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PubMed2005

Non-thyroid autoantibodies in autoimmune thyroid disease.

Autoimmune thyroid disease is frequently accompanied by other organ-specific and non-organ-specific diseases, most likely because there is sharing of genetic and possibly environmental susceptibility factors. These associations are well recognized in the autoimmune polyglandular syndromes; autoimmune thyroid disease is one of the three major endocrinopathies in the type 2 syndrome and occurs in around 4% of type 1 patients. This review considers the frequency of disease-specific autoantibodies in patients with thyroid autoimmunity and briefly examines the role of such antibodies in performing screening for the associated conditions. Recommendations are made for using such autoantibody tests in the setting of patients with autoimmune thyroid disorders, and also for the utility of screening for thyroid autoimmunity in patients with pernicious anaemia, Addison's disease, coeliac disease, primary biliary cirrhosis, myasthenia gravis, lymphocytic hypophysitis, systemic lupus erythematosus and rheumatoid arthritis. At present, however, there are no large-scale trials that have shown the cost-benefit ratio of autoantibody screening for autoimmunity screening, and clinicians must use individual judgement combined with heightened awareness to identify who to test.

Autoantibodies↗
PubMed2005

[Diagnosis of autoimmune thyroid disease].

Autoimmune thyroid disease (AITD) is the most common organ specific autoimmune disorder usually resulting in dysfunction (hyperfunction, hypofunction or both) of the thyroid gland. The syndromes comprising autoimmune thyroid disease are many intimately related illnesses: Graves' disease with goitre, hyperthyroidism and, in many patients, associated ophthalmopathy, Hashimoto's thyroiditis with goitre and euthyroidism or hypothyroidism but also thyroid dysfunction occurring independently of pregnancy and in 5-6% of postpartum women and thyroiditides induced by different drugs and other environmental influences. The immunological mechanisms involved in these diseases are closely related, while the phenotypes probably differ because of the specific type of immunological response that occurs. The syndromes are connected together by their similar thyroid pathology, similar immune mechanisms, co-occurrence in family groups, and transition from one clinical picture to another within the same individual over time. In some patients, other organ specific and nonorgan specific autoimmune syndromes are associated with autoimmune thyroid disease, including pernicious anemia, vitiligo, myasthenia gravis, primary adrenal autoimmune disease, celiac disease, rheumatoid arthritis or lupus. Thyroid peroxydase, TPO, the primary enzyme involved in thyroid hormonogenesis, was initially identified in 1959 as the 'thyroid microsomal antigenn. It is uncertain whether TPO autoantibodies or TPO-specific T cells are the primary cause of thyroid inflammation, which can lead, in some individuals, to thyroid failure and hypothyroidism. TPOAbs are the hallmark of AITB and are present in almost all patients with Hashimoto's thyroiditis, in two-thirds of patients with postpartum thyroiditis and also in 75% of patients with Graves' hyperthyroidism. The antibodies are mainly produced by lymphocytic infiltrate in the thyroid gland and only to a small extent by regional lymph nodes or the bone marrow. Unlike antibodies against thyroglobulin (Tg), TPO antibodies are capable of inducing antibody-dependent cell-mediated cytotoxicity. Antibodies to TSH-R mimic the function of TSH, and cause disease by binding to the TSH-R and stimulating (or inhibiting) thyroid cells. The TSHR, a member of the G protein-coupled receptor family with seven membrane-spanning segments. Patients with autoimmune thyroid disease may have both stimulating and blocking antibodies in their sera, the clinical picture being the result of the relative potency of each species; blocking antibodies seem more common in Graves' patients with ophthalmopathy compared to those without this complication. The major T cell epitopes are heterogeneous and T cell reactivity against certain TSH-R epitopes has been present in high proportion in normal subjects. More diversified response to TSH-R, with heterogeneity of epitope recognition by TSAb, is predictive of likely remission after antithyroid drug treatment for Graves' disease.

Autoimmune Diseases↗
PubMed1999

[B-cell, T-cell surface phenotypes and epitopes in autoimmune thyroid diseases].

Autoimmune thyroid diseases (AITD) are categorized as organ specific autoimmune diseases, including Graves' disease (GD), Hashimoto's thyroiditis and idiopathic myxoedema. In this article, B-, T-cell surface phenotypes and epitopes in AITD were reviewed. It has been reported that the proportion and absolute number of B and T lymphocyte subpopulation or CD4/8 ratio in peripheral blood from AITD was not different from normal subjects. Those of CD5+ B cells and gamma delta T cells known as autoreactive clones were, however, increased in peripheral blood from GD. In the thyroid tissue of AITD, B-cells with activated markers were predominantly infiltrated rather than T-cells. The CD4/8 ratio and the proportion of CD8+CD11b+ T (suppressor T) cells was decreased in contrast to the increase of CD8+CD11b- T (cytotoxic T) cells. The CD4+4B4+ T (helper/inducer) cells were more predominant than CD4+2H4+ T (suppressor/inducer) cells in thyroid tissue from GD. These abnormality might cause the cell destruction and the enhanced autoantibody production in the tissue of AITD. Thyroglobulin, thyroid peroxidase and thyroid stimulating hormone receptor are known as major autoantigens in AITD. Recently, B-cell and T-cell epitopes on these autoantigen molecules have been defined, using monoclonal antibodies, proteolytic or synthetic peptides with molecular gene engineering. These epitope analysis would be contributed to the autoimmune tolerance in AITD.

Autoimmune Diseases↗
PubMed1998

Somatic hypermutation in autoimmune thyroid disease.

Autoimmune thyroid disease is one of the most common autoimmune diseases. There is typically patient antibody (Ab) reactivity to one or more of the antigens thyroglobulin (Tg), thyroid peroxidase (TPO) and the thyroid simulating hormone receptor (TSHr). With the advent of combinatorial library technology, there has been an enormous increase in the number of sequences from Ab to Tg and TPO. The repertoire of both Tg and TPO Ab is restricted and indicates the importance of somatic hypermutation in the development of the high affinity Ab response. However, there are still too few sequences to determine patterns in which the mutation occurs, which residues are introduced during substitution and how individual substitutions affect the affinity of the Ab. Ab to the TSHr are of far greater pathological significance than those to Tg and TPO, but the current repertoire of Ab to the TSHr has yet to include the high affinity IgG Ab characteristic of patient serum Ab. Instructive analysis of the role of somatic hypermutation in the development of TSHr Ab therefore still awaits the isolation of the pathologically active repertoire. Despite this, the Ab response in thyroid autoimmunity remains one of the best characterised of human autoimmune diseases.

Amino Acid Sequence↗
PubMed2005

[Differentiated thyroid carcinoma in previously manifested autoimmune thyroid disease].

Autoimmune thyroid diseases are frequently associated with differentiated thyroid carcinomas. The role of autoimmune phenomena in the origin and clinical course of coexisting papillary and follicular carcinomas is still controversial. In Graves' patients, the prevalence of palpable thyroid nodules is 15.8%, and by using ultrasonography, the prevalence increases to 33.6%. Since the malignancy rate of palpable thyroid nodules in Graves' patients is 16.9%, approximately threefold higher than in general population, it seems that a thyroid nodule diagnosed in Graves' patients is at higher risk for malignancy. In addition, radioiodine therapy for Graves' disease was found to be associated with increased incidence of thyroid cancer in some studies. These studies however, were not able to confirm the carcinogenic effect of radioiodine therapy since the late growth of occult carcinomas could not be excluded. The frequency of the association of Hashimoto's thyroiditis and differentiated thyroid carcinomas is approximately 30%. The presence of coexistent Hashimoto's thyroiditis does not affect the diagnostic evaluation and management of papillary thyroid cancer. The frequent presentation of differentiated thyroid carcinomas in Graves' disease and Hashimoto's thyroiditis opens the possibility that some mutual pathogenethic mechanisms might be involved in the development of these diseases.

Adenocarcinoma, Follicular↗
PubMed2003

CTLA-4 and its role in autoimmune thyroid disease.

Autoimmune thyroid disease (AITD) occurs in two common forms: Graves' disease and Hashimoto thyroiditis. On the basis of functional and experimental data, it has been suggested that the gene encoding cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4) is a candidate gene for conferring susceptibility to thyroid autoimmunity. In this review, we critically evaluate the evidence for pathogenetic involvement of CTLA-4 in the various forms of AITD and focus on the possible role of genetic variation of the CTLA4 locus. Population genetics data strongly suggest a role for the CTLA4 region in susceptibility to AITD. However, further functional studies are required to understand the significance of CTLA4 polymorphisms in the pathogenic mechanism of AITD.

Antigens, CD↗
PubMed2003

Autoantibodies against glutamic acid decarboxylase and 21-hydroxylase in Brazilian patients with type 1 diabetes or autoimmune thyroid diseases.

Autoimmune thyroid diseases (ATD) are often associated with Type 1 diabetes mellitus (T1DM) and Addison's disease (AD), characterizing the autoimmune polyendocrine syndrome. We evaluated the frequency of autoantibodies against glutamic acid decarboxylase isoform 65 (GAD65Ab) and 21-hydroxylase (21OHAb) in the sera of 65 [58 females (F)/7 males (M), 17-70 yr] patients with Graves' disease (GD) and 47 (45 F/2 M, 12-77 yr) with Hashimoto's thyroiditis (HT), none of whom had either diabetes or AD. The sera of 30 recently diagnosed T1DM patients (16 M/14 F, 1-39 yr) and of 97 (54 F/43 M, 7-69 yr) healthy controls were also examined. GAD65Ab were detected in the sera of 18 (60%) T1DM, 8 (12%) GD and in none of the HT patients or the controls (p = 0.03 for GD vs HT, p = 0.002 for GD vs controls, and p < 0.001 for GD vs T1DM). 21OHAb were detected in the sera of 2 (3%) GD, 1 (2%) HT and in none of the T1DM patients or the controls. GAD65Ab levels were significantly lower in GD than in T1DM patients (median: -0.06 vs 0.28, p < 0.001). Six of the 8 GD GAD65Ab-positive patients submitted to an intravenous glucose tolerance test showed no diminished first phase insulin secretion. All 21OHAb positive patients had normal basal cortisol and adrenocorticotropin (ACTH), normal cortisol response after ACTH stimulation, but high plasma renin activity. In conclusion, despite the genetic diversity of the Brazilian population, the frequency of GAD65Ab and 21OHAb in our patients is similar to that observed in other countries. GAD65Ab were more prevalent in GD than in HT patients, suggesting a difference in the immune response between these disorders. Long-term follow-up is necessary to determine the clinical relevance of these autoantibodies in the Brazilian population.

Addison Disease↗
PubMed2002

Disease associations with autoimmune thyroid disease.

Autoimmune thyroid disease (AITD) is common and occurs frequently in conjunction with other diseases. Many putative disease associations have been suggested for AITD but the validity of these associations is not clear in all cases. It is important to define disease associations correctly because this may offer a means to rationally screen for true associations, may shed light on shared pathophysiologic mechanisms and may be important if the associated disease impacts on patient management. This review has examined the evidence base for a large number of the suggested associations.

Digestive System Diseases↗
PubMed2004

SNPs in the promoter of a B cell-specific antisense transcript, SAS-ZFAT, determine susceptibility to autoimmune thyroid disease.

Autoimmune thyroid disease (AITD) is caused by an immune response to self-thyroid antigens and has a significant genetic component. Antisense RNA transcripts have been implicated in gene regulation. Here we have identified a novel zinc-finger gene, designated ZFAT (zinc-finger gene in AITD susceptibility region), as one of the susceptibility genes in 8q23-q24 through an initial association analysis using the probands in the previous linkage analysis and a subsequent association analysis of the samples from a total of 515 affected individuals and 526 controls. The T allele of the single-nucleotide polymorphism (SNP), Ex9b-SNP10 located in the intron 9 of ZFAT, is associated with increased risk for AITD (dominant model: odds ratio = 1.7, P = 0.000091). The Ex9b-SNP10 falls into the 3'-UTR of truncated-ZFAT (TR-ZFAT) and the promoter region of the small antisense transcript of ZFAT (SAS-ZFAT). In peripheral blood lymphocytes, SAS-ZFAT is exclusively expressed in CD19+ B cells and expression levels of SAS-ZFAT and TR-ZFAT seemed to correlate with the Ex9b-SNP10-T-associated ZFAT-allele, inversely and positively, respectively. The Ex9b-SNP10 is critically involved in the regulation of SAS-ZFAT expression in vitro and this expression results in a decreased expression of TR-ZFAT. These results suggested that the SNP-associated ZFAT-allele plays a critical role in B cell function by affecting the expression level of TR-ZFAT through regulating SAS-ZFAT expression and that this novel regulatory mechanism of SNPs might be involved in controlling susceptibility or resistance to human disease.

B-Lymphocytes↗
PubMed1995

Cellular immunity in autoimmune thyroid disease.

Autoimmune thyroid disease occurs in a genetically susceptible patient after triggering events including bacterial and viral infections, environmental insults, drugs or hormones. These triggering events may break the tolerance to self-antigen, leading to emergence of autoreactive T cells. One or more T cell clones that recognize the self-antigen is(are) assumed to be involved in initiating autoimmune processes. Following this, T cell clones expand and migrate from the peripheral blood into the thyroid gland. Migration of mononuclear cells is controlled by inflammatory cytokines and adhesion molecules. Intrathyroidal T cells may interact with dendritic-like cells, thyrocytes expressed with HLA-DR antigens, B cells and extracellular matrix, resulting in the proliferation of T cells, production of cytokines and autoantibodies. These interactions are also regulated by inflammatory cytokines and adhesion molecules. When the initial immune response is completed, a secondary immune response ensues, that may be of considerable complexity involving reaction of infiltrating T cells to a variety of tissue-specific and tissue-non-specific antigens. These immune responses may contribute to the recurring immunologic activity and maintenance of autoantibody overproduction.

Animals↗
PubMed2004

The genetics of autoimmune thyroid disease.

Autoimmune thyroid diseases (AITDs), such as Graves' hyperthyroidism, are common disorders involving multiple genes and the environment. Some pathogenetic genes are probably shared between these diseases and non-endocrine autoimmune diseases, whereas others are disease specific. Population studies show that major histocompatibility complex alleles and CTLA4 confer risk for AITDs. Genetic studies have identified over 20 potential loci; only one, mapping to 5q31, has been convincingly replicated. Despite its recent emergence as an autoimmunity gatekeeper gene, linkage of CLTA4 to AITDs was described in only one Caucasian population subset. Like in the case of many complex genetic disorders, identifying AITD pathogenetic genes is limited by the ability of data analysis methods to discern the influence of genes of minor effect in a relatively small database.

Autoimmune Diseases↗
PubMed2006

[Susceptibility genes for the development of autoimmune thyroid disease].

Autoimmune thyroid disease (AITD) is caused by an immune response to self thyroid antigens. Twin studies and familial aggregation indicated that AITD is a complex disease with genetic factors and major histocompatibility complex is the most clearly established genetic factor. We confirmed the association of the co-receptor CTLA4 with AITD. We have identified the association of the SNP in the Fc receptor-like 3 with several autoimmune diseases, including AITD, SLE and rheumatoid arthritis, which SNP affected the level of autoantibody production. Furthermore, we have identified ZFAT as a susceptibility gene in 8q24 for AITD by whole-genome linkage analysis and further SNP-based dense mapping. The associated SNP in ZFAT affected the antisense transcript of ZFAT, which in turn affected the ZFAT expression.

Antigens, CD↗
PubMed1999

[Immunoregulatory genes in autoimmune thyroid disease].

Autoimmune thyroid diseases (AITD) has a strong genetic basis. Although several candidate genes have been studied, the AITD causing genes are still unknown. Major candidate immune regulatory genes include human leukocyte antigen (HLA) gene, Ig heavy chain genes, T cell receptor genes, IL-1 receptor antagonist gene, IL-1 alpha gene and cytotoxic T lymphocyte antigen-4 (CTLA-4) gene. The relation between HLA and AITD has extensively been studied. In addition, polymorphism of the 3'-untranslated region and codon 17 of the CTLA-4 gene has been reported to associate positively with AITD. However, no linkage analyses have showed positive relation between AITD and these candidate genes except for HLA.

Abatacept↗
PubMed2005

[Surgical procedures in patients with thyroid autoimmune disease].

Autoimmune thyroid disease is a serious medical problem in which various operative procedures are performed. The objective of the study is to explore the type of applied surgical procedures in autoimmune thyroid disease, advantages and disadvantages of various procedures, and criteria they have to meet. This is retrospective clinical study on 1478 patients, operated for Graves' toxic goiter (117 males and 795 females mean age 37.7) and Hashimoto thyroiditis (27 males and 539 females mean age 50.6) from 1995 to April 2005. Cancer in Graves' disease was found in 61 patients (6.7%), papillary in 60 (occult in 53 or 6.6%) and metastatic in 1, Hashimoto thyroiditis and thyroid cancer was found in 141 patients (24.9%), papillary in 116 or 20.5% (occult in 55 or 9.7%), follicular in 2 (0.3%), Hurthle in 11 (1.9%), medullary in 8 (1.4%), anaplastic in 2 (0.3%) and lymphoma in 3 (0.5%). We performed subtotal bilateral lobectomy in 344 (312 in Graves and 32 in Hashimoto), total lobectomy on one side with subtotal on the oposite in 307 (228 in Graves and 79 in Hashimoto); out of them, in 59 patients, the remnant was left in the region of the upper pole which we called atypic lobectomy. The most common procedure, total or near by total thyroidectomy, performed in 719 (371 in Graves and 349 in Hashimoto). One side lobectomy was performed in 103 patients with Hashimoto thyroiditis. Lymph node dissection was performed in 21 (1 in Graves and 20 in Hashimoto), in all central, in 10 lateral functional and in 6 mediastinal, in 15 patients with cancer and in 6 patients with benign disease. There was no operative mortality. In Graves' disease, there was postoperative bleeding in 4 (0.4%), wound infection in 2 (0.2%) recurrent pulsy in 18 (2%) and permanent hypoparathyroidism in 13 (1.4%). In Hashimoto thyroiditis, there was postoperative bleeding in 2 (0.4%), recurrent nerve pulsy in 11 (1.9%) and permanent hypoparathyroidism in 6 (1.1%). The most common surgical procedure in autoimmune thyroid disease is total thyroidectomy which is followed by low complication rate in specialised centers. Cancer is more frequent in Hashimoto than in Graves' disease.

Adult↗
PubMed1987

Autoimmune thyroid disease: an expanding spectrum.

Autoimmune thyroid disease classically has included Hashimoto's thyroiditis and Graves' disease. Hashimoto's thyroiditis probably also includes focal thyroiditis, fibrous thyroiditis, primary myxedema, and Hashitoxicosis as variants. Graves' disease is associated with ophthalmopathy and dermopathy, and recent evidence suggests that these manifestations are autoimmune phenomena as well. Other associated autoimmune disorders include idiopathic thrombocytopenic purpura and antigen-antibody complex nephritis. Nonthyroid endocrine autoimmune deficiency disorders also have been classified as part of the spectrum of thyroid autoimmune disease. With the recent recognition of the spectrum of autoimmune mechanisms and antibody types and methods to distinguish antibody functions or types, our understanding of postpartum and neonatal thyroid disorders has been advanced considerably. The spectrum of neonatal thyroid disorders in the infants of women with autoimmune disease relates to the levels and types of antithyroid antibodies acquired from the mother. Finally, there is suggestive evidence that nonspecific goiter, including simple adolescent goiter and multinodular goiter as well as some cases of sporadic cretinism, may be part of an even more expanded spectrum of autoimmune thyroid disease.

Autoimmune Diseases↗
PubMed1993

[Basedow-Graves disease development in 2 patients with primary hypothyroidism: exceptional development of the autoimmune thyroid disease].

Autoimmune thyroid disease has multiple manifestations and its presentation may change with time. We report two patients with primary hypothyroidism due to Hashimoto's disease that unexpectedly, developed a hyperthyroidism due to Basedow-Graves disease. This phenomenon may be explained by variations in the types and proportions of anti TSH receptor antibodies, that can stimulate or block thyroid gland function and growth. It is deducted that the hypothyroidism of these patients was not due to a definitive gland destruction, but to the action of function blocking antibodies.

Adult↗
PubMed1993

Lack of disease associated HLA-DQ restriction fragment length polymorphisms in families with autoimmune thyroid disease.

Autoimmune thyroid disease (AITD) is often familial and serological HLA disease associations have been described in many different populations. However, such HLA disease associations are weak and the precise molecular contribution of HLA antigens to thyroid disease susceptibility remains unknown. Much of the data available are cross-sectional and few studies have explored familial inheritance of AITD at the molecular level. We have, therefore, examined the inheritance of AITD in multiplex and multi-generational families using restriction fragment length polymorphism (RFLP) analysis of DNA digested with the restriction enzyme BamH1 and probed with a full length human HLA-DQ beta cDNA probe. Thirty seven subjects in 7 informative families were available for study. Eleven subjects had Graves' disease and 4 were diagnosed as having Hashimoto's thyroiditis. Segregation of polymorphic fragments enabled genotyping of each individual to produce fully informative families. LOD scores were computed, using the LIPED program, for dominant and recessive models of inheritance, for recombination fractions of 0.01 to 0.5 for each sex, and for penetrances of 0.1 to 1.0. The results showed that maximum LOD scores were negative for all of the inheritance models tested. If the primary locus for AITD were in the HLA region, LOD scores would be highly positive. These data, therefore, provide strong evidence against a disease locus for AITD in linkage disequilibrium with the HLA-DQ beta locus.

Adult↗
PubMed2005

[Autoimmune thyroid disease and associated diseases].

Autoimmune thyroid disease (ATD) is a multifactorial, genetic disease. It is the sequelae of the impaired immunoregulation, tolerance and poor recognition of one's own proteins, oligopolysaccharides and polypeptides, due to development of somatic lymphocyte mutations. It is manifested by different clinical and morphological entities, inter-related by etiopathogenetic association, i.e., all of them are caused by disorder of immune system regulation. Chronic autoimmune thyroidism (Thyreoiditis lymphocytaria Hashimoto, HT), as well as immunogenic hyperthyroidism (Morbus Graves Basedow, MGB) are frequently associated with autoimmune diseases of other organs, such as: chronic insufficiency of salivary glands (Sy Sjögren), autoimmune hemolytic anemia, megalocytic pernicious anemia, thrombocytopenia, Rheumatoid arthritis, Diabetes mellitus (more often type 2, but also type 1), Morbus Addison, Coeliakia, and other autoimmune diseases such as systemic diseases of connecting tissue (Lupus erythematosus-SLE, Sclerodermia, Vasculitis superficialis). The incidence of autoimmune diseases has been at increase in all age groups of our population. The prevalence of organ-specific and organ-nonspecific antibodies increases with the age. Antigenicity of thyroid epithelial cell may be triggered by different chemical and biological agents (repeated viral infections), repeated stress, and in individuals with genetic propensity. Unrecognized ATD progressively leads to hypothyroidism with hyperlipidemia, blood vessel changes, osteoporosis, deformities, invalidity which substantially reduces the quality of life of patient and requires medical attention and expensive treatment on what account it is medically and socio-economically significant. Multiple diagnostic procedures contribute to faster recognition of this condition. The goal of the primary health care physician (given that preclinical phase of ATD and other associated diseases have different duration) and other specialists is to recognize ATD and, by early diagnosis and multidisciplinary treatment, to take secondary preventive measures of manifestation of above-mentioned associated autoimmune diseases, and in that way, to avoid the development of comorbidity and complications. It is particularly supported by medical doctrine based on evidence of application of corticosteroids, cytostatics, thyro-suppressive and substitution therapy, antilipemics, bisphosphonates and other drugs, significant for autoimmune diseases.

Autoimmune Diseases↗