Autoimmune Lymphocytic Thyroiditis Research Articles

The effect of vitamin D on the development of Hashimoto's disease and the reduction of the inflammatory process in its course - review

Introduction Hashimoto's disease is an autoimmune chronic lymphocytic thyroiditis. It is a common condition, more frequent in women. Its diagnosis is based on the presence of specific antithyroid antibodies in the patient's blood which lead to the destruction of the thyroid gland. This can result in the development of hypothyroidism, requiring levothyroxine replacement therapy. Aim of the review A summary of the information gathered so far on the involvement of vitamin D in the development and course of Hashimoto's disease. Results The articles analyzed have mixed results. Most of them show a positive correlation between vitamin D and Hashimoto's disease, paying particular attention to the contribution of vitamin D in moderating the inflammatory process in HT. Other studies show significant differences in vitamin D levels between groups with different HT severity. Others show a negative correlation between vitamin D levels and the development of Hashimoto's disease. Conclusions Large well-controlled randomized double blind trials are needed in order to determine the exact role of vitamin D in Hashimoto’s disease.

Understanding and approach of Ayurveda management towards a unique case of Hashimoto Thyroiditis - A Case Report

Hashimoto thyroiditis is also known as chronic autoimmune thyroiditis and chronic lymphocytic thyroiditis, is an autoimmune disease in which thyroid cells are destroyed via cell and antibody-mediated immune processes. It is the most common cause of hypothyroidism in developed countries. The Pathophysiology of Hashimoto Thyroiditis involves the formation of antithyroid antibodies that attack the thyroid tissue, causing progressive fibrosis. The condition is sometimes not diagnosed until late in the disease process. The most common laboratory findings demonstrate elevated Thyroid-Stimulating Hormone (TSH) and low Thyroxine (T4) levels, coupled with increased anti thyroid peroxidase (anti-TPO) antibodies. In Ayurveda, it can be correlated with Rasavaha Sroto Vikara, Dhatwagnimandya, Vataja Pandu, Pittavruta Vata based on symptoms. Case Report: In this present study a female patient aged 37 years, known case of Hashimoto Thyroiditis since 8 years was treated with Shiro Takradhara, Sarvanga Abhynaga, Virechana and specific Shamanaushadhi’s as per signs and symptoms. Results: After 2 months of treatment there was a significant reduction in the signs and symptoms of the disease with 70% improvement in the condition.

Hashimoto's Thyroiditis among Patients with Thyroid Disorders Visiting a Tertiary Care Centre.

Hashimoto's thyroiditis is a chronic autoimmune lymphocytic thyroiditis characterised by thyroid autoantibodies. Early detection and treatment of this condition help in reducing the morbidity and mortality associated with it. The aim of the study was to find out the prevalence of Hashimoto's thyroiditis among patients with thyroid disorders visiting a tertiary care centre. A descriptive cross-sectional study was conducted among patients visiting the outpatient department of a tertiary care centre. Data from 14 April 2017 to 13 April 2019 was collected between 30 June 2022 to 15 September 2022 from medical records. Ethical approval was obtained from the Nepal Health Research Council. Hashimoto's thyroiditis was diagnosed based on clinical presentation and positive antibodies to thyroid antigens. Convenience sampling method was used. The point estimate was calculated at a 95% Confidence Interval. Among 813 patients with thyroid disorders, 393 (48.33%) (44.89-51.77, 95% Confidence Interval) had Hashimoto's thyroiditis. The manifestation of the spectrum of Hashimoto's thyroiditis were euthyroid in 215 (54.70%), subclinical hypothyroidism in 102 (25.95%), subclinical hyperthyroidism in 23 (5.85%), overt hyperthyroidism in 9 (2.30%) and overt hypothyroidism in 4 (1.02%). The prevalence of Hashimoto's thyroiditis among patients with thyroid disorders was higher than in other studies done in similar settings. anti-thyroid peroxidase antibodies; Hashimoto's thyroiditis; thyroid disorders.

The clinical, laboratory and anatomical pathology profiles of Hashimoto’s Thyroiditis patients at Dr. Soetomo General Academic Hospital Surabaya 2015 – 2020

The primary cause of hypothyroidism in the ​​sufficient iodine area is Hashimoto's thyroiditis. Hashimoto's thyroiditis, also known as chronic autoimmune thyroiditis or chronic lymphocytic thyroiditis, is an autoimmune condition in which B cells and T cells slowly destroy the thyroid gland. To determine the diagnosis, we need the clinical, laboratory, cytological, and/or histopathology profiles. It aims to distinguish Hashimoto's thyroiditis from other diseases such as nontoxic goiter and Graves' disease. This retrospective descriptive study used data from the medical record of Dr. Soetomo General Hospital from 2015-2020. This study used total sampling and got 18 patients in total. The patients were mostly females (n=15), in the age group of 40-49 years old (n=8). The main complaint was an enlargement or nodule in the neck. The TSH (thyroid stimulating hormone) levels were majorly higher than the normal range (n=8) meanwhile the FT4 levels were mostly normal (n=6) and low (n=6). The positivity of TPOAb (antibody against thyroid peroxidase) is merely found in one patient. The majority of the result of the Doppler ultrasound examinations revealed Hashimoto’s thyroiditis (n=7). FNAB (fine needle aspiration biopsy) was performed on 11 patients. A histopathology examination was also conducted on 9 patients who underwent thyroidectomy. All of the cytology and histopathology examinations confirmed Hashimoto’s thyroiditis. Non-Hodgkin Lymphoma was found to coexist with 2 Hashimoto's thyroiditis cases. The findings were similar to the previous studies, except that among all the subjects, those who are 40-49 in age were primarily found in this study.

Cell Component and Function of Tumor Microenvironment in Thyroid Cancer.

Thyroid cancer is the most common cancer in the endocrine system. Most thyroid cancers have good prognosis, but some of them are resistant to treatment or show aggressive behavior. Like other tumors, thyroid cancers harbor tumor microenvironment (TME) composed of cancer associated fibroblasts (CAF) and immune cells. Autoimmune lymphocytic thyroiditis can occur in the thyroid, and it may be associated with cancer development. TME is involved in tumor progression through various mechanisms: (1) CAF is involved in tumor progression through cell proliferation and extracellular matrix (ECM) remodeling; and (2) immune cells are involved in tumor progression through cell proliferation, angiogenesis, epithelial mesenchymal transformation (EMT), and immune suppression. These events are activated by various cytokines, chemokines, and metabolites secreted from cells that comprise TME. This review is focused on how CAF and immune cells, two important cell components of thyroid cancer TME, are involved in tumor progression, and will explore their potential as therapeutic targets.

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

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.

Thyroid cancer associated with Hashimoto thyroiditis: similarities and differences in an endemic area

BackgroundHashimoto thyroiditis (HT) is an autoimmune lymphocytic thyroiditis and is the most common form of thyroid inflammatory diseases. The association of HT with papillary thyroid carcinoma (PTC) has been described. PTC is the most common form of malignancy associated with HT. When papillary carcinoma develops on top of Hashimoto thyroiditis, the disease tends to be less aggressive and lymph node and extra-thyroidal invasion are infrequent.ResultsWe retrospectively examined the pathological features of our patients who were diagnosed with concomitant HT and thyroid cancer. In Egyptian patients, PTC was the main type of malignancy associated with HT (96.2%) and was often multifocal (46.2%). In contrast to the published literature, lymph node invasion and extra-thyroidal extension were as frequent in association with HT as in other cancer cohorts. We also observed the frequent occurrence of Hürthle cell metaplasia (23.1%) and the appreciable incidence of aggressive histological types of PTC (32%).ConclusionThyroid carcinoma with HT may have some aggressive features in areas with endemic goiter background.

Enfermedad tiroidea: una aproximación clínica y genética

La glándula tiroides, es uno de los órganos endocrinos encargado de la regulación de diferentes procesos metabólicos, sintetiza las hormonas tiroideas, tiroxina y triyodotironina, necesarias para el funcionamiento del organismo. El hipotiroidismo, es una condición en la cual la glándula tiroides no puede producir la suficiente cantidad de hormonas tiroideas necesarias para cumplir con el requerimiento tisular, es el desorden más común de la tiroides y una de las principales alteraciones endocrinas. Las causas más comunes son la deficiencia de yodo y la tiroiditis autoinmune linfocítica crónica. El cuadro clínico del hipotiroidismo es bastante amplio afectando diferentes órganos y sistemas. El manejo de esta patología se hace con reemplazo hormonal, para ello levotiroxina es la indicación. El hipertiroidismo por su parte, hace referencia al incremento sostenido de las hormonas tiroideas debido al aumento de biosíntesis y secreción de la tiroides. Entre las principales causas se encuentra la enfermedad de Graves Basedow (EG). Su presentación clínica es amplia y varía de asintomática a una tormenta tiroidea que compromete la vida del paciente. El tratamiento está basado en medicamentos antitiroideos pero también se han diseñado otras alternativas como yodo radioactivo y tiroidectomía. También las enfermedades que afectan directamente la tiroides, como el cáncer, son de gran importancia; la evidencia obtenida en numerosos estudios sugiere que los polimorfismos genéticos influencian el riesgo de carcinogénesis y que la susceptibilidad genética es un factor importante para el desarrollo del cáncer. Los avances genéticos en esta patología han permitido una compresión mas a fondo de las diferencias en el comportamiento de los trastornos tiroideos entre una persona y otra, así mismo han generado un nuevo punto de partida para el tratamiento farmacológico.

Autoimmunity, Intestinal Lymphoid Hyperplasia, and Defects in Mucosal B-Cell Homeostasis in Patients With PTEN Hamartoma Tumor Syndrome

The Phosphatase And Tensin Homolog Deleted On Chromosome 10 (PTEN) regulates the phosphoinositol-3-kinase (PI3K)-AKT signaling pathway. In a series of 34 patients with PTEN mutations, we described gastrointestinal lymphoid hyperplasia, extensive hyperplastic tonsils, thymus hyperplasia, autoimmune lymphocytic thyroiditis, autoimmune hemolytic anemia, and colitis. Functional analysis of the gastrointestinal mucosa-associated lymphoid tissue revealed increased signaling via the PI3K-AKT pathway, including phosphorylation of S6 and increased cell proliferation, but also reduced apoptosis of CD20(+)CD10(+) B cells. Reduced activity of PTEN therefore affects homeostasis of human germinal center B cells by increasing PI3K-AKT signaling via mammalian target of rapamycin as well as antiapoptotic signals.

Cross-talk between NO and HMGB1 in lymphocytic thyroiditis and papillary thyroid cancer

The controversy on whether or not inflammatory infiltrates in chronic lymphocytic thyroiditis predispose to cancer, has now merged into a debate over the role of the inflammatory infiltrates. The question is how and why some cells become transformed and what factors allow them to spread and in some cases become invasive. Here, we show that the amount of inflammatory mediators such as nitric oxide (NO) and high mobility group Box 1 protein (HMGB1) produced in thyroiditis microenvironment increases in tumors and could be involved in the cellular transformation process. NO and HMGB1 are known to attract macrophages that would promote angiogenesis, matrix remodelling and suppression of an efficient immune response. Inflammatory infiltrates could increase the risk of papillary cancer in patients with autoimmune lymphocytic thyroiditis. Cytokines and soluble inflammatory mediators involved in cancer-related inflammation are not only a target for innovative diagnostic and therapeutic strategies but they also represent a future challenge for oncologists.

Substernal Thyroid Masses

Substernal Thyroid Masses

Increased genetic risk or protection for canine autoimmune lymphocytic thyroiditis in Giant Schnauzers depends on DLA class II genotype

Dogs represent an excellent comparative model for autoimmune thyroiditis as several dog breeds develop canine lymphocytic thyroiditis (CLT), which is clinically similar to Hashimoto's thyroiditis in human. We obtained evidence that dog leukocyte antigen (DLA) class II genotype function as either genetic risk factor that predisposes for CLT or as protective factor against the disease. Genetic diversity at their DLA-DRB1, -DQA1, and -DQB1 loci were defined and potential association to major histocompatibility complex II haplotypes and alleles was analyzed. Giant Schnauzers carrying the DLA-DRB1*01201/DQA1*00101/DQB1*00201 haplotype showed an increased risk (odds ratio of 6.5) for developing CLT. The same risk haplotype has, to date, been observed in three different breeds affected by this disease, Giant Schnauzer, Dobermann, and Labrador Retriever, indicating that it is a common genetic risk factor in a variety of breeds affected by this disease. Importantly, protection for development of the disease was found in dogs carrying the DLA-DRB1*01301/DQA1*00301/DQB1*00501 haplotype (odds ratio of 0.3).

Prevalence of diagnostic characteristics indicating canine autoimmune lymphocytic thyroiditis in giant schnauzer and hovawart dogs

To investigate prevalence of autoantibodies to thyroglobulin (TgAA) and/or elevated levels of thyroid stimulating hormone (TSH), indicating canine autoimmune lymphocytic thyroiditis (CLT) and/or hypothyroidism, in two high-risk dog breeds. A cohort study was conducted in two birth cohorts of giant schnauzer and hovawart dogs. The cohorts were three to four and six to seven years of age at the time of blood sampling and screening for TgAA and TSH levels. Blood sampling was accompanied by one initial and one follow-up questionnaire to the dog owners. A total number of 236 giant schnauzers and 95 hovawarts were included in the study. Seventeen (7.2 per cent) giant schnauzers and three (3.2 per cent) hovawarts had been diagnosed as hypothyroid at the time of sampling. Out of the remaining dogs, 22 giant schnauzers (10.0 per cent) and nine hovawarts (10.1 per cent) had elevated TgAA and/or TSH levels. Prevalence of elevated TgAA and TSH levels varied with age. The high prevalence of diagnostic characteristics indicating CLT/hypothyroidism in these two breeds suggests a strong genetic predisposition. It would be advisable to screen potential breeding stock for TSH and TgAA as a basis for genetic health programmes to reduce prevalence of CLT in these breeds.

Ductal Metaplasia in Chronic Lymphocytic Thyroiditis as a Manifestation of Phylogenic Regression to an Exocrine Structure

From a morphologic and functional point of view the thyroid can be considered as both an exocrine and endocrine organ. Firstly, thyroglobulin is secreted at the apical pole of the thyrocyte. Secondly, after endocytosis thyroglobulin is lysed and T3 and T4 are secreted at the basal pole into the bloodstream. However, usually exocrine glands are constituted of 2 well separate components: an acinus/alveolar component and an exocrine duct component. Under particular conditions such as chronic injury the acinus/alveolar component is rapidly destroyed, whereas the ductal component seems to be far more resistant and can proliferate giving rise to a tubular network described as "ductulus reaction" or "ductal metaplasia." Normal exocrine ducts and metaplastic ducts exhibit common genetic and phenotypic features directly related to their tubular morphology. In this study, we describe in lymphocytic autoimmune thyroiditis the appearance of ductal-like structures which displayed the features of ductal metaplasia.

Iodine and IFN-γ Synergistically Enhance Intercellular Adhesion Molecule 1 Expression on NOD.H2h4 Mouse Thyrocytes

NOD.H2(h4) mice spontaneously develop autoimmune lymphocytic thyroiditis that mimics human Hashimoto's thyroiditis, a disease where iodine, IFN-gamma, and adhesion molecules have all been implicated in the pathogenesis. To study how iodine and IFN-gamma modulate the expression of ICAM-1, we analyzed NOD.H2(h4) thyrocytes in baseline conditions (day 0) and at several time points following supplementation of iodine in the drinking water. On day 0, a small percentage ( approximately 10%) of thyrocytes constitutively expressed ICAM-1. The expression gradually increased to 13, 25, and 41% on days 7, 14 and 28, respectively, returning to baseline (9%) on day 35. The initial ICAM-1 kinetics was paralleled by thyroidal infiltration of CD45(+) hemopoietic cells, which increased from an average of 4% on day 0 to an average of 13, 21, and 24% on days 14, 28, and 35, respectively. To distinguish whether the observed ICAM-1 increase was a direct effect of iodine or a consequence of the immune infiltrate, we treated mouse primary thyrocyte cultures with 0.01 mM sodium iodine and showed a 3-fold increased ICAM-1 expression. To assess interaction between IFN-gamma and iodine, we analyzed CD45 and ICAM-1expression on thyrocytes from NOD.H2(h4) wild-type and NOD.H2(h4) thyr-IFN-gamma transgenic littermates. Strikingly, IFN-gamma interacted synergistically with iodine to enhance ICAM-1 expression on thyrocytes. These findings suggest that iodine and IFN-gamma cooperate to promote thyroidal expression of ICAM-1 in this mouse model of thyroiditis, highlighting the complex interplay present in the pathogenesis of Hashimoto's thyroiditis.

5: Diagnosis and management of hyperthyroidism and hypothyroidism

The most common cause of hyperthyroidism in Australia is Graves disease, caused by a defect in immunoregulation in genetically predisposed individuals, leading to production of thyroid-stimulating antibodies. Each of the three modalities of therapy for Graves disease--thionamide drugs, subtotal or total thyroidectomy, and radioactive iodine ablation--can render the patient euthyroid, but all have potential adverse effects and may not eliminate recurrences. Hypothyroidism occurs in about 5% of the adult population; most present with "subclinical" hypothyroidism (mild thyroid failure), characterised by raised levels of serum thyroid stimulating hormone (TSH) but normal free thyroxine (T(4)). The most common cause of hypothyroidism in Australia is autoimmune chronic lymphocytic thyroiditis, characterised by raised circulating levels of thyroid peroxidase antibody. Symptoms and signs of hypothyroidism are often mild or subtle and, when there is clinical suspicion, thyroid function tests are needed; if serum TSH level is raised, free T(4) and thyroid peroxidase antibody should be measured. Replacement therapy with thyroxine is the cornerstone of therapy (1.6 microg/kg lean body weight daily, taken on an empty stomach); combination therapy with thyroxine and liothyronine (T(3)) is promoted, but there is little evidence of its clinical benefit. Despite the development of highly sensitive laboratory tests, clinical assessment and judgement remain paramount

P53 and p21WAF1Expression in Lymphocytic Thyroiditis and Thyroid Tumors

To clarify the roles of increased apoptosis and cell proliferation in chronic autoimmune lymphocytic thyroiditis and thyroid tumorigenesis, expression of p53 and p21WAF1proteins was immunohistochemically investigated in a series of 158 cases. Positive epithelial cells were quantified to give numbers per unit square and to score for distribution. They were found scattered in nontumorous thyroid tissue, their numbers increasing with the severity of thyroiditis and the correlation between expression of the two proteins, regardless of the presence or absence of thyroid neoplasms. Simultaneous expression of both proteins was occasionally found in the same cells by analysis of serial histologic sections. In thyroid tumors, increased expression was found to be diffuse, focal, or scattered for the distribution of p53- or p21WAF1-immunopositive cells in accordance with tumor cell dedifferentiation, showing significant correlation between expression of the two proteins. Correlated with these findings, enhanced apoptosis along with decreased Bcl-2 expression and increased Ki-67 labeling in lymphocytic thyroiditis and thyroid tumors was also confirmed in the same series, usingin situDNA nick-end labeling and immunohistochemical methods. Increased expression of p53 and/or p21WAF1proteins was thus suggestive of possible DNA damage and increased apoptosis in autoimmune thyroiditis. In addition, a significant correlation between protein overexpression and dedifferentiation of thyroid tumor cells was apparent.

Dehydroepiandrosterone sulfate does not prevent spontaneous and iodine-induced lymphocytic thyroiditis and diabetes mellitus in the BB/Wor rat.

Chronic feeding of dehydroepiandrosterone (DHEA) and its sulfated metabolite, dehydroepiandrosterone sulfate (DHEAS), has previously been reported to decrease hyperglycemia, obesity, cancer, and autoantibody generation in a number of animal models and to increase muscle mass and physiological and psychological well-being in elderly humans, although these latter studies remain controversial. The present study was carried out to determine whether large amounts of DHEAS given orally would prevent the occurrence of spontaneous and iodine-induced autoimmune lymphocytic thyroiditis (LT) and/or spontaneous insulin-dependent diabetes mellitus (DM) in male and female BB/Wor rats. DHEAS was administered by gavage (44 mg/rat/day) or in the chow (133 mg/rat/day) to LT- and DM-prone rats from 30 to 120 days of life; some of these rats also received iodine in the drinking water to enhance the incidence and intensity of LT. Onset of DM requiring protamine zinc insulin and its maintenance dose were assessed. Rats were killed at 90 or 120 days of age and blood, thyroid, adrenals, pancreases, testes, and ovaries were removed. Serum glucose, DHEA, DHEAS, thyroxine (T4), tri-iodothyronine (T3) and thyrotropin (TSH) concentrations were measured in all rats in both experiments. Serum DHEAS concentrations were 10-fold higher in the rats given the steroid by gavage or in the diet compared with levels in control rats. DHEAS administered over a prolonged period of time had no significant effect on body weight, incidence and severity of DM, incidence and intensity of spontaneous and iodine-induced LT, and thyroid, pancreas and testes weights but did significantly decrease adrenal and ovarian weights. Serum T4, T3, and TSH concentrations were similar in control and DHEAS-treated rats. In conclusion, DHEAS did not prevent the occurrence of iodine-induced or spontaneous autoimmune LT or spontaneous DM in the BB/Wor rat, at variance with its reported immunosuppressive effects in other animal models.

Expression of tenascin in lymphocytic autoimmune thyroiditis.

AIMS: To study the distribution of tenascin by immunocytochemistry in autoimmune diseases of the thyroid. METHODS: Thyroids from patients with inflammatory lesions of the thyroid (lymphocytic thyroiditis Hashimoto, Grave's disease,...

New tests for the assessment of thyroid function in dogs

As the techniques of thyroid imagery are not suitable for use in veterinary practice, laboratory tests are of special interest in the confirmation of thyroid disease. As many thyroidal function tests exist for use in dogs, but all are controversial, we assessed two new tests which have recently been commercially developed: the canine TSH assay and the canine thyroglobulin autoantibody assay. The TSH values assayed with the DPC kit in dogs were usually under 0.55 ng/1. TSH assay could not totally replace thyroid stimulation with T4 measurement in hypothyroidism but permitted distinction between a thyroidal disease (high TSH) and an extrathyroidal disease (low TSH). TSH should be considered as complementary to thyroid stimulation for the determination of hypothyroidal aetiology. TSH measurement could also be used to confirm pituitary aetiology in nanism (TSH undetectable), and to evaluate the therapeutic efficacy of treatments of hypothyroidism with thyroidal aetiology, the dose being suitable when the TSH value returns to normal. The main aetiology of hypothyroidism seemed to be autoimmune lymphocytic thyroiditis. Thyroglobulin autoantibodies were the most frequent autoantibodies found in dogs with thyroiditis. It was not possible to use a commercial canine thyroglobulin autoantibody assay kit to refute or confirm this in a population of dogs with hypothyroidism and high TSH. Further technical developments will be required before the canine thyroglobulin autoantibody immunoassay can be used to diagnose thyroiditis.