimmune conditions of mankind and make up a large proportion of the caseload for endocrinologists. This topic collection brings together the latest papers on autoimmunity as related to the thyroid which will be of broad interest to both clinicians and non-clinical scientists alike.

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Autoimmune thyroid diseases

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Maja Hjelm Lundgaard Department of Clinical Biochemistry, Aalborg University Hospital, Aalborg, Denmark

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Allan Carlé Department of Clinical Medicine, Aalborg University, Aalborg, Denmark
Department of Endocrinology, Aalborg University Hospital, Aalborg, Denmark

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Ulla Birgitte Christiansen Department of Gynaecology and Obstetrics, Aalborg University Hospital, Aalborg, Denmark

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Anne Sørensen Department of Clinical Medicine, Aalborg University, Aalborg, Denmark
Department of Gynaecology and Obstetrics, Aalborg University Hospital, Aalborg, Denmark

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Søren Risom Kristensen Department of Clinical Biochemistry, Aalborg University Hospital, Aalborg, Denmark
Department of Clinical Medicine, Aalborg University, Aalborg, Denmark

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Stine Linding Andersen Department of Clinical Biochemistry, Aalborg University Hospital, Aalborg, Denmark
Department of Clinical Medicine, Aalborg University, Aalborg, Denmark

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Introduction

Thyroid disorders have been linked to abnormalities in the coagulation system, and a hypocoagulant state has been proposed in hypothyroidism. The assessment of thyroid function is, however, not routinely recommended as part of the assessment for coagulation disorders.

Case presentation

We present a 32-year-old woman who had no history of thyroid disease and who recently gave birth preterm because of severe preeclampsia and intrauterine growth restriction. Due to severe placental dysfunction, she underwent a routine biochemical assessment of the coagulation system 6 months postpartum, and a prolonged activated partial thromboplastin time (APTT) (43 s) was identified along with a low level of coagulation factor VIII (0.44 IU/mL), and a low level of von Willebrand factor (vWF) antigen (0.35 IU/mL), vWF activity (0.38 IU/mL) as well as reduced generation of thrombin. The assessment of thyroid function in the patient identified autoimmune, overt hypothyroidism with a thyroid-stimulating hormone (TSH) concentration of 139 mIU/L, low levels of the peripheral thyroid hormones (total thyroxine: 43 nmol/L, total triiodothyronine: 0.9 nmol/L), and high levels of thyroid peroxidase antibodies (296 U/mL) as well as thyroglobulin antibodies (927 U/mL).

Conclusion

In this case, prolonged APTT provided a diagnostic clue for the assessment of thyroid function in a young woman with a recent history of severe placental dysfunction. The identification of autoimmune, overt hypothyroidism emphasizes that measurement of TSH may be of clinical importance in cases of unexplained prolonged APTT or other biochemical signs of abnormalities in the coagulation system.

Established facts

  • Hypothyroidism has been associated with alterations of the coagulation system suggesting a hypocoagulant state.

  • At present, measurement of thyroid-stimulating hormone is not routinely recommended as part of the assessment for coagulation disorders.

Novel insights

  • In this case, biochemical assessment of the coagulation system was routinely performed following a pregnancy complicated by severe placental dysfunction.

  • Overt hypothyroidism of autoimmune origin was identified secondary to prolonged activated partial thromboplastin time (APTT) postpartum along with low levels of coagulation factor VIII, von Willebrand factor, and thrombin generation.

  • Measurement of thyroid-stimulating hormone may be considered in cases of unexplained prolonged APTT.

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Sébastien Verdickt Department of Endocrinology, University Hospitals of Leuven, Leuven, Belgium

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Falco Van Nes Department of Endocrinology, University Hospitals of Leuven, Leuven, Belgium

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Carolien Moyson Department of Endocrinology, University Hospitals of Leuven, Leuven, Belgium

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Toon Maes Department of Endocrinology, Imeldaziekenhuis Bonheiden, Bonheiden, Belgium

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Paul Van Crombrugge Department of Endocrinology, OLV Ziekenhuis Aalst-Asse-Ninove, Aalst, Belgium

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Annick Van den Bruel Department of Endocrinology, AZ Sint Jan Brugge, Brugge, Belgium

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Brigitte Decallonne Department of Endocrinology, University Hospitals of Leuven, Leuven, Belgium

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Objective

We investigated whether a positive thyroid peroxidase antibody (TPO Ab) status before radioactive iodine (RAI) therapy in patients with Graves’ hyperthyroidism is a predictive factor for developing hypothyroidism post RAI.

Methods

We performed a retrospective study of patients with Graves’ hyperthyroidism with known TPO Ab status, receiving the first administration of RAI. Patients from four thyroid outpatient centres in Belgium receiving their first RAI therapy between the years 2011 and 2019 were studied. Clinical, laboratory, imaging, and treatment data were recorded from medical charts. Hypothyroidism and cure (defined as combined hypo- and euthyroidism) were evaluated in period 1 (≥2 and ≤9 months, closest to 6 months post RAI) and period 2 (>9 months and ≤24 months post RAI, closest to 12 months post RAI).

Results

A total of 152 patients were included of which 105 (69%) were TPO Ab-positive. Compared to TPO Ab-negative patients, TPO Ab-positive patients were younger, had a larger thyroid gland, and had more previous episodes of hyperthyroidism. In period 1, 89% of the TPO Ab-positive group developed hypothyroidism and 72% in the TPO Ab-negative group (P = 0.007). In period 2, the observation was similar: 88% vs 72% (P = 0.019). In the multivariate logistic regression analysis, a positive TPO Ab status was associated with hypothyroidism in period 2 (adjusted OR: 4.78; 95% CI: 1.27–20.18; P = 0.024). In period 1, the aOR was 4.16 (95% CI: 1.0–18.83; P = 0.052).

Conclusion

A positive TPO Ab status in patients with Graves’ hyperthyroidism receiving the first administration of RAI is associated with a higher risk of early hypothyroidism.

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Hippolyte Dupuis Department of Endocrinology, Diabetology and Metabolism, Huriez Hospital, Lille University Hospital, Lille, France
University of Lille, Lille, France

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Emilie Merlen Department of Endocrinology, Diabetology and Metabolism, Huriez Hospital, Lille University Hospital, Lille, France

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Arnaud Jannin Department of Endocrinology, Diabetology and Metabolism, Huriez Hospital, Lille University Hospital, Lille, France
University of Lille, Lille, France

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Philippe Jamme University of Lille, Lille, France
Department of Dermatology, Lille University Hospital, Lille, France

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Alexandre Fagart Department of Nuclear Medicine, Valenciennes Hospital Center, Valenciennes, France

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Marie-Christine Vantyghem Department of Endocrinology, Diabetology and Metabolism, Huriez Hospital, Lille University Hospital, Lille, France
University of Lille, Lille, France

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Miriam Ladsous Department of Endocrinology, Diabetology and Metabolism, Huriez Hospital, Lille University Hospital, Lille, France

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Introduction

Immune checkpoint inhibitors (ICI) are used to treat cancers including metastatic melanomas and can induce endocrine side effects. The thyroid is frequently affected with classically transient thyrotoxicosis followed by hypothyroidism. The evolution of thyroid nodules and goiters under ICI therapy is poorly described.

Case presentation

A 72-year-old male presenting with hyperthyroidism due to a toxic nodule in a multinodular goiter (MNG) started ICI therapy combining ipilimumab and nivolumab to treat metastatic melanoma. After an initial worsening of thyrotoxicosis, treated with carbimazole, he developed profound hypothyroidism, persisting after carbimazole discontinuation, needing a long-term levothyroxine supplementation. Ultrasound control performed 6 months after ICIs treatment initiation revealed diffuse thyroid atrophy with involution of all nodules. 123I-scintigraphy confirmed a destructive mechanism.

Discussion

The evolution of MNG and toxic nodules is poorly described in patients treated with ICI since systematic US evaluations are lacking. We describe for the first time a toxic nodule cured by ICI therapy inducing destructive thyroiditis.

Conclusion

Pre-existing nodules and MNG, even if toxic, are not a contraindication for ICI treatment provided the patients are carefully monitored.

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Giovanna Rotondo Dottore Department of Clinical and Experimental Medicine, Endocrinology Unit II, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Marenza Leo Department of Clinical and Experimental Medicine, Endocrinology Unit II, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Roberta Ricciardi Department of Clinical and Experimental Medicine, Neurology Unit, University of Pisa and University Hospital of Pisa, Pisa, Italy
Department of Surgical, Medical and Molecular Pathology, Division of Thoracic Surgery, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Michelangelo Maestri Department of Clinical and Experimental Medicine, Neurology Unit, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Ilaria Bucci Department of Clinical and Experimental Medicine, Endocrinology Unit II, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Marco Lucchi Department of Surgical, Medical and Molecular Pathology, Division of Thoracic Surgery, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Franca Melfi Department of Surgical, Medical and Molecular Pathology, Division of Thoracic Surgery, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Melania Guida Department of Clinical and Experimental Medicine, Neurology Unit, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Anna De Rosa Department of Clinical and Experimental Medicine, Neurology Unit, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Loredana Petrucci Department of Clinical and Experimental Medicine, Neurology Unit, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Ilaria Ionni Department of Clinical and Experimental Medicine, Endocrinology Unit II, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Giulia Lanzolla Department of Clinical and Experimental Medicine, Endocrinology Unit II, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Francesca Nicolì Department of Clinical and Experimental Medicine, Endocrinology Unit II, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Michele Mantuano Department of Clinical and Experimental Medicine, Endocrinology Unit II, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Debora Ricci Department of Clinical and Experimental Medicine, Endocrinology Unit II, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Francesco Latrofa Department of Clinical and Experimental Medicine, Endocrinology Unit II, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Stefano Mariotti Department of Medical Sciences and Public Health, University of Cagliari, Monserrato, Italy

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Claudio Marcocci Department of Clinical and Experimental Medicine, Endocrinology Unit II, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Michele Marinò Department of Clinical and Experimental Medicine, Endocrinology Unit II, University of Pisa and University Hospital of Pisa, Pisa, Italy

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Objectives: The thymus plays a central role in immune tolerance, which prevents autoimmunity. Myasthenia gravis (MG) is commonly associated with thymoma or thymus hyperplasia, and it can coexist with autoimmune thyroid diseases. However, the role of the thymus in thyroid autoimmunity remains to be clarified, which we investigated here. Study Design: The study design entailed the inclusion of consecutive MG patients and the measurement of anti-thyroid autoantibodies at baseline and, limited to autoantibody-positive patients, also at 24 and 48 weeks. One hundred and seven MG patients were studied. The main outcome measure was the behaviour of anti-thyroglobulin autoantibodies (TgAbs) and anti-thyroperoxidase autoantibodies (TPOAbs) over time in relation to thymectomy. Results: Serum TgAbs and/or TPOAbs were detected in ∼20% of patients in the absence of thyroid dysfunction. The prevalence of positive serum TgAbs and/or TPOAbs decreased significantly (p = 0.002) over the follow-up period in patients who underwent thymectomy, but not in patients who were not thymectomized. When the analysis was restricted to TgAbs or TPOAbs, findings were similar. On the same line, there was a general trend towards a reduction in the serum concentrations of anti-thyroid autoantibodies in patients who underwent thymectomy, which was significant for TPOAbs (p = 0.009). Conclusions: Our findings suggest a role of the thymus in the maintenance of humoral thyroid autoimmunity.

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Yuan Li Department of Endocrinology, Peking University First Hospital, Beijing, China

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Chenxu Zhao Department of Endocrinology, Peking University First Hospital, Beijing, China
Department of Endocrinology, The First Hospital of Hebei Medical University, Shijiazhuang, China

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Keli Zhao Institute of Biophysics, Chinese Academy of Sciences, Beijing, China
College of Life Science, University of the Chinese Academy of Sciences, Beijing, China

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Nan Yu Department of Endocrinology, Peking University First Hospital, Beijing, China

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Yan Li Institute of Biophysics, Chinese Academy of Sciences, Beijing, China
College of Life Science, University of the Chinese Academy of Sciences, Beijing, China

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Yang Yu Department of Endocrinology, Peking University First Hospital, Beijing, China

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Yang Zhang Department of Endocrinology, Peking University First Hospital, Beijing, China

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Zhijing Song Institute of Biophysics, Chinese Academy of Sciences, Beijing, China
College of Life Science, University of the Chinese Academy of Sciences, Beijing, China

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Youyuan Huang Department of Endocrinology, Peking University First Hospital, Beijing, China

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Guizhi Lu Department of Endocrinology, Peking University First Hospital, Beijing, China

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Ying Gao Department of Endocrinology, Peking University First Hospital, Beijing, China

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Junqing Zhang Department of Endocrinology, Peking University First Hospital, Beijing, China

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Xiaohui Guo Department of Endocrinology, Peking University First Hospital, Beijing, China

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Objective: Thyroglobulin antibodies (TgAb), principally comprising immunoglobulin G (IgG), are frequently found in healthy individuals. Previously, we showed that the glycosylation levels of TgAb IgG differed across various thyroid diseases, suggesting an important role of glycosylation on antibodies in the pathogenesis of thyroid diseases. Since IgG1 and IgG4 are the primary TgAb IgG subclasses, this study aimed to investigate the glycosylation of TgAb IgG1 and IgG4 subclasses in thyroid diseases. Methods: TgAb IgG was purified by affinity chromatography from the serum of patients with Hashimoto’s thyroiditis (HT) (n = 16), Graves’ disease (GD) (n = 8), papillary thyroid carcinoma (PTC) (n = 6), and PTC with histological lymphocytic thyroiditis (PTC-T) (n = 9) as well as healthy donors (n = 10). TgAb IgG1 and IgG4 concentrations were determined by enzyme-linked immunosorbent assay, and a lectin microassay was used to assess TgAb IgG1 and IgG4 glycosylation. Results: Significantly elevated mannose, sialic acid, and galactose levels on TgAb IgG1 were found in HT and PTC patients compared to GD patients and healthy controls (all p < 0.05). The mannose, sialic acid, and core fucose levels on TgAb IgG1 in PTC-T patients were higher than in healthy controls (all p < 0.05). Additionally, TgAb IgG1 from PTC-T patients exhibited lower sialylation than that from patients with PTC and higher fucosylation than that from patients with HT (both p < 0.05). However, TgAb IgG4 glycosylation did not differ among the five groups (p < 0.05). Conclusion: Our study describes different distributions of TgAb IgG1 glycosylation in various thyroid diseases. The aberrantly increased glycosylation levels of TgAb IgG1 observed in HT, PTC, and PTC-T might be indicative of immune disorders and participate in the pathogenesis of these diseases.

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Bing Han Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China

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Chi Chen Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China

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Yi Chen Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China

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Ningjian Wang Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China

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Jie Yu Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China

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Jing Cheng Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China

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Yingchao Chen Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China

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Chunfang Zhu Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China

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Yingli Lu Institute and Department of Endocrinology and Metabolism, Shanghai Ninth People’s Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, China

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Background/Aims: Hashimoto thyroiditis, characterized by positive thyroid peroxidase antibodies (TPOAbs), is caused by the interaction of genetic and environment factors. The aim of this study was to clarify the interaction of gene polymorphisms and iodine intake in the incidence of TPOAb positivity. Methods: 1,733 subjects were included in this study. Genomic DNA was extracted from peripheral blood white cells. Four SNPs (rs11675434 [TPO], rs3094228 [HCP5], rs9277555 [HLA-DPB1], and rs301799 [RERE]) were selected for genotyping. Weighted TPOAb genetic risk score (GRS) was calculated based on these 4 SNPs. Thyroid hormones and autoimmune antibodies (TPOAb and thyroglobulin antibody) were determined using the electrochemiluminescence immunoassay method. Results: The mean serum thyrotropin level in TPOAb-positive subjects was higher than in TPOAb-negative subjects (p < 0.01). Genotype GG of rs9277555 was associated with an increased risk of TPOAb positivity (OR = 1.64, 5–95% CI 1.09, 2.47, p = 0.02). Genotype TT of rs11675434 showed marginal increased risk of TPOAb positivity (OR = 1.57, 5–95% CI 1.01, 2.43, p = 0.048). Logistic regression analysis showed TPOAb-GRS and rs9277555 were associated with TPOAb positivity (OR = 5.09, 5–95% CI 1.30, 19.91, p = 0.02 and OR = 1.30, 5–95% CI 1.05, 1.61, p = 0.02). Subjects with a high TPOAb-GRS had a 52% increased risk of TPOAb positivity compared to subjects with a low TPOAb-GRS (OR 1.52, 5–95% CI 1.05, 2.21, p = 0.03). Conclusion: TPOAb-GRS was associated with an increased risk of TPOAb positivity in a Chinese Han population. This effect might be attribute to rs9277555.

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Clotilde Saïe Thyroid and Endocrine Tumors Unit, Pitié-Salpêtrière Hospital APHP, Sorbonne University, Paris, France

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Cécile Ghander Thyroid and Endocrine Tumors Unit, Pitié-Salpêtrière Hospital APHP, Sorbonne University, Paris, France

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Samir Saheb Apheresis Unit, Pitié-Salpêtrière Hospital, AP-HP, Sorbonne University, Paris, France

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Christel Jublanc Department of Endocrinology, Pitié-Salpêtrière Hospital APHP, Sorbonne University, Paris, France

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Denis Lemesle Department of Anaesthesia, Pitié-Salpêtrière Hospital APHP, Sorbonne University, Paris, France

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Charlotte Lussey-Lepoutre Nuclear Medicine Department, Pitié-Salpêtrière Hospital APHP, Sorbonne Université, Inserm U970, Paris, France

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Laurence Leenhardt Thyroid and Endocrine Tumors Unit, Pitié-Salpêtrière Hospital APHP, Sorbonne University, Paris, France

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Fabrice Menegaux Department of Surgery, Pitié-Salpêtrière Hospital APHP, Sorbonne University, Paris, France

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Christophe Tresallet Department of Surgery, Avicennes Hospital, Paris, France

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Camille Buffet Thyroid and Endocrine Tumors Unit, Pitié-Salpêtrière Hospital APHP, Sorbonne University, Paris, France

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Introduction: Hyperthyroid patients who are unresponsive to medical treatment remain a challenging clinical problem. Objective: The goal of our study was to evaluate the use of therapeutic plasma exchange (TPE) in hyperthyroid patients and their outcome after TPE. Method: We retrospectively reviewed 22 patients who underwent TPE for refractory thyrotoxicosis in our institution: 13 with Graves’ disease, 7 with amiodarone-induced thyrotoxicosis (AIT), 1 with toxic goiter, and 1 pregnant patient with familial nonautoimmune thyrotoxicosis. Results: Before TPE, all patients had severe hyperthyroidism, and antithyroid drugs were either contraindicated or not sufficiently effective to restore euthyroidism promptly. After all the TPEs, free T<sub>4</sub> (fT4) decreased significantly by 48% (p = 0.001) and fT3 by 52% (p = 0.0001). The median number of TPE sessions per patient was 4 (range: 1–10). There were no complications during the 91 TPE sessions. Total thyroidectomy with no severe side effects was performed on 16/22 patients and 1 other patient was treated with radioactive iodine. One patient died from severe thyrotoxicosis during medical care. The remaining 4 patients were followed up without any radical treatment. For all 7 patients with AIT, iterative TPE led to a significant clinical improvement, and amiodarone was continued for 1 patient. Available treatments were continued between TPE sessions (cholestyramine for 13 patients [60%] and glucocorticoids for 16 patients [73%]). Conclusion: TPE allowed a safe decrease of 50% in thyroid hormone levels, and it should be considered for refractory hyperthyroid patients when medical treatments are contraindicated or have failed to restore euthyroidism, irrespective of the etiology of the thyrotoxicosis.

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