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      The association between serum adenosine deaminase levels and Graves’ disease

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          Abstract

          Background

          Adenosine deaminase (ADA) is essential for the differentiation and maturation of lymphocytes, while lymphocytes infiltration in thyroid tissue is a vital pathological feature of Graves’ disease (GD). The aim of the present study was to compare the concentration of ADA between healthy controls (HC) and patients with GD, and evaluate the association between ADA and GD.

          Methods

          A total of 112 GD patients and 77 matched HC were enrolled in this study. Each participant was examined for thyroid hormones and autoantibodies, ADA concentration, and thyroid ultrasonography.

          Results

          Serum ADA levels in GD patients were significantly higher than that in HC subgroup ( P < 0.001). In GD patients, serum ADA levels were positively associated with serum-free triiodothyronine (FT3), free thyroxine (FT4), thyroid peroxidase antibody (TPOAb), thyroid-stimulating hormone receptor antibody (TRAb) levels, and total thyroid gland volume (thyroid VolT) and negatively associated with serum thyroid-stimulating hormone receptor (TSH) levels (all P < 0.05). There were no similar correlations in the HC subgroup. Multiple linear regression analysis suggested that serum TSH, FT3, and ADA levels played an important role in serum TRAb levels.

          Conclusions

          Our results demonstrated that serum ADA levels were closely associated with GD.

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          Most cited references31

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          2018 European Thyroid Association Guideline for the Management of Graves’ Hyperthyroidism

          Graves’ disease (GD) is a systemic autoimmune disorder characterized by the infiltration of thyroid antigen-specific T cells into thyroid-stimulating hormone receptor (TSH-R)-expressing tissues. Stimulatory autoantibodies (Ab) in GD activate the TSH-R leading to thyroid hyperplasia and unregulated thyroid hormone production and secretion. Diagnosis of GD is straightforward in a patient with biochemically confirmed thyrotoxicosis, positive TSH-R-Ab, a hypervascular and hypoechoic thyroid gland (ultrasound), and associated orbitopathy. In GD, measurement of TSH-R-Ab is recommended for an accurate diagnosis/differential diagnosis, prior to stopping antithyroid drug (ATD) treatment and during pregnancy. Graves’ hyperthyroidism is treated by decreasing thyroid hormone synthesis with the use of ATD, or by reducing the amount of thyroid tissue with radioactive iodine (RAI) treatment or total thyroidectomy. Patients with newly diagnosed Graves’ hyperthyroidism are usually medically treated for 12–18 months with methimazole (MMI) as the preferred drug. In children with GD, a 24- to 36-month course of MMI is recommended. Patients with persistently high TSH-R-Ab at 12–18 months can continue MMI treatment, repeating the TSH-R-Ab measurement after an additional 12 months, or opt for therapy with RAI or thyroidectomy. Women treated with MMI should be switched to propylthiouracil when planning pregnancy and during the first trimester of pregnancy. If a patient relapses after completing a course of ATD, definitive treatment is recommended; however, continued long-term low-dose MMI can be considered. Thyroidectomy should be performed by an experienced high-volume thyroid surgeon. RAI is contraindicated in Graves’ patients with active/severe orbitopathy, and steroid prophylaxis is warranted in Graves’ patients with mild/active orbitopathy receiving RAI.
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            Thyroid hormone action in the heart.

            The heart is a major target organ for thyroid hormone action, and marked changes occur in cardiac function in patients with hypo- or hyperthyroidism. T(3)-induced changes in cardiac function can result from direct or indirect T(3) effects. Direct effects result from T(3) action in the heart itself and are mediated by nuclear or extranuclear mechanisms. Extranuclear T(3) effects, which occur independent of nuclear T(3) receptor binding and increases in protein synthesis, influence primarily the transport of amino acids, sugars, and calcium across the cell membrane. Nuclear T(3) effects are mediated by the binding of T(3) to specific nuclear receptor proteins, which results in increased transcription of T(3)-responsive cardiac genes. The T(3) receptor is a member of the ligand-activated transcription factor family and is encoded by cellular erythroblastosis A (c-erb A) genes. T(3) also leads to an increase in the speed of diastolic relaxation, which is caused by the more efficient pumping of the calcium ATPase of the sarcoplasmic reticulum. This T(3) effect results from T(3)-induced increases in the level of the mRNA coding for the sarcoplasmic reticulum calcium ATPase protein, leading to an increased number of calcium ATPase pump units in the sarcoplasmic reticulum.
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              Reactive oxygen species in living systems: source, biochemistry, and role in human disease.

              Reactive oxygen species are constantly formed in the human body and removed by antioxidant defenses. An antioxidant is a substance that, when present at low concentrations compared to that of an oxidizable substrate, significantly delays or prevents oxidation of that substrate. Antioxidants can act by scavenging biologically important reactive oxygen species (O2-., H2O2.OH, HOCl, ferryl, peroxyl, and alkyl), by preventing their formation, or by repairing the damage that they do. One problem with scavenging-type antioxidants is that secondary radicals derived from them can often themselves do biologic damage. These various principles will be illustrated by considering several thiol compounds.

                Author and article information

                Journal
                Endocr Connect
                Endocr Connect
                EC
                Endocrine Connections
                Bioscientifica Ltd (Bristol )
                2049-3614
                02 September 2021
                01 October 2021
                : 10
                : 10
                : 1227-1233
                Affiliations
                [1 ]Department of Endocrinology , Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China
                [2 ]Department of Geriatrics , Affiliated Hospital 2 of Nantong University and First People’s Hospital of Nantong City, Nantong, China
                Author notes
                Correspondence should be addressed to F Xu or J Su or X Wang: xufeng5205529@ 123456163.com or sujbzjx@ 123456163.com or wangxueqin108@ 123456163.com

                *(C Lu, W Liu and X Ge contributed equally to this work)

                Author information
                http://orcid.org/0000-0002-2138-0263
                Article
                EC-21-0344
                10.1530/EC-21-0344
                8494409
                34473081
                26003d05-7e89-45fb-8e10-22ca2001061e
                © The authors

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                History
                : 16 August 2021
                : 02 September 2021
                Categories
                Research

                adenosine deaminase,graves’ disease,thyroid-stimulating hormone receptor antibody

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