scholarly journals Hashimoto's Thyroiditis Autoimmune Disease: Background and Current Status, Update Overview of Biotechnological and Biomedical Fields and Future Trends for 3D Models

2021 ◽  
Author(s):  
Arnaud Martino Capuzzo
Keyword(s):  
Thyroid Tissue ◽  
Disease Process ◽  
Hashimoto Thyroiditis ◽  
3D Models ◽  
Current Status ◽  
Thyroid Peroxidase ◽  
Chronic Lymphocytic Thyroiditis ◽  
Laboratory Findings ◽  
Thyroid Cells ◽  
Immunological Mechanisms

Hashimoto thyroiditis, also known as chronic autoimmune thyroiditis or chronic lymphocytic thyroiditis, is an autoimmune illness in which thyroid cells are damaged by immunological mechanisms involving cells and antibodies. Thyroid peroxidase and/or thyroglobulin autoantibodies in the serum are biochemical indicators of the condition, with females having a higher incidence than males and increasing with age. It's the leading cause of hypothyroidism in affluent countries. Inadequate dietary iodine intake, on the other hand, is the most common cause of hypothyroidism worldwide. The development of antithyroid antibodies that target the thyroid tissue, causing gradual fibrosis, is the pathogenesis of Hashimoto thyroiditis. The diagnosis can be difficult, and as a result, the problem is frequently not detected until late in the disease process. The most prevalent laboratory findings are raised TSH and low thyroxine (T4) levels, as well as enhanced antithyroid peroxidase (anti-TPO) antibodies. The pathogenesis, diagnosis, and management of Hashimoto thyroiditis are discussed in this article.

scholarly journals Hashimoto’s Thyroiditis Autoimmune Disease: Background and Current Status, Update Overview of Biotechnological and Biomedical Fields and Future Trends for 3D Models

2021 ◽  
Vol 4 (2) ◽  
Author(s):  
Arnaud Martino Capuzzo
Keyword(s):  
Thyroid Tissue ◽  
Disease Process ◽  
Hashimoto Thyroiditis ◽  
3D Models ◽  
Current Status ◽  
Thyroid Peroxidase ◽  
Chronic Lymphocytic Thyroiditis ◽  
Laboratory Findings ◽  
Thyroid Cells ◽  
Immunological Mechanisms

Hashimoto thyroiditis, also known as chronic autoimmune thyroiditis or chronic lymphocytic thyroiditis, is an autoimmune illness in which thyroid cells are damaged by immunological mechanisms involving cells and antibodies. Thyroid peroxidase and/or thyroglobulin autoantibodies in the serum are biochemical indicators of the condition, with females having a higher incidence than males and increasing with age. It’s the leading cause of hypothyroidism in affluent countries. Inadequate dietary iodine intake, on the other hand, is the most common cause of hypothyroidism worldwide. The development of antithyroid antibodies that target the thyroid tissue, causing gradual fibrosis, is the pathogenesis of Hashimoto thyroiditis. The diagnosis can be difficult, and as a result, the problem is frequently not detected until late in the disease process. The most prevalent laboratory findings are raised TSH and low thyroxine (T4) levels, as well as enhanced antithyroid peroxidase (anti-TPO) antibodies. The pathogenesis, diagnosis, and management of Hashimoto thyroiditis are discussed in this article.

scholarly journals The effects of vitamins and trace minerals on chronic autoimmune thyroiditis

2014 ◽  
Vol 83 (2) ◽  
pp. 167-172
Author(s):  
Małgorzata Włochal ◽  
Marcin A. Kucharski ◽  
Marian Grzymisławski
Keyword(s):  
Thyroid Gland ◽  
Hashimoto’S Thyroiditis ◽  
Essential Element ◽  
Hashimoto Thyroiditis ◽  
Hashimoto's Thyroiditis ◽  
Thyroid Peroxidase ◽  
Chronic Lymphocytic Thyroiditis ◽  
Thyroid Cells ◽  
Thyroglobulin Antibodies ◽  
Chronic Autoimmune Thyroiditis

Hashimoto’s thyroiditis (HT), also known as chronic lymphocytic thyroiditis is one of the most frequent types of inflammation of the thyroid gland. The prevalence of the overt HT is about 2% but it is believed that Hashimoto thyroiditis is more frequent than expected. Hashimoto’s thyroiditis is characterized by dysfunction of the immune system, which leads to impaired tolerance of own tissues and increased production of autoantibodies against the thyroid cells. Thyroid peroxidase antibodies (anti-TPO), thyroglobulin antibodies (anti-Tg) and/or TSH receptors antibodies are the principal markers of the disease. The essential element of the treatment of HT is the supplementation of L-thyroxine. In Hashimoto’s disease, like in many other autoimmune diseases, researchers attempted to support pharmacological treatment by adequate nutrition. The aim of this paper was to review the existing literature on the levels of antioxidants (vitamin A, C, E, selenium, zinc) and vitamin D in patients with HT, as well as the influence of the nutritional supplementation of the above mentioned elements on the metabolism of the thyroid gland hormones and the level of anti-thyroid peroxidase (anti-TPO) antibodies.

EUTHYROID GOITERS IN CHILDREN: CORRELATION OF NEEDLE BIOPSY WITH OTHER CLINICAL AND LABORATORY FINDINGS IN CHRONIC LYMPHOCYTIC THYROIDITIS AND SIMPLE GOITER

PEDIATRICS ◽  
1969 ◽  
Vol 44 (5) ◽  
pp. 695-708
Author(s):  
Shun M. Ling ◽  
Solomon A. Kaplan ◽  
Jordan J. Weitzman ◽  
George B. Reed ◽  
Gertrude Costin ◽  
...  
Keyword(s):  
Thyroid Function ◽  
Needle Biopsy ◽  
Biopsy Specimen ◽  
Disease Process ◽  
Chronic Lymphocytic Thyroiditis ◽  
Red Cell ◽  
Thyroid Antibodies ◽  
Thyroid Extract ◽  
Laboratory Findings ◽  
Lymphocytic Thyroiditis

All children with euthyroid goiters examined over a period of 3 years underwent study of thyroid function, needle biopsy, and measurement of thyroid antibodies. Sixty-six of 71 children studied had satisfactory biopsies of the thyroid. Of these, 43 (65%) had chronic lymphocytic thyroiditis and 23 (35%) had simple goiter as determined by histologic examination of the biopsy specimen. Elevated titers of anti-thyroid antibodies were found in 50% of the patients with thyroiditis by the tanned red cell method and in 63% by the indirect Coons method. Neither antibody was present in significant quantity in 20% of the patients. Abnormal levels of antibody were rarely detected in children with histologic evidence of simple goiter. Treatment with thyroid extract has little effect on the progression of the disease process to fibrosis and atrophy. Such treatment may be necessary to anticipate the development of hypothyroidism or for replacement if thyroid function is already diminished. There is no evidence that simple goiter is associated with hypothyroidism, and treatment of this disease with thyroid preparations is necessary only for cosmetic purposes. Needle biopsy is the most useful means for making a distinction between thyroiditis and simple goiter.

scholarly journals RECURRENT PAINFUL HASHIMOTO THYROIDITIS SUCCESSFULLY TREATED BY THYROIDECTOMY

2020 ◽  
Vol 6 (1) ◽  
pp. e9-e13
Author(s):  
Carol Chiung-Hui Peng ◽  
Kashif M. Munir ◽  
Linda Song ◽  
John C. Papadimitriou ◽  
Majorie A. Pennant
Keyword(s):  
Neck Pain ◽  
Hashimoto Thyroiditis ◽  
Thyroid Stimulating Hormone ◽  
Thyroid Peroxidase ◽  
Ultrasound Images ◽  
Upper Respiratory Tract ◽  
Anterior Neck ◽  
Laboratory Findings ◽  
Thyroid Goiter ◽  
Oral Corticosteroids

Objective: Painful Hashimoto thyroiditis (HT) is a rare HT variant characterized by neck pain. The clinical differentiation between painful HT and subacute thyroiditis is challenging, as the diagnosis cannot be confirmed without histopathological evidence. Here we present a patient who had anterior neck pain who was diagnosed with HT. Methods: We present the patient's clinical examinations and laboratory findings (white blood cell count, thyroid-stimulating hormone, free thyroxine, thyroid peroxidase antibody, and erythrocyte sedimentation rate). Ultrasound images of the thyroid gland and pathology images representative of marked HT with positive IgG4 immunohistochemical stain after thyroidectomy are also presented. Results: A 42-year-old female with a 3-year history of HT developed recurrent anterior neck pain with bilateral radiation to the ears as well as a tender, enlarging thyroid goiter. She had no signs of fever or a preceding infection of the upper respiratory tract. Her pain was only temporarily alleviated by oral corticosteroids. According to the serial ultrasound records, both thyroid lobes decreased in size after 2 pain episodes. She eventually underwent total thyroidectomy and remained pain-free for 1.5 years, up to the last office follow-up visit. Histopathology confirmed the diagnosis of HT. Conclusion: In patients with HT, recurrent thyroid pain despite steroid treatment is the clinical hallmark of diagnosis of painful HT. The reference standard of diagnosis is pathology. Thyroidectomy may be considered after recurrent painful episodes.

scholarly journals Increased Expression of the Na+/I− Symporter in Cultured Human Thyroid Cells Exposed to Thyrotropin and in Graves’ Thyroid Tissue*

1997 ◽  
Vol 82 (10) ◽  
pp. 3331-3336 ◽  
Author(s):  
Tsukasa Saito ◽  
Toyoshi Endo ◽  
Akio Kawaguchi ◽  
Masato Ikeda ◽  
Minoru Nakazato ◽  
...  
Keyword(s):  
Thyroid Tissue ◽  
Human Thyroid ◽  
Thyroid Peroxidase ◽  
Graves Disease ◽  
Intracellular Camp ◽  
Normal Thyroid Tissue ◽  
Thyroid Cells ◽  
Normal Thyroid ◽  
Hormone Synthesis ◽  
Messenger Ribonucleic Acid

Abstract The Na+/I− symporter (NIS) is important in hormone synthesis in the thyroid gland. NIS activity, as reflected by I− uptake, was increased by TSH (1 mU/mL) or forskolin (10μ mol/L) in primary cultured human thyroid cells. Northern blot analysis revealed that incubation of these cells with TSH or forskolin for 24 h increased the abundance of NIS messenger ribonucleic acid (mRNA) 2.3- and 2.5-fold, respectively. Immunoblot analysis revealed 2.7- and 2.4-fold increases, respectively, in the amount of NIS protein after 48 h, suggesting that elevated levels of intracellular cAMP induced the expression of NIS in human thyrocytes. We then studied the levels of NIS mRNA and protein in Graves’ thyroid tissue and found that the amount of NIS mRNA in thyroid tissue from individuals with Graves’ disease (n = 5) was 3.8 times that in normal thyroid tissue (n = 5). The abundance of NIS mRNA was significantly correlated with that of thyroid peroxidase or thyroglobulin mRNAs, but not with that of TSH receptor mRNA, in the Graves’ and normal thyroid tissue specimens. The amount of NIS protein was also increased 3.1-fold in Graves’ thyroid tissue compared with that in normal thyroid tissue. The increased expression of NIS may thus contribute to the development of Graves’ disease.

Activation of the thyroid peroxidase gene in human thyroid cells: effect of thyrotrophin, forskolin and phorbol ester

1989 ◽  
Vol 3 (1) ◽  
pp. 1-5 ◽  
Author(s):  
K. S. Collison ◽  
J. P. Banga ◽  
P. S. Barnett ◽  
A. W. C. Kung ◽  
A. M. McGregor
Keyword(s):  
Phorbol Ester ◽  
Oligonucleotide Probe ◽  
Thyroid Tissue ◽  
Human Thyroid ◽  
Thyroid Peroxidase ◽  
Maximal Effect ◽  
Mrna Levels ◽  
Thyroid Cells ◽  
Autoimmune Attack ◽  
Wide Range

ABSTRACT The enzyme thyroid peroxidase (TPO) plays a central role in thyroid hormone synthesis and is the target for the autoimmune attack in lymphocytic thyroiditis. We have examined the activation of the TPO gene in cultured human thyrocytes using slotblot hybridization with a synthetic 40 mer oligonucleotide probe derived from the nucleotide sequence of the human TPO gene. The oligonucleotide probe was shown by Northern blotting to hybridize specifically to an approximately 3 kb RNA species from thyroid tissue of patients with Graves' disease, but not to RNA preparations from human or bovine retinal tissue, providing compelling evidence for the specificity of the probe for TPO mRNA. Addition of TSH (10 mU/ml) to primary thyroid cultures for 4 h led to increased TPO mRNA levels which were maximal after 48 h and significantly higher than basal even after 7 days of co-culture. Activation of TPO mRNA by TSH showed dose dependency over a wide range (0·01–100 mU/ml), with a maximal effect at 10 mU TSH/ml in cells cultured for a period of 72 h. Comparison of TPO mRNA levels with the accumulation of thyroglobulin mRNA levels following stimulation by TSH indicated that the induction of the gene encoding thyroglobulin precedes transcription of the TPO gene. The adenylate cyclase activator forskolin (1–100 μm) mimicked TSH in increasing TPO mRNA levels whilst, in contrast, the phorbol ester 12-O-tetradecanoyl phorbol 13-acetate (TPA; 0·01–1 μm) led to levels of TPO mRNA that were lower than basal. Thus TSH induces a specific dose-dependent activation of TPO mRNA which is mimicked by agents which increase cyclic AMP. In contrast, TPA-induced activation of protein kinase C inhibits this response.

scholarly journals Association of Duoxes with Thyroid Peroxidase and Its Regulation in Thyrocytes

2010 ◽  
Vol 95 (1) ◽  
pp. 375-382 ◽  
Author(s):  
Yue Song ◽  
Jean Ruf ◽  
Philippe Lothaire ◽  
Didier Dequanter ◽  
Guy Andry ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Protein Kinase ◽  
Plasma Membranes ◽  
Cell Damage ◽  
Thyroid Tissue ◽  
Human Thyroid ◽  
Thyroid Peroxidase ◽  
Thyroid Cells ◽  
Hormone Synthesis ◽  
Thyroid Hormone Synthesis

Abstract Context: Thyroid hormone synthesis requires H2O2 produced by dual oxidases (Duoxes) and thyroperoxidase (TPO). Defects in this system lead to congenital hypothyroidism. H2O2 damage to the thyrocytes may be a cause of cancer. Objective: The objective of the study was to investigate whether Duox and TPO, the H2O2 producer and consumer, might constitute a complex in the plasma membrane of human thyroid cells, thus maximizing efficiency and minimizing leakage and damage. Design: The interaction between Duox and TPO was studied by coimmunoprecipitation and Western blotting of plasma membranes from incubated follicles prepared from freshly resected human thyroid tissue from patients undergoing thyroidectomy, and COS-7 cells transiently transfected with the entire Duoxes or truncated [amino (NH2) or carboxyl (COOH) terminal]. Results: The following results were reached: 1) Duox and TPO from membranes are coprecipitated, 2) this association is up-regulated through the Gq-phospholipase C-Ca2+-protein kinase C pathway and down-regulated through the Gs-cAMP-protein kinase A pathway, 3) H2O2 increases the association of Duox1 and Duox2 to TPO in cells and in membranes, and 4) truncated NH2- or COOH-terminal Duox1 and Duox2 proteins show different binding abilities with TPO. Conclusion: Coimmunoprecipitations show that Duox and TPO locate closely in the plasma membranes of human thyrocytes, and this association can be modulated by H2O2, optimizing working efficiency and minimizing H2O2 spillage. This association could represent one part of a postulated pluriprotein complex involved in iodination. This suggests that defects in this association could impair thyroid hormone synthesis and lead to thyroid insufficiency and cell damage.

Auto-antigen presentation of thyroid cells derived from autoimmune thyroid tissue

1985 ◽  
Vol 110 (1_Suppla) ◽  
pp. S83
Author(s):  
B. E. WENZEL ◽  
T. MANSKY ◽  
P. C. SCRIBA
Keyword(s):  
Antigen Presentation ◽  
Thyroid Tissue ◽  
Thyroid Cells ◽  
Autoimmune Thyroid

AN INVESTIGATION OF THE PATHOGENESIS OF HASHIMOTO'S DISEASE BY THYROID TISSUE CULTURE

1960 ◽  
Vol 20 (2) ◽  
pp. 83-NP ◽  
Author(s):  
W. J. IRVINE
Keyword(s):  
Tissue Culture ◽  
Alternative Hypothesis ◽  
Thyroid Tissue ◽  
Human Thyroid ◽  
Rabbit Serum ◽  
Thyroid Cell ◽  
Thyroid Extract ◽  
Thyroid Cells ◽  
Hashimoto’S Disease ◽  
Hashimoto's Disease

SUMMARY Human thyroid cells were grown in tissue culture in media containing normal human serum, Hashimoto serum, and rabbit sera containing antibodies to purified human thyroglobulin and to crude thyroid extract, respectively. The thyroid cells grew equally well in all media, with the exception of the rabbit serum containing antibodies to crude thyroid extract. Intact thyroid cells obtained from tissue culture failed to fix Hashimoto antibodies in the presence of complement, whereas the constituents of disrupted thyroid cells gave a strongly positive complement-fixation test with Hashimoto serum. It is therefore suggested that the intact thyroid cell is impermeable to complement-fixing Hashimoto antibody. The evidence afforded by the present work adds further weight to the belief that Hashimoto's disease may not be due to a simple auto-immunizing process consequent upon the interaction of thyroid antigen and the known circulating auto-antibodies. Evidence in support of an alternative hypothesis involving 'cell-bound' antibodies with disruption of the follicular basement membrane is discussed.

The revised 8307 base pair coding sequence of human thyroglobulin transiently expressed in eukaryotic cells

1997 ◽  
Vol 136 (5) ◽  
pp. 508-515 ◽  
Author(s):  
Simone A R van de Graaf ◽  
Erwin Pauws ◽  
Jan J M de Vijlder ◽  
Carrie Ris-Stalpers
Keyword(s):  
Nucleotide Sequence ◽  
Expression System ◽  
Thyroid Tissue ◽  
Initiation Site ◽  
Human Thyroid ◽  
Translation Initiation Site ◽  
Thyroid Cells ◽  
Coding Sequence ◽  
Reverse Transcription Pcr ◽  
Human Sequence

Abstract We developed a transient transfection system for human thyroglobulin (TG) cDNA in both human thyroid cells and in COS-1 cells. Four overlapping TG cDNA fragments were amplified by reverse transcription-PCR from RNA of normal thyroid tissue. The most 5′ fragment includes the natural translation initiation site and the sequence encoding the signal peptide (SP). After subcloning, the nucleotide sequence was determined and compared with the published human sequence, resulting in the detection of 30 nucleotide variations. For validation purposes, all variations were screened in 6–12 normal human alleles. Twenty-one were present in all screened alleles and have to be revised in the published nucleotide sequence. Since one variation concerns a triplet insertion, the coding sequence of the mature human thyroglobulin is 8307 nucleotides encoding 2750 amino acids. The TG cDNA constructs were transiently transfected in HTori 3 and COS-1 cells and protein expression was detected using a polyclonal anti-human-TG on fixed cells and after SDS-PAGE. In both cell-lines all four TG protein fragments were expressed. The mannose structures detected on the proteins by lectins and localization after expression in the cells suggest that only the N-terminal TG fragment (containing the SP) is directed to the endoplasmatic reticulum but is unable to reach the Golgi complex. The described expression system in human thyrocytes will be a helpful tool in studying the structure–function relationship of human TG in thyroid hormonogenesis. European Journal of Endocrinology 136 508–515

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