scholarly journals Gluten intolerance and hashimoto thyroiditis: an integrated review

2021 ◽  
Vol 14 (3) ◽  
Author(s):  
Etianne Andrade Araújo ◽  
Sabrina Portela Kerkhoff
Keyword(s):  
Intestinal Permeability ◽  
Hashimoto’S Thyroiditis ◽  
Familial Aggregation ◽  
Hashimoto Thyroiditis ◽  
Food Intolerance ◽  
Hashimoto's Thyroiditis ◽  
Gluten Free ◽  
Interesting Phenomenon ◽  
Autoimmune Thyroid ◽  
Number Of Individuals

The advent of agriculture about 10,000 years ago enabled the massive and widespread use of grains containing gluten in food. Thus, it represented an evolutionary challenge that has not yet been overcome and created the conditions for the development of diseases related to exposure to gluten in humans. The so-called hypersensitivity involves any abnormal reaction resulting from eating a particular food. We are now looking at another interesting phenomenon that is causing great confusion among healthcare professionals. The number of individuals embracing a gluten-free diet appears far greater than the predicted number of celiac patients, fueling a global gluten-free product market approaching $2.5 billion (US) in global sales in 2010. This trend is supported by the notion that, along with celiac disease, other conditions related to gluten intake have emerged as health concerns. Hashimoto's Thyroiditis is an autoimmune disease and the most common cause of hypothyroidism in our environment. It occurs with high familial aggregation and there seems to be a clear genetic predisposition, with an apparent autosomal dominant inheritance of autoantibodies in affected individuals. Food intolerance and allergies and intestinal permeability can accompany hypothyroidism. Food (food intolerance and allergies), bacteria, viruses, chemicals, excess bacterial growth in the intestine, intestinal permeability, and contaminants are the main culprits for the autoimmune thyroid disease – Hashimoto's thyroiditis.

scholarly journals Defect of a subpopulation of natural killer immune cells in Graves’ disease and Hashimoto’s thyroiditis: normalizing effect of dehydroepiandrosterone sulfate

2005 ◽  
Vol 152 (5) ◽  
pp. 703-712 ◽  
Author(s):  
Sebastiano Bruno Solerte ◽  
Sara Precerutti ◽  
Carmine Gazzaruso ◽  
Eleonora Locatelli ◽  
Mauro Zamboni ◽  
...  
Keyword(s):  
Nk Cells ◽  
Hashimoto’S Thyroiditis ◽  
Nk Cell ◽  
Secretory Activity ◽  
Thyroid Diseases ◽  
Hashimoto's Thyroiditis ◽  
Graves Disease ◽  
Autoimmune Thyroid Diseases ◽  
Autoimmune Thyroid ◽  
Tnf Α

Background: The study of the natural killer (NK) immune compartment could provide important findings to help in the understanding of some of the pathogenetic mechanisms related to autoimmune thyroid diseases (Graves’ disease (GD) and Hashimoto’s thyroiditis (HT)). Within this context, it was suggested that alterations in NK cell cytotoxicity (NKCC) and NK production of cytokines might occur in subjects with GD and HT, whereas the normalization of NK functions could potentially contribute to the prevention of the onset or the progression of both diseases. Objective: Due to the hypothesis of alterations in NK in autoimmune thyroid diseases, we were interested to evaluate NKCC in GD and HT patients and to modulate NK function and secretory activity with cytokines and dehydroepiandrosterone sulfate (DHEAS) in an attempt to normalize NK cell defect. Design: We studied 13 patients with recent onset Graves’ disease, 11 patients with Hashimoto’s thyroiditis at first diagnosis and 15 age-matched healthy subjects. Methods: NK cells were concentrated at a density of 7.75 × 106 cells/ml by negative immunomagnetic cell separation and validated by FACScan as CD16 + /CD56 + cells. NK cells were incubated with interleukin-2 (IL-2) and interferon-β (IFN-β) and co-incubated with DHEAS at different molar concentrations for measuring NKCC and the secretory pattern of tumor necrosis factor-α (TNF-α) from NK cells. Results: Lower spontaneous, IL-2- and IFN-β-modulated NKCC was demonstrated in GD and HT patients compared with healthy subjects (P < 0.001). A decrease in spontaneous and IL-2-modulated TNF-α release from NK cells was also found in both groups of patients (P < 0.001). The co-incubation of NK cells with IL-2/IFN-β + DHEAS at different molar concentrations (from 10−8 to 10−5 M/ml/NK cells) promptly normalized NKCC and TNF-α secretion in GD and HT patients. Conclusions: A functional defect of a subpopulation of NK immune cells, involving both NKCC and the secretory activity, was demonstrated in newly-diagnosed GD and HT patients. This defect can be reversed by a dose-dependent treatment with DHEAS. The impairment of NK cell activity in autoimmune thyroid diseases could potentially determine a critical expansion of T/B-cell immune compartments leading to the generation of autoantibodies and to the pathogenesis of thyroid autoimmunity.

scholarly journals Immune Disorders in Hashimoto’s Thyroiditis: What Do We Know So Far?

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Aleksandra Pyzik ◽  
Ewelina Grywalska ◽  
Beata Matyjaszek-Matuszek ◽  
Jacek Roliński
Keyword(s):  
Hashimoto’S Thyroiditis ◽  
T Regulatory Cells ◽  
Hashimoto Thyroiditis ◽  
Hashimoto's Thyroiditis ◽  
Regulatory Cells ◽  
Review Of Literature ◽  
Immune Disorders ◽  
Cd4 Cells ◽  
Immune Defect

This review of literature attempts to identify the factors that are involved in the pathogenesis of Hashimoto thyroiditis, an immune defect in an individual with genetic susceptibility accompanied with environmental factors. The frequency of Hashimoto’s disease is a growing trend and among Caucasians it is estimated at approximately 5%. The dysfunction of the gland may be clinically evident (0.1–2% of the population) or subclinical (10–15%). The pathology is diagnosed five to ten times more often in women than men and its incidence increases with the age (the peak of the number of cases is between 45 and 65); however, it can also be diagnosed in children. The pathogenesis of Hashimoto’s thyroiditis is still not fully comprehended. In the etiology of Hashimoto thyroiditis excessively stimulated T CD4+ cells are known to play the most important role. Recent research has demonstrated an increasing role of newly discovered cells such as Th17 (CD4+IL-17+) or T regulatory cells (CD4+CD25+highFoxP3+) in the induction of autoimmune disorders. The process of programmed cell death also plays an equally important role in the pathogenesis and the development of hypothyroidism.

scholarly journals Hyperthyroid Phase of Hashimoto's Thyroiditis

2019 ◽  
Vol 26 (1) ◽  
pp. 123
Author(s):  
Siti Nurul Hapsari ◽  
Sidarti Soehita
Keyword(s):  
Hashimoto’S Thyroiditis ◽  
Benign Lesion ◽  
Peripheral Blood Smear ◽  
Liver Function Tests ◽  
Hashimoto Thyroiditis ◽  
Ca 125 ◽  
Hashimoto's Thyroiditis ◽  
Thyroid Function Tests ◽  
Chronic Autoimmune Thyroiditis ◽  
Function Tests

Hashimoto thyroiditis (chronic autoimmune thyroiditis) is the most common cause of hypothyroidism in iodine-sufficient areas of the world. This condition, however, can sometimes show hyperthyroidism. A 39-year-old femalewas admitted to hospital due to shortness of breath and tremor four hours before hospitalization. There were nausea, chestpain, cold chills, and palpitation. She was diagnosed with Hashimoto's thyroiditis and routinely received tyrosol,propranolol, and dexamethasone. Physical examination showed cervical mass, afebrile, blood pressure of 130/70 mmHg,pulse rate of 110 beats/minute and respiratory rate of 20 breaths/minute. Laboratory examinations showed WBC 7.53 x 109/L, Hb 11.0 g/dL and platelet count of 168 x 109/L. Chest X-Ray: negative for infiltrates. Several laboratory testswere performed, abnormal results were as follows: FT4 level of 2.96 ng/dL (increased), TSH level of 0.003 µIU/mL(decreased), anti-TPO (antithyroid microsomal antibody) level of 306 IU/ml (increased), and IgE level of 213.6 IU/mL(increased). Peripheral blood smear, coagulation test, serum electrolytes, liver function tests, renal function tests, urinalysis,CEA and Ca 125 were within normal limits. Thyroid ultrasound was performed and showed a benign lesion. Fine needleaspiration biopsy showed lymphocytic Hashimoto's thyroiditis. Echocardiography showed hyperthyroid heart disease. Dueto an increase of anti-TPO and FT4 levels, a decrease of TSH levels and lymphocytic thyroiditis from FNAB, this patient wasdiagnosed with a hyperthyroid phase of Hashimoto's thyroiditis. Thyroid function tests and thyroid antibody tests must bemonitored to distinguish between the hyperthyroid and hypothyroid phase of Hashimoto thyroiditis.

scholarly journals Polymorphisms of IKZF3 Gene and Autoimmune Thyroid Diseases: Associated with Graves’ Disease but Not with Hashimoto’s Thyroiditis

2018 ◽  
Vol 45 (5) ◽  
pp. 1787-1796 ◽  
Author(s):  
Ling Li ◽  
Xiaolian Ding ◽  
Xuan Wang ◽  
Qiuming Yao ◽  
Xiaoqing Shao ◽  
...  
Keyword(s):  
Hashimoto’S Thyroiditis ◽  
Zinc Finger Protein ◽  
Thyroid Diseases ◽  
Hashimoto's Thyroiditis ◽  
Control Group ◽  
Graves Disease ◽  
Autoimmune Thyroid Diseases ◽  
Autoimmune Thyroid ◽  
Significant Difference ◽  
Proliferation And Differentiation

Background/Aims: The IKZF3 gene encodes a zinc-finger protein that plays an important role in the proliferation and differentiation of B lymphocytes. Autoimmune thyroid diseases (AITDs), mainly include Graves’ disease (GD) and Hashimoto’s thyroiditis (HT), are probably caused by the aberrant proliferation of B cells. The objective of this study was to explore the association between IKZF3 polymorphisms and AITDs. Methods: We examined 915 AITD patients (604 GD and 311 HT) and 814 healthy controls. IKZF3 variants (rs2941522, rs907091, rs1453559, rs12150079 and rs2872507) were tested by PCR-ligase detection reaction. Results: It was manifested that that the minor alleles of the five loci increased susceptibility to GD (p<0.05 for rs2941522, and p<0.01 for rs907091, rs1453559, rs12150079 and rs2872507) but in HT patients, these loci showed no significant difference compared with controls. Similarly, the genotype distributions of GD patients manifested obvious differences in all these loci compared with the control group, whereas no statistical differences were observed between HT patients and controls. Furthermore, bioinformatics tools were used to analyze rs1453559, rs12150079 and rs907091. These variants were believed to be the transcription regulator. Conclusion: It is the first time we reported the association between the IKZF3 polymorphisms and GD, indicating that IKZF3 gene tends to bean important risk factor for the development of GD.

Familial Aggregation Study of Hashimoto’s Thyroiditis

2001 ◽  
Vol 3 (2) ◽  
pp. 75-79
Author(s):  
Aditi Sengupta ◽  
M.P. Sacheva ◽  
Col.R. Sankar ◽  
W. Selvamurthy
Keyword(s):  
Hashimoto’S Thyroiditis ◽  
Familial Aggregation ◽  
Hashimoto's Thyroiditis

scholarly journals The Relationship Between the Impairment of Endothelial Function and Thyroid Antibodies in Hashimoto’s Thyroiditis Patients with Euthyroidism

2020 ◽  
Vol 52 (09) ◽  
pp. 642-646
Author(s):  
Yanjin Hu ◽  
Zhi Yao ◽  
Guang Wang
Keyword(s):  
Endothelial Dysfunction ◽  
Endothelial Function ◽  
Hashimoto’S Thyroiditis ◽  
Reactive Hyperemia ◽  
Density Lipoprotein ◽  
Hashimoto Thyroiditis ◽  
Hashimoto's Thyroiditis ◽  
Thyroid Peroxidase ◽  
Healthy Controls ◽  
Negatively Associated

AbstractEndothelial dysfunction is the important early step in the development of atherosclerosis. Hypothyroidism caused by Hashimoto’s thyroiditis and other thyroid disease is one of the risk factors of endothelial dysfunction. The present study tried to investigate the endothelial function and its associated factors in Hashimoto thyroiditis with euthyroidism. A total of 95 newly diagnosed Hashimoto’s thyroiditis patients with euthyroidism and 45 healthy controls were studied. Hashimoto’s patients were divided into 3 subgroups namely, single thyroglobulin antibody (TGAb) positive subgroup, single thyroid peroxidase antibody (TPOAb) positive subgroup, and both TGAb and TPOAb positive subgroup. Endothelial function was tested by the reactive hyperemia index (RHI). Hashimoto’s thyroiditis patients had lower RHI than healthy controls (1.73±0.42 vs 1.96±0.51, p<0.05). Hashimoto’s thyroiditis with single TGAb positive patients had higher RHI than single TPOAb positive (1.98±0.57 vs. 1.69±0.33, p<0.05) and TGAB + TPOAb positive patients (1.98±0.57 vs. 1.68±0.42, p<0.05). RHI were negatively associated with total cholesterol (TC, r=−0.215, p<0.05), low density lipoprotein cholesterol (LDL-C, r=−0.268, p<0.05), triglyceride (TG, r=−0.192, p<0.05), and TPOAb (r=−0.288, p<0.05). In the regression analysis, LDL-C (β=−0.146, p<0.05), TG (β=−0.034, p<0.05) and TPOAb (β=−0.001, p<0.05) were independently associated with RHI. Hashimoto’s patients had poor endothelial function. TPOAb levels were negatively associated with endothelial function.

scholarly journals IRF7 Gene Variations Confer Susceptibility to Autoimmune Thyroid Diseases and Graves’ Ophthalmopathy

2019 ◽  
Vol 2019 ◽  
pp. 1-7
Author(s):  
Qiuming Yao ◽  
Xiaofei An ◽  
Jing Zhang ◽  
Kaida Mu ◽  
Ling Li ◽  
...  
Keyword(s):  
Hashimoto’S Thyroiditis ◽  
Susceptibility Gene ◽  
Thyroid Diseases ◽  
Minor Allele ◽  
Hashimoto's Thyroiditis ◽  
Graves Disease ◽  
Autoimmune Thyroid Diseases ◽  
Autoimmune Thyroid ◽  
Graves Ophthalmopathy ◽  
Significant Difference

The objective of this study was to investigate whether IRF7 polymorphisms are associated with autoimmune thyroid diseases (AITDs). We selected three single nucleotide polymorphisms (SNPs) of IRF7, namely, rs1061501, rs1131665, and rs1061502 for genotyping using PCR-based ligase detection reaction (LDR) method in a total of 1659 participants (592 with Graves’ disease, 297 with Hashimoto’s thyroiditis, and 770 healthy controls). Gene-disease and genotype-clinical phenotype associations were evaluated for the three SNPs. Our results showed that the AG genotype and the minor allele G frequency of rs1131665 and rs1061502 in AITD patients were both higher than those of the controls (rs1131665: AG genotype: P=0.017, OR=1.968; allele G: P=0.018, OR=1.946; rs1061502: AG genotype: P=0.029, OR=1.866; allele G: P=0.031, OR=1.847). Subgroup analysis also showed that the AG genotype and the minor allele G frequency of rs1131665 and rs1061502 in Graves’ disease patients were both higher than those of the controls (rs1131665: AG genotype: P=0.015, OR=2.074; allele G: P=0.016, OR=2.048; rs1061502: AG genotype: P=0.034, OR=1.919; allele G: P=0.035, OR=1.898). Furthermore, the allele G frequency of rs1061501 was associated with Graves’ ophthalmopathy (P=0.035, OR=1.396). No significant difference in IRF7 polymorphisms was found between Hashimoto’s thyroiditis patients and controls. Our study has revealed for the first time that IRF7 is a susceptibility gene for AITD, especially for Graves’ disease and Graves’ ophthalmopathy.

scholarly journals Autoantibodies from patients with autoimmune thyroid disease do not interfere with the activity of the human iodide symporter gene stably transfected in CHO cells

2001 ◽  
pp. 611-618 ◽  
Author(s):  
M Tonacchera ◽  
P Agretti ◽  
G Ceccarini ◽  
R Lenza ◽  
S Refetoff ◽  
...  
Keyword(s):  
Cell Line ◽  
Cho Cells ◽  
Hashimoto’S Thyroiditis ◽  
Time Course ◽  
Hashimoto's Thyroiditis ◽  
Graves Disease ◽  
Dependent Manner ◽  
Iodide Uptake ◽  
Autoimmune Thyroid ◽  
A Cell

OBJECTIVE: The human sodium iodide symporter (hNIS) is a candidate autoantigen in autoimmune thyroid diseases. To investigate the possible existence of autoantibodies able to interfere with the biological activity of hNIS, an assay was developed using a cell line stably expressing hNIS. METHODS: hNIS complementary cDNA cloned in pcDNA3 and a neomycin resistance gene vector were co-transfected into CHO cells. After selection with geneticin, a cell line termed PA4, showing the highest level of Na(125)I uptake, was characterized. The time course of iodide uptake was evaluated by incubating PA(4) cells with 10 micromol/l NaI and 0.1 microCi Na(125)I for a period up to 90 min. The accumulation of iodide increased linearly between 2 and 10 min, reaching a plateau at 45 min. The curve of iodide efflux mirrored that of iodide influx. Both perchlorate and thiocyanate inhibited iodide uptake in PA(4) cells in a dose-dependent manner starting from concentrations as low as 0.01 and 0.1 micromol/l respectively and complete inhibition was obtained at concentrations of 100 micromol/l perchlorate and 1000 micromol/l thiocyanate. The sensitivity of the inhibition assay was further improved using both inhibitors after 5 min incubation and in the absence of cold NaI. RESULTS: Included in the study were 42 patients with Graves' disease (25 had active hyperthyroidism, ten were euthyroid and seven had hypothyroidism); 34 patients with Hashimoto's thyroiditis (one was euthyroid, four had subclinical hypothyroidism and 29 were overtly hypothyroid); and 19 with atrophic thyroiditis (all hypothyroid). Four out of eight whole sera from patients with Hashimoto's thyroiditis, and 8 out of 25 whole sera from patients with Graves' disease caused an inhibition of iodide uptake in PA(4) cells greater than 20% but also in 4 out of 15 sera from normal subjects. This inhibition activity exerted by sera from patients and controls was lost after dialyzing against buffer. Accordingly, IgGs purified from sera of all patients with Graves' disease and with Hashimoto's thyroiditis or atrophic thyroiditis were devoid of any effect on iodide uptake. CONCLUSIONS: In conclusion, we believe that autoantibodies able to block the function of hNIS are very rare.

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