Comparison of thyroglobulin and thyroid peroxidase antibodies measured by five different kits in autoimmune thyroid diseases

Nishihara, Eijun; Amino, Nobuyuki; Kudo, Takumi; M, Ito; Fukata, Shuji; Nishikawa, Mitsushige; Nakamura, Hirotoshi; Miyauchi, Akira

doi:10.1507/endocrj.ej17-0164

Cited by 16 publications

(8 citation statements)

References 34 publications

(37 reference statements)

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“…It is also important to recall that the diagnostic accuracy of thyroid autoantibodies is more dependent on the type of assay used than is usually acknowledged. In a survey using 5 different assay kits, there was the discordance between positive and negative results for thyroglobulin and TPO antibodies, and correlation between kits ranged widely [38]. For 4 of the assays, thyroglobulin antibodies were more frequent (99%) that TPO antibodies (81%) in HT, making the former the test of choice in this Japanese cohort.…”

Section: Thyroid Autoantibodiesmentioning

confidence: 86%

An update on the pathogenesis of Hashimoto’s thyroiditis

Weetman

2020

J Endocrinol Invest

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It is 70 years since Noel Rose embarked on his pioneering studies that lead to the discovery of autoimmune thyroiditis and the elucidation of Hashimoto’s thyroiditis. This short review to honour his passing focuses on the developments in our understanding of the causes and pathogenesis of HT over the last five years. Recent genetic studies have reported heritability estimates for HT and associated diseases for the first time, and emphasised the complexity of the genetic factors involved, including monogenic forms of HT. Environmental factors continue to be elucidated, especially as a side effect of drugs which modulate the immune system therapeutically. Regarding pathogenetic mechanisms, multiple cytokine networks have been identified which involve the thyroid cells in a circuit of escalating proinflammatory effects, such as the expression of inflammasome components, and an array of different defects in T regulatory cells may underlie the loss of self-tolerance to thyroid autoantigens. Finally, a number of studies have revealed fresh insights into disease associations with HT which may have both pathological and clinical significance, the most intriguing of which is a possible direct role of the autoimmune process itself in causing some of the persistent symptoms reported by a minority of patients with levothyroxine-treated HT.

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Section: Thyroid Autoantibodiesmentioning

confidence: 86%

An update on the pathogenesis of Hashimoto’s thyroiditis

Weetman

2020

J Endocrinol Invest

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“…In present case, however, both anti-TG and anti-TPO antibodies were negative. Anti-thyroglobulin and anti-TPO antibodies prevalence in painless thyroiditis have been reported to be 70 and 30%, respectively [19]. The patient had an history of acute pancreatitis.…”

Section: Discussionmentioning

confidence: 86%

A case of thyrotoxicosis-induced anemia in a patient with painless thyroiditis

Komiya¹,

Tomoyose

Yagi³

et al. 2021

Thyroid Res

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Background There have been several reports of secondary anemia associated with Graves’ disease. There are no reports of secondary anemia resulting from thyrotoxicosis due to painless thyroiditis (silent thyroiditis). We report the case of a patient with pancreatic diabetes who developed anemia caused by thyrotoxicosis due to painless thyroiditis. Case presentation The patient was a 37-year-old man who visited the hospital complaining of fatigue, palpitations, and dyspnea. His hemoglobin was 110 g/l (reference range, 135–176), and mean corpuscular volume was 81.5 fl (81.7–101.6). His free thyroxine (FT4) was high, at 100.4 pmol/l (11.6–21.9); the free triiodothyronine (FT3) was high, at 27.49 pmol/l (3.53–6.14); TSH was low, at < 0.01 mIU/l (0.50–5.00); and TSH receptor antibody was negative. Soluble IL-2 receptor (sIL-2R) was high, at 1340 U/ml (122–496); C-reactive protein (CRP) was high, at 6900 μg/l (< 3000); and reticulocytes was high, at 108 109 /l (30–100). Serum iron (Fe) was 9.5 (9.1–35.5), ferritin was 389 μg/l (13–401), haptoglobin was 0.66 g/l (0.19–1.70. Propranolol was prescribed and followed up. Anemia completely disappeared by 12 weeks after disease onset. Thyroid hormones and sIL-2R had normalized by 16 weeks after onset. He developed mild hypothyroidism and was treated with L-thyroxine at 24 weeks. Conclusions This is the first case report of transient secondary anemia associated with thyrotoxicosis due to painless thyroiditis. The change in sIL-2R was also observed during the clinical course of thyrotoxicosis and anemia, suggesting the immune processes in thyroid gland and bone marrow.

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“…Thyroid peroxidase (tpo) is an enzyme that attaches iodine to thyroglobulin (tg), an important protein in the production of thyroid hormones (Nishihara et al 2017). Decreased transcription of the tpo gene after avobenzone and octinoxate exposure indicates that these substances inhibit tpo activity in a manner similar to BP-2, thereby reducing thyroid hormone production (Lee et al 2018).…”

Section: Discussionmentioning

confidence: 99%

Waterborne Exposure to Avobenzone and Octinoxate Induces Thyroid Endocrine Disruption in Wild-Type and Thrαa-/- Zebrafish Larvae

2022

Preprint

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Avobenzone and octinoxate are frequently used as organic ultraviolet filters, and these chemicals are widely detected in water. This study evaluated the potential of avobenzone and octinoxate to disrupt thyroid endocrine system in wild-type and thyroid hormone receptor alpha a knockout (thrαa−/−) zebrafish embryos/larvae. Following a 120 h exposure to various concentrations of avobenzone and octinoxate, larvae mortality and developmental toxicity in wild-type and thrαa−/− fish were assessed. Triiodothyronine (T3) and thyroxine (T4) levels as well as transcriptional levels of ten genes associated with the hypothalamus-pituitary-thyroid (HPT) axis were measured in wild-type fish. Significantly lower larvae survival rate in thrαa−/− fish exposed to ≥ 3 µM avobenzone and octinoxate suggests that the thyroid hormone receptor plays a crucial role in the toxic effects of avobenzone and octinoxate. A significant increase in the deio2 gene level in avobenzone-exposed zebrafish supports the result of an increased ratio of T3 to T4. Significant decrease of T4 level with upregulation of trh, tshβ, and tshr genes indicates feedback in the hypothalamus and pituitary gland to maintain hormonal homeostasis. Our observation indicates that exposure to avobenzone and octinoxate affects the feedback mechanisms of the HPT axis.

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Comparison of thyroglobulin and thyroid peroxidase antibodies measured by five different kits in autoimmune thyroid diseases

Cited by 16 publications

References 34 publications

An update on the pathogenesis of Hashimoto’s thyroiditis

An update on the pathogenesis of Hashimoto’s thyroiditis

A case of thyrotoxicosis-induced anemia in a patient with painless thyroiditis

Waterborne Exposure to Avobenzone and Octinoxate Induces Thyroid Endocrine Disruption in Wild-Type and Thrαa-/- Zebrafish Larvae

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