Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THYROID DISEASES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 865 records · Page 48Linked to original sources
PubMed2004

Presence of systemic autoimmune disorders in patients with autoimmune thyroid diseases.

OBJECTIVE: To evaluate the prevalence of antinuclear antibodies (ANA) in patients with autoimmune thyroid diseases (ATD) and the presence of systemic autoimmune disorders among ANA positive patients with ATD. METHODS: 168 consecutive patients with ATD with positive antithyroid antibodies and 75 healthy subjects were tested for the presence of ANA. ANA positive patients were further evaluated by complete history, physical examination, blood and urine tests, and immunological studies. Patients with subjective xerophthalmia and xerostomia were examined by objective tests. RESULTS: 58/168 (35%) patients with ATD were ANA positive compared with 7/75 (9%) healthy controls (p = 0.001). Of 58 ANA positive patients, 6 (10%) had anti-Ro antibodies, 1 had anti-Ro and anti-La antibodies, 7 (12%) had anti-dsDNA antibodies, and 7 (12%) had medium levels of IgG and/or IgM anticardiolipin antibodies (aCL). No healthy subjects had positive anti-dsDNA, antibodies against the extractable nuclear antigens, or aCL. 5/58 (9%) patients fulfilled the criteria for Sjögren's syndrome (SS). Two patients had features related to systemic lupus erythematosus. No healthy subjects had clinical or laboratory characteristics of systemic autoimmune disorders. CONCLUSION: ANA are detected in 1/3 of patients with ATD. Anti-dsDNA, anti-Ro, and aCL can also be found in ANA positive patients with ATD. SS occurs in about 1/10 of ANA positive patients with ATD.

Adult↗
PubMed1998

Induction of oral tolerance in human autoimmune thyroid disease.

Our laboratory has reported suppression of experimental autoimmune thyroiditis in mice by oral feeding with antigen. Based on these data, we considered it possible that oral feeding of animal thyroglobulin (TG) might induce tolerance to antigen in human autoimmune thyroid disease (AITD). Thirteen patients receiving thyroid hormone replacement with synthetic thyroxine (T4) (five patients with Graves' disease, treated with radioiodine 4 to 11 years ago and eight patients with Hashimoto's thyroiditis) were randomly assigned to a test group (switched to replacement with desiccated thyroid from porcine thyroids) and a control group (maintained on synthetic T4). Humoral and cellular immunologic parameters were evaluated in addition to clinical parameters before and every 3 months after the onset of study for a year. At the onset of study, there was no difference in clinical parameters, or humoral and cellular immunity to thyroid autoantigens, except a finding that one thyroid peroxidase (TPO) peptide (100 approximately 119) appeared to stimulate peripheral blood mononuclear cells (PBMC) during in vitro microproliferation assay more in the test group than control group (p = 0.051 by t test). Additionally, almost all of TPO and thyrotropin receptor extracellular domain (TSHR) peptides were slightly more stimulatory to PBMC from the test group than the control group, although this was not statistically significant. After treatment, all variables were analyzed at each time point between groups (t test), and also were analyzed over time in each group (analysis of variance, ANOVA). Among the clinical parameters, thyrotropin (TSH) levels were unchanged and equal. Total serum T4 levels (p < 0.05 at 6 and 12 months after treatment) and free thyroxine indices (FT4I) (p < 0.05 at all time points after treatment) were lower in the test group than the control group. This is an expected result of treatment with desiccated thyroid. We found no change over time nor any difference between groups at time points for titers of antibodies to thyroid autoantigens, ie, human TG, human TPO, and recombinant human TSHR from Escherichia coli. However, cellular immunity, measured by in vitro microproliferation of PBMC to peptides of TPO or TSHR, showed significant differences between groups. At 12 months, stimulatory indices (SI) of PBMC to six peptides, containing the indicated amino acids (764 approximately 95, 100 approximately 119, 110 approximately 129, 261 approximately 275, 441 approximately 448, 708 approximately 727) of 10 TPO peptides, and one peptide (145 approximately 163) of 14 TSHR peptides were lower in the test group than control group (p < 0.05). SI of PBMC to phytohemagglutinin, purified protein derivative from mycobacteria, and tetanus toxoid were not different between groups nor changed over time in any group. In conclusion, treating patients with AITD with an antigen related to the autoantigen TG did not produce changes in humoral immunity parameters, while cellular immunity to certain peptides were apparently suppressed. While the results are both surprising and intriguing, we need more evidence to justify the use of autoantigen as a form of immunospecific therapy in patients with AITD.

Administration, Oral↗
PubMed2006

Decreased nerve growth factor levels in hyperthyroid Graves' ophthalmopathy highlighting the role of neuroprotective factor in autoimmune thyroid diseases.

Nerve growth factor (NGF), which is a neurotrophic factor, is involved in autoimmune and inflammatory processes. Serum NGF levels were investigated in 131 patients with autoimmune (95 with Graves' disease, of whom 57 had ophthalmopathy, 19 with Hashimoto's thyroiditis) and nonimmune thyroid diseases (17 with toxic nodular goitre), and 20 controls. NGF levels were measured via enzyme-linked immunosorbent assay. Twenty-nine positive cases for NGF were detected: 21 cases in Graves' disease, 7 cases in Hashimoto's thyroiditis, no case in toxic nodular goitre and one case in controls. NGF levels were higher in patients with Graves' disease and particularly with Hashimoto's thyroiditis compared with controls (1786.47+/-34.79 pg/ml and 1996.27+/-77.71pg/ml vs 1579.16+/-57.45pg/ml, P<0.049 and P<0.0001, respectively). Increased NGF levels associated with Graves' hyperthyroidism and correlated with FT(3) (P<0.01). Patients with the presence of antibodies against TSH receptor showed higher NGF levels than those with no antibodies (1938.61+/-56.44pg/ml vs 1712.12+/-54.22pg/ml, P<0.009). Decreased NGF levels were demonstrated in hyperthyroid Graves' ophthalmopathy compared with those without eye symptoms (1746.65+/-51.98pg/ml vs 1910.47+/-55.62pg/ml, P<0.036). NGF may be involved in the pathomechanism of autoimmune thyroid diseases. Decreased NGF levels in hyperthyroid Graves' ophthalmopathy highlight the importance of NGF in the neuroprotection of orbital tissues.

Adult↗
PubMed1994

Thyrotropin receptor and leukocyte adhesion molecules in autoimmune thyroid disease: a study of their gene expression by northern blot analysis and in situ hybridization.

In order to characterize the role of leukocyte-activating antigens and other immunological parameters in autoimmune thyroid disease, mRNA levels of intercellular adhesion molecule 1 (ICAM-1), endothelial leukocyte adhesion molecule 1 (ELAM-1, E-selectin), invariant chain (Ii) and the thymic hormone thymosin beta (T beta 4) were investigated in 18 human thyroid glands, including eight Graves' thyroids, two Hashimoto's thyroids, two endemic goiters and six healthy controls. Northern blot analysis showed that in autoimmune thyroid disease, expression of ICAM-1 and T beta 4 was correlated to transcript levels of Ii, whereas in the healthy controls, expression of T beta 4, ICAM-1 and ELAM-1 was low or nearly absent. ELAM-1 and TSH receptor (TSH-R) expression, the latter serving as a thyroid specific marker, was increased in some diseased gland but showed no relation to the immunological parameters mentioned above. Localization of the specific mRNAs by in situ hybridization demonstrated a cell-specific expression of TSH-R (thyrocytes), ELAM-1 (vascular endothelial cells) and T beta 4 (cells of hematopoietic origin). In contrast, transcripts of Ii and ICAM-1 were found in thyrocytes, leukocytes and endothelial cells. Our results implicate a coordinate expression of ICAM-1, T beta 4 and Ii in autoimmune thyroid disease, yielding distinct cellular expression patterns. Differential expression of ICAM-1, Ii and the TSH-R in thyroid epithelial cells indicates active regulatory events within the thyrocyte.

Autoimmune Diseases↗
PubMed2005

Non-cancer thyroid diseases among children in the Kaluga and Bryansk regions of the Russian Federation exposed to radiation following the Chernobyl accident.

This paper presents results of estimated radiation risks of non-cancer thyroid diseases in the people from Kaluga and Bryansk regions of the Russian Federation exposed in their childhood to radioiodine as a result of the Chernobyl accident. This work was carried out under the Joint Medical Research Project on non-cancer thyroid diseases conducted by Sasakawa Memorial Health Foundation and the Medical Radiological Research Center of the Russian Academy of Medical Sciences. The subjects were 2,457 people who underwent health examinations from 1997 to the end of 1999 who had individual radiometric thyroid data obtained between May and June 1986 and were aged 10 y or less at the time of exposure. The thyroid absorbed doses from incorporated 131I were estimated on the basis of measurements of exposure dose rate in the vicinity of the subject's thyroid and liver. A compartment model accounting for 131I metabolism in humans and cows was used. The estimated dose varied from 0 to 6 Gy, and its distribution was approximately lognormal with a mean of 0.132 Gy and standard deviation of 0.45 Gy. The prevalence of diffuse goiter in males showed a significant dose-response (p = 0.03) with an estimated odds ratio 1.36 at 1 Gy.

Chernobyl Nuclear Accident↗
PubMed1994

The potential immunological role of the thyroid cell in autoimmune thyroid disease.

Over the last decade it has become evident that thyroid follicular cells express a number of immunologically active molecules in autoimmune thyroid disease that may endow them with the capacity to interact with cells of the classical immune system. Expression of major histocompatibility complex class II molecules is induced by gamma-interferon, but there is no evidence yet that thyroid follicular cells can concurrently express the costimulatory signals necessary for class II expression to result in T cell stimulation: in this situation, class II expression may have a protective role, inducing T cell anergy. Thyroid follicular cells also express a variety of cell surface proteins (in particular CD59) that may protect the cells from complement attack. On the other hand, the expression of adhesion molecules and cytokines by thyrocytes would seem to be harmful, as these are likely to exacerbate autoimmune injury. Further study of the immunological role of thyroid follicular cells will shed new light on the pathogenesis of Graves' disease and autoimmune hypothyroidism, and may lead to novel therapeutic approaches to these disorders.

Animals↗
PubMed1996

Efficacy of fine needle aspiration cytology in the management of thyroid diseases.

To find out the values of fine needle aspiration cytology (FNAC) in the management of thyroid diseases, 1123 cases have been analysed as regards clinical details, thyroid hormone levels and thyroid scans. Cytologically, 96.35% were benign, 0.98% follicular neoplasm, 1.24% malignant, 0.80% extrathyroidal and 0.63% inconclusive. One hundred twenty eight cases were selected for surgery. Correlation of cytology with histology revealed nil false positive. Efficacy as regards narrow definition was 92.3% sensitive, 100% specific with positive and negative predictive values of 92.3% and 98.9% respectively.

Adolescent↗
PubMed1994

Thyroid diseases in cohort studies of A-bomb survivors.

A fixed population of about 120,000 subjects was selected from those A-bomb survivors and unexposed controls for the purpose of follow-up studies on their late health effects. One hundred twelve cases of thyroid cancer were found in the study period between 1958 to 1979. The relative risk increased with thyroid dose: the excess relative risk per Gray was 1.1. The prevalence of thyroid diseases was evaluated in 2,587 subjects in Nagasaki: one or more diagnoses for thyroid diseases were made in 447.

Cohort Studies↗
PubMed1986

Immunohistochemical localization of thyroglobulin (Tg), thyroxine (T4), and triiodothyronine (T3) in thyroid diseases.

Thyroglobulin (Tg), thyroxine (T4), and triiodothyronine (T3) were detected by the immunoperoxidase method in 51 cases of the following thyroid diseases: euthyroid goiter, Basedow's disease, Hashimoto's thyroiditis, folliculo-papillary carcinoma, follicular carcinoma, anaplastic carcinoma, and medullary carcinoma. Tg, T3, and T4 are present in most of the examined disorders, excepting anaplastic and medullary carcinoma. The pattern of Tg, T3, and T4 distribution between the cases of a benign lesion is rather similar; Tg and T4 are localized both in the epithelium and the colloid; T3 is disposed especially in the follicular cells. The pattern of Tg, T3, and T4 distribution in differentiated carcinomas is more heterogeneous. In half of the cases, T3 distribution resembled that of Tg. In 2 cases, a predominance of T4 was noted. In the other specimens, T3 and T4 showed a weak or a negative immunostaining.

Adenocarcinoma↗
PubMed1981

Normal immunoregulation of in vitro antibody secretion in autoimmune thyroid disease.

Defective suppressor cell function may be a causative factor in autoimmune disease in animals and man. In autoimmune thyroid disease, decreased suppressor cell activity could, under appropriate conditions, account for excess production of thyroid autoantibodies. We evaluated suppressor cell function in patients with Graves' disease and Hashimoto's thyroiditis and in normal controls. The method used is based on the principle that immunoglobulin synthesis by pokeweed mitogen (PWM)-stimulated lymphocytes is inhibited by Concanavalin A (Con A) stimulation of suppressor T cells. We studied suppressor cell control of polyclonal immunoglobulin G (IgG) and the thyroid-specific autoantibody, antimicrosomal antibody. PWM-stimulated IgG secretion (mean +/- SD) by lymphocytes from patients with Graves' disease (2797 +/- 718 ng/ml) and Hashimoto's thyroiditis (2201 +/- 423 ng/ml) did not differ from normal subjects (2431 +/- 485 ng/ml). The addition of Con A to PWM-stimulated lymphocytes suppressed IgG production in all three groups: Graves', 475 +/- 137 ng/ml; Hashimoto's, 507 +/- 74 ng/ml; and normal subjects, 460 +/- 156 ng/ml. The degree of suppression by the disease groups did not differ from the normal controls. Antimicrosomal antibody was detected in the concentrated, PWM-stimulated culture media of two of four Hashimoto's lymphocytes, three of five Graves' lymphocytes, and none of nine normal controls. Con A induced marked suppression of this organ-specific antibody in all cases. We conclude that Con A-stimulated lymphocytes from patients with Hashimoto's thyroiditis and Graves' disease can suppress antimicrosomal antibody and polyclonal IgG synthesis. These findings do not support the postulate of a generalized defect of suppressor cell function in these thyroid disorders.

Adult↗
PubMed1994

Expression and function of multiple regulators of complement activation in autoimmune thyroid disease.

Membrane attack complexes of complement occur around thyroid follicles in Graves' disease and Hashimoto's thyroiditis. The lytic potential of such complexes is controlled by membrane-bound and fluid phase regulators and we have investigated the role of these in autoimmune thyroid disease. By immunohistochemical staining, clusterin and S-protein were found in all nine thyroid specimens from patients with Graves' disease and S-protein was found in one of two Hashimoto glands. CD46, CD55 and CD59 were found on thyroid cells in all specimens. CD46 and CD55 expression occurred on thyroid cells cultured in vitro and was increased significantly by culture with interleukin-1 (IL-1) and interferon-gamma (IFN-gamma), which are known to be released by the lymphocytic infiltrate in these conditions. Blocking CD55 had a weak and inconsistent effect on complement-mediated thyroid cell killing in vitro but, in four of five experiments, blocking CD46 enhanced killing. However, the effect of blocking CD59 was greater in all cases than blocking CD46 or CD55. Expression of these fluid phase and membrane-bound proteins may be important in determining the severity of thyroid damage produced by complement fixation in Graves' disease and Hashimoto's thyroiditis.

Antigens, CD↗
PubMed2002

Genetic dissection of familial autoimmune thyroid diseases using whole genome screening.

The autoimmune thyroid diseases (AITDs) are multifactorial disease which are caused by genetic susceptibility and environmental triggers. Various epidemiological and genetic techniques can be employed to study the genetic contribution to disease development. Most epidemiologic data support an important genetic contribution to the development of AITD. The genetic susceptibility to AITD involves several genes with varying effects. Some AITD susceptibility genes are most likely immune modifying genes which increase the susceptibility to autoimmunity in general (e.g. HLA, CTLA-4) while others may be thyroid-specific (e.g. thyroglobulin). These genes probably act in concert to increase the autoimmune reactions in susceptible individuals and direct them towards the thyroid.

Abatacept↗
PubMed1981

Thyroid disease in the elderly in the community.

In a clinical and biochemical study of 559 subjects over the age of 65 years living in the community, in residential homes and in hospital, seven patients with thyroid disease were found. This gave a prevalence rate of 0.94% of hypothyroidism and 0.47% of hyperthyroidism in people aged 80 years or more. Five of these seven subjects were suspected clinically of having thyroid disease. Therefore routine biochemical screening does not appear to be justified. Within each of the age strata there was no significant change in serum thyroxine with age. Women had significantly higher serum thyroxine levels than men, in the group aged 75 years or more.

Aged↗
PubMed2002

HLA study on two Mexican Mestizo families with autoimmune thyroid disease.

Several studies have been done regarding the genetic susceptibility to autoimmune thyroid disease, particularly those related to the role of Major Histocompatibility Complex (MHC) genes in the etiology of the disease. In the present study, we report class I and class II MHC haplotypes in nine individuals affected by Hashimoto thyroiditis and Graves' disease who belong to two distinct Mexican families. In one of the families, Hashimoto thyroiditis was associated with the Human Leukocyte Antigen (HLA) HLA-DR3 allele whereas in the other family the disease was associated with homozygosity for the HLA-DR4 (DRB1*0407), HLA-DQ3 (DQB1*0302) haplotype. On the other hand, Graves' disease was found to be associated in one of the families with HLA-DR2 (DRB1*1501) and in the other with homozygosity for the HLA-DR7 (DRB*0701) and HLA-DQ2 (DQB1*0201) haplotype. These results confirm that in Mexicans as in other ethnic groups, genes located within the MHC region are related to the genetic susceptibility to develop autoimmune thyroid disease.

Family↗
PubMed1989

[An ultrasonic study in the differential diagnosis of thyroid diseases].

The correlation of clinical, echo and morphological findings demonstrated ultrasound potentialities in the differential diagnosis of thyroid cancer. Ultrasound permitted the detection of nodes up to 3 cm in diameter. False-negative results were obtained in 6.5% of cases, there were no true false positive results. Adenomas are often characterized by mixed echogenicity of a node and hypoechogenic lining around it. Chronic nonspecific thyroid diseases are characterized by inhomogeneous echogenicity of the organ. Thyroid cancer is characterized by hypoechogenicity of a node with its inhomogeneous structure and irregular contours as if consisting of several nodules. The probability of malignancy grows with an increase in the number of these features combining in a particular patient.

Adenocarcinoma↗
PubMed1994

Epidemiology of thyroid diseases of dogs and cats.

Data regarding the epidemiology of the thyroid diseases in companion animals are sparse. Published studies providing information regarding the epidemiology of canine hypothyroidism and thyroid neoplasia and feline hyperthyroidism are summarized. Future studies should seek to refine diagnoses, include control animals for comparison, and target the elucidation of causes that may lead to preventative recommendations.

Adenoma↗
PubMed1992

[Role of immune complexes in thyroid diseases].

To elucidate the immune complex (thyroglobulin-antibody, Tg-Ab) role in thyroid hormone formation, in vitro iodination of Tg--AB immune complex, bovine intact Tg and that of the patient with euthyroid goiter and partially purified AB to Tg were studied. We compared the amount of iodamine acids (MIT, DIT, T4/mole of Tg) forming during iodination in immune complex with other samples. The results suggest that Tg being in complex with antibodies (up to 30-40 mole of antibodies/mole of Tg) is iodinated forming the enough amount of MIT, decreased amount of DIT and T4. A MIT fraction increase is connected with additional iodination of complex antibodies. We suggest that such processes may take place in the patient body and be involved in pathogenesis of thyroid disease.

Animals↗
PubMed2001

Identification of antigenic domains on the human sodium-iodide symporter which are recognized by autoantibodies from patients with autoimmune thyroid disease.

The sodium-iodide symporter (NIS) is a novel autoantigen in autoimmune thyroid disease. In the present study we have characterized the antigenic domains on the human symporter which are recognized by autoantibodies from patients with either Graves' disease (GD) or autoimmune hypothyroidism (AH). Deletion derivatives of complementary DNA (cDNA) encoding the Na(+)/I(-) symporter were constructed using polymerase chain reaction (PCR) amplification. These deletion constructs were translated in vitro with the concomitant incorporation of [(35)S]methionine into the protein products. The reactivity of seven GD and six AH sera, which were known to contain symporter-binding antibodies, to each of the radiolabelled modified symporters was then determined in immunoprecipitation experiments. Analyses of the results obtained in the radiobinding assays suggest the existence of multiple antibody binding sites on human NIS (hNIS), including regions between amino acids (aa) 1--134, 191--286, 290--411, 411--520 and 520--588. Computer prediction of the potential B cell epitopes on the symporter revealed that, apart from aa 134--191, all the epitope domains identified overlapped, at least in part, with areas predicted to be highly antigenic. Interestingly, the antigenic domains represented by aa 191--286, 290--411 and 411--520 include regions of the polypeptide which form putative extracellular domains in the secondary structure model of the rat symporter. No correlation between the recognition of specific epitopes on the human symporter and the type of autoimmune thyroid disease was demonstrated.

Adult↗