Expression of Thyroid Peroxidase Antibody, Thyroglobulin Antibody, and Thyrotropin Receptor Antibody in Breast Cancer and Their Associations with Clinical Characteristics of Breast Cancer

Author(s):  
Xiaoyi Liu ◽  
Zhengju Fu ◽  
Hongmei Xu ◽  
Kui Che ◽  
Jingwei Chi ◽  
...  
Author(s):  
Jing Song ◽  
Rongxin Sun ◽  
Yuanyuan Zhang ◽  
Ying Fu ◽  
Dong Zhao

Abstract Objective Resolvins are produced by the catabolism of polyunsaturated fatty acids (PUFAs) and play vital roles in inflammation resolution. Resolvins have been associated with autoimmune disorders. This study aimed to measure the level of Resolvin D1 (RVD1) in the serum of Hashimoto's thyroiditis (HT) patients and healthy controls (HCs) and to further analyse its correlation with thyroid autoantibodies and inflammatory factors. Methods Sixty-three participants were recruited, namely, 30 untreated HT patients and 33 sex- and age-matched HCs. Serum RVD1 and inflammatory chemokine (MCP-1 and IP-10) levels were measured by ELISA according to the manufacturer’s protocol. Serum total T3 (TT3), TT4, free T3 (FT3), FT4, thyroglobulin antibody (TgAb), thyroid peroxidase antibody (TPOAb) and thyroid-stimulating hormone (TSH) levels were measured using an electrochemiluminescence immunoassay. Thyroid homeostasis parameters, including the thyroid secretory capacity (SPINA-GT), the total deiodinase activity (SPINA-GD), Jostel’s TSH index (TSHI) and the thyrotroph thyroid hormone sensitivity index (TTSI), were calculated. Results Serum RVD1 levels in HT patients (134.76, 85.35–201.36 pg/mL) were significantly lower than those in HCs (187.64, 131.01–326.85 pg/mL) (P=0.004). As the TPOAb level increased, the RVD1 level showed a decreasing trend (P for trend=0.002). Both multinomial and ordinal logistics analyses revealed that serum RVD1 levels were negatively correlated with TPOAb levels in the adjusted models. Moreover, RVD1 showed a negative correlation with the inflammatory chemokine IP-1 0 (r=–0.276, P=0.034), TSHI (r=–0.269, P=0.036) and TTSI (r=–0.277, P=0.031). Conclusions Thyroid autoimmunity may be associated with low levels of RVD1. Decreased RVD1 levels indicate impaired resolution of inflammation in HT patients.


Thyroid ◽  
2021 ◽  
Author(s):  
Daniele Cappellani ◽  
Giuseppina De Marco ◽  
Eleonora Ferrarini ◽  
Liborio Torregrossa ◽  
Agostino Maria Di Certo ◽  
...  

2019 ◽  
Vol 64 ◽  
pp. 44-48 ◽  
Author(s):  
Yuyan Li ◽  
Ting Xu ◽  
Qinyun Mo ◽  
Weiling Fu ◽  
Chunyan Yao

1989 ◽  
Vol 4 (2) ◽  
pp. 118-125 ◽  
Author(s):  
Young Kee Shong ◽  
Bo Youn Cho ◽  
Sung Kwan Hong ◽  
Hong Kyu Lee ◽  
Chang Soon Koh ◽  
...  

1998 ◽  
pp. 281-285 ◽  
Author(s):  
M Akuzawa ◽  
M Murakami ◽  
M Yamada ◽  
T Satoh ◽  
H Shimizu ◽  
...  

Clinical evaluation was conducted to ascertain whether thyrotropin receptor antibody (TRAb) in the normal range may still be involved in the regulation of thyroid function after prolonged treatment for Graves' disease. All patients (n = 33) were treated with antithyroid drugs for an average of 10.6 years and were under euthyroid conditions in which normal blood levels of tri-iodothyronine (T3) were significantly correlated with blood thyrotropin (TSH) levels, but not with titers of TRAb. A significant correlation was observed between TRAb titer and thyroid-stimulating antibody (TSAb) activity. In contrast, this correlation was not found in normal subjects. After administration of T3 (75 microg daily for 8 days), the patients showed increased levels of T3 with concomitant suppression of TSH levels. Under these conditions, linear regression analysis showed significant correlations of TRAb titer and TSAb activity with 24-h thyroid radioiodine uptake (r = 0.641 and 0.621 respectively, P < 0.01), in contrast to declining blood thyroxine levels. Moreover, the immunoglobulin G (IgG) of the patients precipitated to a greater extent than IgG from normal subjects a peptide consisting of the amino acid sequence near the terminus of the human TSH receptor. These findings indicated that TRAb at normal levels possessed significant unremitting activities on thyroid function despite long-term treatment in euthyroid patients with Graves' disease.


2020 ◽  
Vol 26 (6) ◽  
pp. 595-603
Author(s):  
Yanan Zhang ◽  
Xinmei Huang ◽  
Zaoping Chen ◽  
Qian Yang ◽  
Xiaoying Li ◽  
...  

Objective: Previous studies have reported an association between iron deficiency (ID) and increased thyroid peroxidase antibody (TPO-Ab) during early pregnancy. The objective of this study was to explore the relationship between ID and thyroid dysfunction, as well as thyroid autoantibodies, during the second trimester of pregnancy. Methods: A total of 1,592 pregnant women (13 to 28 weeks gestation) were enrolled in this cross-sectional study. According to serum ferritin (SF) concentrations, they were divided into ID (SF <20 μg/L) or non-ID (SF ≥20 μg/L) groups. Logistic regression analysis was used to evaluate the association between ID and subclinical hypothyroidism (thyroid-stimulating hormone [TSH] >4.0 mIU/L and free thyroxine [FT4] within the reference range) and thyroid autoimmunity. Results: The prevalence of ID was 23.43% (373/1,592). Compared with the non-ID group, the ID group had lower FT4 levels (13.94 pmol/L [8.91 to 29.82 pmol/L] versus 14.63 pmol/L [8.22 to 47.24 pmol/L]; P<.001]) and higher TSH levels (1.85 mIU/L [0.01 to 7.84 mIU/L] versus 1.69 mIU/L [0.01 to 10.2 mIU/L]; P<.05). Logistic regression analysis confirmed ID as a risk factor for increased thyroglobulin antibody (TG-Ab) (odds ratio 1.974; 95% confidence interval 1.065, 3.657; P<.05), but not for subclinical hypothyroidism or increased TPO-Ab. Conclusion: ID is associated with increased TG-Ab during the second trimester of pregnancy. Abbreviations: BMI = body mass index; CV = coefficient of variation; FT4 = free thyroxine; Hb = hemoglobin; ID = iron deficiency; IDA = iron deficiency anemia; SF = serum ferritin; T3 = triiodothyronine; T4 = thyroxine; TAI = thyroid autoimmunity; TG = thyroglobulin; TG-Ab = thyroglobulin antibody; TPO = thyroid peroxidase; TPO-Ab = thyroid peroxidase antibody; TSH = thyroid-stimulating hormone


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