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PubMed2001

The role of Fas-mediated apoptosis in thyroid disease.

Recent evidence has emphasized the importance of apoptosis in the maintenance of tissue homeostasis and the pathogenesis of malignant and immune diseases. Autoimmune thyroid diseases such as Hashimoto's thyroiditis and Graves' disease, as well as other autoimmune endocrine diseases, have been associated with dysregulation of apoptotic signaling pathways. In particular, dysfunction of the Fas apoptotic pathway or production of soluble factors including soluble Fas and soluble Fas ligand may be involved in the pathogenesis of these disorders. On the other hand, malignant thyroid cells may avoid Fas-mediated suicide possibly by expression of inhibitors of apoptosis and evade the immune system by inducing apoptosis on infiltrating lymphocytes. The delicate balance between cell proliferation and cell death through the Fas pathway may also play an important role in the control of thyroid cell mass and goitrogenesis. This review analyzes the current evidence on the role of Fas-mediated apoptosis in the pathogenesis of thyroid diseases including Hashimoto's thyroiditis, Graves' disease, thyroid cancer and goiter. However, the exact mechanisms involved in the regulation of apoptosis in thyroid disease remain unclear. Further investigation is needed.

Animals↗
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↗
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↗
PubMed1986

Prescribing in pregnancy. Thyroid disease.

When treating thyroid disease, as with other conditions in pregnancy, one is concerned with the welfare of both mother and developing child. Thyroid disease causes few maternal problems; thyrotoxicosis in fact tends to improve in pregnancy, allowing medical management with lower drug doses than usual. Relapse of thyroid disease may occur postpartum, when transient hypo- and hyperthyroidism are relatively common. In contrast, the fetus and neonate are threatened in a number of ways by drugs given to the mother and by transplacental passage of maternal antibodies capable of inducing thyroid disease. Antithyroid drugs may cause fetal goitre with airway obstruction, and are associated with mild neonatal hypothyroidism. Thyroid antibodies in primary myxoedema and Hashimoto's thyroiditis are occasionally implicated in neonatal hypothyroidism and may even cause thyroid dysgenesis. Neonatal hyperthyroidism has a high morbidity and mortality and may have long-term skeletal effects such as craniosynostosis. Fetal problems may not be apparent at birth but may emerge in the next eight to ten days, especially in hyperthyroidism when the mother has been on treatment. Close monitoring throughout pregnancy and for the first ten days postpartum is required to minimize risks to the fetus and neonate. Most pregnancies associated with thyroid disease will have a successful outcome. If the occasional at-risk fetus is to be identified and treated successfully there should ideally be close cooperation between obstetrician, endocrinologist and paediatrician.

Antithyroid Agents↗
PubMed2005

Questionnaire on management of nodular thyroid disease (Annual Meeting of the Thyroid Section of the German Society of Endocrinology 2003).

Nodular thyroid disease is highly prevalent in iodine deficient areas. In Germany it affects approximately 30 % of the adult population. Differential diagnosis of thyroid nodules is directed at exclusion of rare thyroid malignancy and assessment of the nodules' functional characteristics in order to determine the best treatment approach. In 2003 the annual meeting of the Sektion Schilddrüse, a thyroid specialist group of the German Society of Endocrinology addressed the topic of "management of benign nodular thyroid disease". To assess the current diagnostic and therapeutic approach to nodular thyroid disease by German thyroid experts we designed a questionnaire, which was sent to all members of the Thyroid Section before the meeting and was answered by 70 % of the participants. We here report the results of the questionnaire, which show a considerable national heterogeneity in the management of thyroid nodules as well as diagnostic and treatment preferences for different thyroid specialist subgroups, e.g. endocrinologists and nuclear medicine specialist. This is in agreement with results of previous questionnaires assessing state-of-the-art practise among members of the European and American Thyroid Associations and underlines the definite need for a consensus process and for carefully planned randomized trials to answer the many unresolved questions in diagnosis and therapy of nodular thyroid disease.

Biopsy, Needle↗
PubMed1995

Simple radioimmunological assay of anti-alpha-galactosyl antibody (anti-Gal): application to autoimmune thyroid diseases and thyroid-associated ophthalmopathy.

Two radioimmunological techniques for the measurement of anti-alpha-galactosyl (anti-Gal) antibodies were developed and we demonstrated that this antibody is present in the serum of most untreated patients with Graves' disease, thyroid-associated ophthalmopathy (TAO) and autoimmune thyroiditis. Thyrotropin-binding inhibiting immunoglobulins (TBII) and Thyroid Stimulating Antibodies (TSAb) are frequently found in serum of patients with Graves' disease but not with autoimmune thyroiditis. Although TBII and anti-Gal were found sometimes simultaneously in the same serum samples, we demonstrated that anti-Gal could be present in the absence of TBII and reciprocally.

Animals↗
PubMed1998

Linkage analysis of candidate genes in autoimmune thyroid disease. II. Selected gender-related genes and the X-chromosome. International Consortium for the Genetics of Autoimmune Thyroid Disease.

Hashimoto's thyroiditis (HT) and Graves' disease (GD) are autoimmune thyroid diseases (AITD) in which multiple genetic factors are suspected to play an important role. Until now, only a few minor risk factors for these diseases have been identified. Susceptibility seems to be stronger in women, pointing toward a possible role for genes related to sex steroid action or mechanisms related to genes on the X-chromosome. We have studied a total of 45 multiplex families, each containing at least 2 members affected with either GD (55 patients) or HT (72 patients), and used linkage analysis to target as candidate susceptibility loci genes involved in estrogen activity, such as the estrogen receptor alpha and beta and the aromatase genes. We then screened the entire X-chromosome using a set of polymorphic microsatellite markers spanning the whole chromosome. We found a region of the X-chromosome (Xq21.33-22) giving positive logarithm of odds (LOD) scores and then reanalyzed this area with dense markers in a multipoint analysis. Our results excluded linkage to the estrogen receptor alpha and aromatase genes when either the patients with GD only, those with HT only, or those with any AITD were considered as affected. Linkage to the estrogen receptor beta could not be totally ruled out, partly due to incomplete mapping information for the gene itself at this time. The X-chromosome data revealed consistently positive LOD scores (maximum of 1.88 for marker DXS8020 and GD patients) when either definition of affectedness was considered. Analysis of the family data using a multipoint analysis with eight closely linked markers generated LOD scores suggestive of linkage to GD in a chromosomal area (Xq21.33-22) extending for about 6 cM and encompassing four markers. The maximum LOD score (2.5) occurred at DXS8020. In conclusion, we ruled out a major role for estrogen receptor alpha and the aromatase genes in the genetic predisposition to AITD. Estrogen receptor beta remains a candidate locus. We found a locus on Xq21.33-22 linked to GD that may help to explain the female predisposition to GD. Confirmation of these data in HT may require study of an extended number of families because of possible heterogeneity.

Aromatase↗
PubMed2001

Routine measurement of serum calcitonin is useful for early detection of medullary thyroid carcinoma in patients with nodular thyroid diseases.

BACKGROUND: Medullary thyroid carcinoma (MTC) is characterized by a high concentration of serum calcitonin. Routine measurement of serum calcitonin concentration has been advocated for detection of MTC among patients with nodular thyroid diseases. However, a minimal to moderate increase of serum calcitonin concentration has been frequently observed in diseases other than MTC. Fine-needle aspiration cytology (FNAC) is not a reliable method for detection of MTC. Therefore, we evaluated the usefulness of routine measurement of serum calcitonin concentration in patients with nodular thyroid diseases, and studied the validity of pentagastrin stimulation test and FNAC in these patients. SUBJECTS AND METHODS: We performed routine measurement of serum calcitonin concentrations in 1,448 patients (male, 285, female, 1,163) with nodular thyroid diseases. The average age was 46 years (range, 14-86 years). Initial examination included thyroid examination, thyroid scan or ultrasonography, measurements of serum free triiodothyronine) (T3), free thyroxine (T4), thyrotropin (TSH) levels, and antithyroid autoantibodies. FNAC was performed in all patients who had palpable or visible thyroid nodule by ultrasonography, and pentagastrin stimulation test was performed in 39 patients who consented. Serum calcitonin concentration was measured with a two-site immunoradiometric assay using commercial kits. We also measured the serum calcitonin concentration in 407 healthy subjects without thyroid or nonthyroid diseases. RESULTS: Serum calcitonin concentration was 10 pg/mL or less in 403 normal subjects (99.0 percentile), and 11-13 pg/mL in the remaining 4 subjects. We found that 56 (3.87%) of 1,448 patients with nodular thyroid diseases had serum calcitonin level above 10 pg/mL. Ten patients (0.69%) with histologically confirmed MTC were detected by the routine measurement of serum calcitonin. The prevalence of MTC was 5.2% in 194 patients with thyroid carcinoma. Five of 10 patients with MTC had basal serum calcitonin level above 100 pg/mL. The remaining 5 patients had minimal or moderate elevation of basal serum calcitonin (range, 12-86 pg/mL). Serum calcitonin concentration increased to more than 100 pg/mL by pentagastrin in all patients with MTC (2.4- to 37.7-fold increase). FNAC suggested MTC in only 2 patients (22.2%), and failed to diagnose MTC in 7 patients. FNAC was not performed in 1 patient with MTC, because he had no visible mass by ultrasonography. CONCLUSION: These results suggested that routine measurement of serum calcitonin is useful in the early detection of MTC among patients with nodular thyroid diseases. Pentagastrin stimulation test may also be a reliable way for evaluating thyroid nodular patients with mild or moderate elevation of serum calcitonin concentrations. However, FNAC was not sensitive in detecting MTC. We recommend routine measurement of serum calcitonin concentration in patients with nodular thyroid diseases.

Adolescent↗
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↗
PubMed1981

The clinical features of diabetes with coexisting autoimmune thyroid disease.

A study was made of the clinical features of diabetics with coexisting Graves' disease (n = 117) or primary hypothyroidism (n = 98). Those with Graves' disease developed thyroid dysfunction and diabetes at an earlier age than patients with primary hypothyroidism. There was, however, no difference between the two groups in respect of sex ratio nor proportion of subjects requiring insulin treatment. In contrast to the general diabetic population, 87% of diabetics with thyroid disease were female, 56% required insulin treatment and of patients requiring insulin from diagnosis, the median age at diagnosis of diabetes was 36 years. A strong correlation was observed between age at diagnosis of diabetes and that of hyperthyroidism (r = 0.71, p less than 0.001) or hypothyroidism (r = 0.65, p less than 0.001). With increasing age at diagnosis of diabetes the interval between diagnosis of diabetes and thyroid disease diminished. The mean +/- SEM interval between diagnosis of diabetes and that of thyroid dysfunction was longer in hypothyroid (6.7 +/- 1.2 years) than in hyperthyroid diabetics (-2.4 +/- 1.2 years). Neither insulin-dependent nor non-insulin dependent diabetics with associated thyroid disease exhibited a significant seasonal variation in diagnosis or symptomatic onset of diabetes. It is conceivable that where diabetes accompanies autoimmune thyroid disease in the same patient, both conditions may share a common and coincident pathogenesis which is unrelated to acute environmental influences.

Adolescent↗
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↗
PubMed1991

Thyroid diseases after treatment of Hodgkin's disease.

BACKGROUND AND METHODS: Thyroid disease, especially hypothyroidism, is common in patients with Hodgkin's disease who have been treated with irradiation. We reviewed the records of 1787 patients (740 women and 1047 men) with Hodgkin's disease who were treated with radiation therapy alone (810 patients), radiation and chemotherapy (920 patients), or chemotherapy alone (57 patients) at Stanford University between 1961 and 1989. Among these patients, 1533 were alive at the last follow-up, and 254 had died of causes other than Hodgkin's disease. (Four other patients were excluded from the analysis because they had undergone thyroidectomy before treatment for Hodgkin's disease. The thyroid was irradiated in 1677 patients. Follow-up averaged 9.9 years. RESULTS: A total of 573 patients had clinical or biochemical evidence of thyroid disease. Among the 1677 patients whose thyroid was irradiated, the actuarial risk of thyroid disease 20 years after treatment was 52 percent, and it was 67 percent at 26 years. Hypothyroidism was found in 513 patients. A total of 486 patients received thyroxine therapy for elevated serum thyrotropin concentrations and either low free thyroxine (208 patients) or normal free thyroxine values (278 patients); 27 had transient elevations of the serum thyrotropin level that were not treated. Graves' hyperthyroidism developed in 30 patients (2 of whom had not undergone thyroid irradiation), and ophthalmopathy developed in 17 of these patients. Ophthalmopathy developed in four other patients with Graves' disease during a period of hypothyroidism (n = 3) or euthyroidism (n = 1). The risk of Graves' disease was 7.2 to 20.4 times that for normal subjects. Silent thyroiditis with thyrotoxicosis developed in six patients. Forty-four patients were found to have single or multiple thyroid nodules, 26 of whom underwent thyroidectomy. Six of the 44 had papillary or follicular cancers. Among the patients who did not undergo operation, 12 had small functioning nodules, 4 had cysts, and 2 had multinodular goiters. The actuarial risk of thyroid cancer was 1.7 percent. The risk of thyroid cancer was 15.6 times the expected risk. CONCLUSIONS: High risks of thyroid disease persist more than 25 years after patients have received radiation therapy for Hodgkin's disease, reinforcing the need for continued clinical and biochemical evaluation. Prolonged follow-up confirms an elevated risk of thyroid cancer and Graves' disease as well as hypothyroidism in these patients.

Adolescent↗
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↗
PubMed1990

Tests of thyroid function: update in the diagnosis and management of thyroid disease.

Current thyroid function tests give the clinician powerful tools for the accurate assessment of thyroid status in the majority of patients encountered. There are, however, a small number of clinical situations in which there appear to be inconsistencies in the interrelationship of the thyroid function tests and/or in which they are apparently inappropriate to the clinical status of the patient. In most instances, there is a rational explanation for these observed alterations. The application of this information should allow clinicians to further refine their diagnostic accuracy and thereby enable them to proceed with an appropriate therapeutic or management program.

Adult↗
PubMed2005

Autoimmune thyroid disease (Graves' disease and hashimoto's thyroiditis) in two patients with Crohn's disease: case reports and literature review.

An increased prevalence of the association between autoimmune thyroid diseases and ulcerative colitis has been suggested, however, not with Crohn's disease, as only 7 cases of thyroid disease coexisting with Crohn's disease have been reported. Herein, we describe 2 patients with Crohn's disease complicated with Graves' disease or autoimmune thyroiditis, and also review other cases with those complications. Some immunological processes are suggested to be implicated in the pathogenesis of this association, however, the exact mechanism remains unclear.

Adult↗