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 469 records · Page 26Linked to original sources

[Ghrelin expression in the tissues of different thyroid diseases].

OBJECTIVE: To investigate whether ghrelin, a novel endogenous ligand of growth hormone secretagogue receptor (GHS-R), was expressed in the thyroid tissues of different thyroid diseases, and its implication. METHODS: The paraffin-embedded specimens of thyroid tissues from 2000 to 2004 were obtained from 57 patients with different thyroid diseases, including 5 subacute thyroiditis, 8 Hashimoto's thyroiditis, 7 hyperthyroidism (Graves disease), 8 nodular goiter, 5 thyroid adenoma, 3 thyroid lymphoma, 8 papillary carcinoma, 3 follicular carcinoma, 5 medullary carcinoma and 5 undifferentiated carcinoma cases. The specimens of normal peri-adenoma thyroid tissues served as controls. Immunohistochemical staining was used to detect ghrelin expression. RESULTS: (1) ghrelin expression was undetectable in the thyroid tissues of normal control, subacute thyroiditis, Hashimoto's thyroiditis and Graves disease. (2) ghrelin expression was also undetected in the tissues of nodular goiter, thyroid adenoma and thyroid lymphoma. (3) ghrelin-positive staining was found in the tumor cells of different types of thyroid carcinoma. Five cases were positive within 8 cases in papillary carcinoma, 2 cases were positive within 3 cases in follicular carcinoma, 3 cases were positive within 5 cases in medullary carcinoma, 3 cases were positive within 5 cases in undifferentiated carcinoma. CONCLUSION: Ghrelin is expressed in malignant epithelial thyroid neoplasms, but not in autoimmune or inflammatory thyroid diseases and benign nodular thyroid diseases. The results indicate that ghrelin expression may play an important role in the occurrence and development of thyroid carcinoma.

Adult↗

Human thyroid phenol sulfotransferase enzymes 1A1 and 1A3: activities in normal and diseased thyroid glands, and inhibition by thyroid hormones and phytoestrogens.

Sulfation by sulfotransferase enzymes (SULTs) is an important pathway for the metabolism of thyroid hormones and phytoestrogens. Intrathyroidal SULTs may contribute to the processing of thyroid hormones for the reutilization of iodide. SULT1A1 and SULT1A3 activities were identified in normal and diseased human thyroid glands. Biochemical properties that included apparent K(m) values, thermal stabilities, and responses to inhibitors were characterized in a normal human thyroid high speed supernatant pool. Apparent K(m) values for SULT1A1 and SULT1A3 activities with the model substrates p-nitrophenol and dopamine were 0.58 +/- 0.04 and 11.3 +/- 1.3 microm, respectively. Activities of SULT1A1 and SULT1A3 determined in individual normal thyroid (n = 35), nodular goiter (n = 26), and autoimmune thyroid disease (n = 25) glands were 0.34 +/- 0.06, 0.52 +/- 0.09, and 0.82 +/- 0.19 U/mg protein for SULT1A1, respectively, and 0.22 +/- 0.04, 0.21 +/- 0.04, and 0.48 +/- 0.11 U/mg protein for SULT1A3, respectively. Both SULT activities in autoimmune thyroid disease glands were significantly higher than those in normal thyroids. Only 3,3'-diiodothyronine (3,3'-T(2)) and the phytoestrogen daidzein served as substrates for the normal thyroid SULT activities, yet each thyroid hormone and phytoestrogen tested were found to inhibit thyroid SULT1A1 and SULT1A3 activities. The preference of thyroid gland SULT activities for 3,3'-T(2) suggests that sulfation may enhance degradation of intrathyroidal 3,3'-T(2) for iodide reutilization. Inhibition of these SULT activities by the exogenous phytoestrogens daidzein and genistein, with a potential decrease in iodide reutilization, presents another mechanism through which these compounds may adversely affect human thyroid function.

Arylsulfotransferase↗

Co-occurrence of autoimmune thyroid disease in a multiple sclerosis cohort.

BACKGROUND: Multiple sclerosis (MS), Hashimoto's disease and Graves' disease are autoimmune diseases that may share similar pathogenic mechanisms. The co-occurrence rates and demographic characteristics of Graves' disease and Hashimoto's disease (HT) in our MS population are compared with the general population. METHODS: The prevalence of thyroid disease in our MS patients was determined by chart review and survey. Previous diagnosis of thyroid disease, age at diagnosis, treatment used, and about the use of disease modifying medications used to treat their MS were asked. Chart reviews were used to estimate the population prevalence of Graves' disease and Hashimoto's disease and to estimate the demographics of patients with thyroid disease. RESULTS: A significant co-occurrence of Graves' disease with MS (p = 0.002), and a non-significant co-occurrence of Hashimoto's disease were noted (p = 0.097). No difference in the age of onset or gender of thyroid disease in MS patients compared to the general population was found. CONCLUSION: There is a significant co-occurrence in patients with MS and Graves' disease, and a trend to co-occurrence in patients with MS and Hashimoto's disease. There are no differences in the demographics of patients with thyroid disease in our MS patients compared to the general population.

Journal Article↗

[High prevalence of subclinical thyroidal disease among individuals attended in health control].

BACKGROUND: There is no information about the prevalence of thyroidal diseases in the general Chilean population. AIM: To assess the prevalence of thyroidal diseases in individuals attended in occupational health examinations. SUBJECTS AND METHODS: Four hundred seventy two individuals were examined between 1998 and 1999. In all, serum levels of thyroid hormones, TSH and anti thyroidal antibodies (anti microsomal, anti thyroid peroxidase and anti thyroglobulin) were measured. RESULTS: Forty four subjects were excluded from the study due to an incomplete medical record and 18 due to a personal history of thyroidal disease. Abnormal serum levels of thyroid hormones or TSH were detected in 28 subjects (6.8%). Four (1%) had hypothyroidism, 23 a subclinical hypothyroidism (5.6%) and one (0.2%) had hyperthyroidism. In 87 subjects (21.2%) at least one of the antibodies was positive. Positive anti thyroid antibodies were found in 14 of 28 subjects (50%) with abnormal thyroid hormone levels, compared with 73 of 382 subjects (19.1%) with normal thyroid hormone levels. Thyroid dysfunction was twice as frequent in women than in men. CONCLUSIONS: In this sample, a 6.8% prevalence of abnormal thyroid function tests was detected.

Adolescent↗

Screening for thyroid disease of 15-17-year-old schoolchildren in an area with normal iodine intake.

OBJECTIVE: The prevalence of thyroid disease in Swedish schoolchildren is today insufficiently known. The aim of the study was therefore to determine the prevalence of abnormal thyroid function and thyroid autoimmunity in teen-age schoolchildren and to compare the findings with a healthy control group of 60-65-year-old inhabitants from the same community. SETTING: A semirural community of approximately 15,000 inhabitants. DESIGN: Cross-sectional study. MAIN OUTCOME MEASURES: Thyroid volume and serum concentrations of serum thyrotropin (TSH), total and free thyroxine (T4), total and free 3,5,3'-triiodothyronine (T3), and antithyroperoxidase antibodies (TPOAb). RESULTS: Four schoolchildren (7%, 59 screened) had elevated TPOAb concentration, three of the subjects being girls (8%). One girl with a goitre was overtly hypothyroid and one girl showed borderline-high serum TSH concentration suggesting subclinical autoimmune thyroid disease. One euthyroid boy had a goitre and high concentration of TPOAb. The serum free T3 concentration was significantly higher in 15-17-year-old than 60-65-year-old (7.4 vs. 6.4 pmol L(-1), P < 0.001). The concentrations of other thyroid hormones and of TSH in 15-17-year-old did not differ from those of the 60-65-year-old. CONCLUSIONS: We found three cases of thyroid disease in need of immediate attention or later follow-up. The prevalence of autoimmune thyroid disease was high as indicated from TPOAb measurements. Thyroid tests including TPOAb measurement should be performed on wide indications when teenagers seek medical advice. The reference intervals for teen-age children for commonly used first line tests (TSH and free T4) do not differ from those for adults.

Adolescent↗

Thyroglobulin messenger ribonucleic acid levels in the peripheral blood of children with benign and malignant thyroid disease.

Reverse transcriptase-PCR has identified thyroglobulin mRNA (Tg mRNA) in peripheral blood of normal adults and adults with thyroid cancer. However, no children were studied. The primary objective of this study was to determine whether whole blood Tg mRNA levels differ between benign and malignant thyroid disease in children. The secondary goals were to determine whether whole blood Tg mRNA levels vary with age or pubertal development among children with thyroid disease. Whole blood Tg mRNA levels were determined in 38 children (29 girls, nine boys; median age, 14.5 y; range, 4.8-20.4 y) with benign and malignant thyroid disease and correlated with diagnosis, age, pubertal status, thyroid size, and serum levels of free thyroxine, TSH, and Tg protein. Tg mRNA levels ranged from 3.3 to 104 pg Eq/microg total thyroid RNA (mean, 28 +/- 20.2 pg Eq/microg total thyroid RNA) and were similar in benign and malignant disorders (p = 0.67). However, in children with previously treated papillary thyroid cancer, Tg mRNA levels directly correlated with total body (131)I uptake (p = 0.026) and serum Tg protein (p = 0.037). There was no difference between boys and girls, and no change with pubertal maturation. In children with benign thyroid disease, Tg mRNA levels correlated with serum TSH (p = 0.031), but not with diagnosis, age, Tanner stage, or thyroid size. We conclude that Tg mRNA levels are similar in children with benign and malignant thyroid disease and unchanged by age or pubertal status, but correlated with tumor burden in previously treated papillary thyroid cancer.

Adolescent↗

Near-total thyroidectomy could be the best treatment for thyroid disease in endemic regions.

HYPOTHESIS: Near-total thyroidectomy, on the basis of its low morbidity rate, is an appropriate treatment option in the surgical management of various thyroid diseases in an endemic region in Turkey. DESIGN: Single-institution study of patients with various thyroid diseases treated by means of near-total thyroidectomy within 2 years in an endemic region, with comparison of the results vs the complication rates of bilateral subtotal and total thyroidectomy reported in the literature. SETTING: Tertiary academic referral center. PATIENTS: One hundred fifty-two patients who underwent near-total thyroidectomy for various thyroid diseases. MAIN OUTCOME MEASURES: Surgical treatments of various benign thyroid diseases were compared according to the complication rates and the achievable benefits of the procedures. RESULTS: In our clinic, near-total thyroidectomy was the principal surgical procedure performed for benign thyroid disease. The temporary recurrent laryngeal nerve palsy rate with respect to the nerves at risk was 3.3% (10 of 304 nerves), whereas temporary hypoparathyroidism was 7.2% (11 of 152 patients). Neither permanent recurrent laryngeal nerve palsy nor permanent hypoparathyroidism occurred. In 1 patient, wound hematoma developed and required re-exploration. Seroma in another patient needed no medical or surgical intervention. Neither wound infection nor mortality were noted. CONCLUSIONS: Near-total thyroidectomy achieves a lower complication rate of hypoparathyroidism and a similar complication rate of recurrent laryngeal nerve palsy and recurrence when compared with the rates reported in the literature for total thyroidectomy. It is an effective and safe surgical treatment option for various benign thyroid diseases.

Adult↗

[The importance of quantitative grey-scale analysis of the sonogram in "diffuse" thyroid diseases].

A sonographic grey scale (gs) analysis of the thyroid gland was retrospectively (1985-1986) performed in 248 patients with normal sized thyroid glands or "diffuse" thyroid diseases. During the examination the physical parameters for gain, far and near gain were constant. The normal value (means +/- 2 s) in 95 patients with normal sized and euthyroid thyroid glands was lower in females (gs: 14 +/- 4) than in males (gs: 16 +/- 6), children had obviously lower patterns (gs: 7.1), adolescents had low normal patterns (gs: 11). The echogenicity increased with increasing thyroid volumes. In patients with autoimmune thyroid diseases an obvious low echogenicity could be demonstrated (Hashimoto's thyroiditis, gs-SEM: 8.3 +/- 1.5; Grave's disease, gs-SEM: 6.7 +/- 1.2) (SEM = standard error of the mean). Euthyroid patients with microsomal antibody titers showed low normal grey scale patterns (gs: 10.9 +/- 3). In patients after subtotal thyroidectomy the grey scale pattern decreased with decreasing volume of the residual thyroid gland. The grey scale pattern increased years after surgery. The subjective grading of the grey scale pattern was different from the quantitatively measured pattern in 18% of the patients with glands of normal size.

Adolescent↗

Antibodies to human immunodeficiency virus (HIV-1) in autoimmune diseases: primary Sjögren's syndrome, systemic lupus erythematosus, rheumatoid arthritis and autoimmune thyroid diseases.

The aetiology of autoimmune diseases remains unknown. The relationship between virus, and more recently retrovirus, has been suggested with this group of diseases. Immunoblotting is a useful method for determining the presence of proteins coded by different retrovirus genes. Since the prevalence of these types of proteins in patients with primary Sjögren's syndrome (SS), systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and autoimmune thyroid diseases has not been fully established, the aim of this work was to determine the prevalence of antibodies to immunodeficiency human virus type 1 (HIV-1) proteins in these diseases and their possible relationship with the presence of anti-nuclear, anti-DNA, anti-SSA (Ro) and anti-SSB (La) autoantibodies. Antibodies to human immunodeficiency virus (HIV-1) were studied in a group of 341 patients with autoimmune diseases (77 SS, 98 SLE, 75 RA, 91 autoimmune thyroid diseases) and 126 blood donors as a control group. A Western blot was used to detect antibodies to HIV-1, and a double polymerase chain reaction (PCR) using nested primers in the gag and pol gene of HIV-1. Antinuclear antibodies, anti-DNA, anti-SSA (Ro) and anti-SSB (La) were determined by enzyme-linked immunosorbent assays. At least one band was shown on immunoblotting in 26% of patients with autoimmune diseases and 35% of controls. The presence of antibodies to p55 or p68 proteins in patients with SS or SLE proved to be the only statistically significant difference between the other autoimmune diseases studied and the control group. These antibodies were not associated with autoantibodies ANA, DNA, SSA (Ro) or SSB (La).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Effect of iodine intake on thyroid diseases in China.

BACKGROUND: Iodine is an essential component of thyroid hormones; either low or high intake may lead to thyroid disease. We observed an increase in the prevalence of overt hypothyroidism, subclinical hypothyroidism, and autoimmune thyroiditis with increasing iodine intake in China in cohorts from three regions with different levels of iodine intake: mildly deficient (median urinary iodine excretion, 84 microg per liter), more than adequate (median, 243 microg per liter), and excessive (median, 651 microg per liter). Participants enrolled in a baseline study in 1999, and during the five-year follow-up through 2004, we examined the effect of regional differences in iodine intake on the incidence of thyroid disease. METHODS: Of the 3761 unselected subjects who were enrolled at baseline, 3018 (80.2 percent) participated in this follow-up study. Levels of thyroid hormones and thyroid autoantibodies in serum, and iodine in urine, were measured and B-mode ultrasonography of the thyroid was performed at baseline and follow-up. RESULTS: Among subjects with mildly deficient iodine intake, those with more than adequate intake, and those with excessive intake, the cumulative incidence of overt hypothyroidism was 0.2 percent, 0.5 percent, and 0.3 percent, respectively; that of subclinical hypothyroidism, 0.2 percent, 2.6 percent, and 2.9 percent, respectively; and that of autoimmune thyroiditis, 0.2 percent, 1.0 percent, and 1.3 percent, respectively. Among subjects with euthyroidism and antithyroid antibodies at baseline, the five-year incidence of elevated serum thyrotropin levels was greater among those with more than adequate or excessive iodine intake than among those with mildly deficient iodine intake. A baseline serum thyrotropin level of 1.0 to 1.9 mIU per liter was associated with the lowest subsequent incidence of abnormal thyroid function. CONCLUSIONS: More than adequate or excessive iodine intake may lead to hypothyroidism and autoimmune thyroiditis.

Adolescent↗

[Impact evaluation of universal salt iodization on spectrum of thyroid diseases in Changzhou area, Jiangsu, China].

OBJECTIVE: To evaluate the impact of universal salt iodization using monitoring data on correctional status of iodine deficiency and hospitalized thyroid diseases. METHODS: Retrospective survey was conducted to collect medical records of hospitalized thyroid disease cases. Routine monitoring data on population iodine nutrition status and goiter prevalence were analyzed. RESULTS: The coverage of adequately iodized salt was consistently above 95%. Hospitalization rate of thyroid diseases rose steadily, and peaked at 54.5 per 100,000. The proportion of hospitalized thyroid disease among hospitalized diseases also rose with female and those aged above 40 years old mostly affected. The proportion of hospitalized hyperthyroidism among total hospitalized thyroid disease rose from 13.6% to 34.7%. CONCLUSIONS: Universal salt iodization might eliminate iodine deficiency while other impact still exists. However, the benefits of universal salt iodization should be far overweight the adverse effects.

China↗

[Autoimmune thyroid disease--clinical symptoms of associated autoimmunity].

Autoimmune diseases are manifested in a broad spectrum. Classic examples of organ-specific autoimmune disease include Addison's disease, insulin-dependent type-1 Diabetes mellitus, Grave's disease (MGB), and Hashimoto thyroiditis (HT). The initial report of this autoimmune thyroid disease (AITD) dates back to Hakira Hashimoto (1912). In HT, as an organ-specific autoimmune disease, massive infiltration of lymphoid cells and parenchyma destruction are a consistent feature. The infiltration appears to be immune-mediated, primarily lymphocytic (T helper, T suppressor cells), NK cells and B cells. The pathological characteristics of AITD include development of the goitre (atrophic form is not so frequent), impaired thyroid gland function (from hyperthyroidism to subclinical and manifested hypothyroidism) and the formation of antithyroidal antibodies against thyroglobulin (AbTg) and the microsomal antigen (Ab TPO). There is a very good correlation between the antibodies against TPO and the histological findings. Morbus Graves Basedow is characterized by autoimmune hyperthyroidism with goitre, and infiltrative orbitopathy. Autoantibodies against the TSH-receptor molecule on the plasma membrane of the thyroid gland follicles cause a nonphysiological activation and an increase of the cellular function. Besides this hyperthyroidal condition, an autoimmune attack against the retrobulbar tissue leading to endocrine orbitopathy, can be noted in about 40% of patients suffering from MGB.

Autoimmune Diseases↗

Thyroid disease in Uganda.

A five-year retrospective study of thyroid disease in an Uganda hospital shows that about 67% of cases are due to goitrous hyperplasia, with colloid diffuse goitre twice as common as nodular goitre. It also notes that goitre rates in neighbouring countries are high, and suggests that a survey to assess its prevalence in Uganda is necessary. I deficiency as an etiological factor and the advantage of a national salt iodization programme are discussed. The rising incidence of thyrotoxicosis (11.4%) is in keeping with its increasing frequency elsewhere in Africa. The incidence of neoplastic diseases of the thyroid is low. Chronic thyroiditis was not seen.

Adolescent↗

Family history of autoimmune thyroid disease and childhood acute leukemia.

The association between a familial history of autoimmune disease and childhood acute leukemia was investigated in a French case-control study that, overall, was designed to assess the role of perinatal, infectious, environmental, and genetic factors in the etiology of childhood acute leukemia. Familial histories of autoimmune disease in first- and second-degree relatives were compared in 279 incident cases, 240 cases of acute lymphocytic leukemia (ALL) and 39 cases of acute non-lymphoblastic leukemia (ANLL), and 285 controls. Recruitment was frequency matched by age, gender, hospital, and ethnic origin. Odds ratios (OR) were estimated using an unconditional regression model taking into account the stratification variables, socioeconomic status, and familial structure. A statistically significant association between a history of autoimmune disease in first- or second-degree relatives and ALL (OR, 1.7; 95% confidence interval (CI), 1.0-2.8) was found. A relationship between thyroid diseases overall and ALL (OR, 2.0; 95% CI, 1.0-3.9) was observed. This association was more pronounced for potentially autoimmune thyroid diseases (Grave's disease and/or hyperthyroidism and Hashimoto's disease and/or hypothyroidism) (OR, 3.5; 95% CI, 1.1-10.7 and OR, 5.6; 95% CI, 1.0-31.1, respectively for ALL and ANLL), whereas it was not statistically significant for the other thyroid diseases (thyroid goiter, thyroid nodule, and unspecified thyroid disorders) (OR, 1.6; 95% CI, 0.7-3.5 and OR, 1.3; 95% CI, 0.2-7.0, respectively, for ALL and ANLL). The results suggest that a familial history of autoimmune thyroid disease may be associated with childhood acute leukemia.

Adolescent↗

Cancer mortality in women with thyroid disease.

A retrospective follow-up study of 7338 women with either nontoxic nodular goiter, thyroid adenoma, hyperthyroidism, hypothyroidism, Hashimoto's thyroiditis, or no thyroid disease was conducted. All women patients at the Massachusetts General Hospital Thyroid Clinic who were seen between 1925 and 1974 and who were treated for a minimum of 1 year were traced. A total of 2231 women (30.4%) were dead and 2012 women (27.4%) were alive as of December 31, 1978. Partial follow-up information was available for the remaining 3095 women (42.2%). The average length of follow-up was 15.2 years. When losses to follow-up were withdrawn at the time of their loss, the standardized mortality ratios (SMR) for all causes of death were 1.2 [95% confidence interval (CI), 1.1-1.3] for women with nontoxic nodular goiter, 1.2 (95% CI 1.0-1.3) for those with thyroid adenoma, 1.4 (95% CI 1.3-1.5) for women with hyperthyroidism, 1.5 (95% CI 1.3-1.7) for hypothyroid women, 1.2 (95% CI 0.9-1.5) for those with Hashimoto's thyroiditis, and 1.5 (95% CI 1.4-1.6) for those without thyroid disease. For deaths from all cancers, the standardized mortality ratios were 1.5 (95% CI 1.2-1.8) for women with nontoxic nodular goiter, 1.5 (95% CI 1.1-1.9) for those with thyroid adenoma, 1.2 (95% CI 1.0-1.4) for women with hyperthyroidism, 1.0 (95% CI 0.7-1.4) for the hypothyroid women, 1.2 (95% CI 0.7-2.1) for those with Hashimoto's thyroiditis, and 1.3 (95% CI 1.0-1.5) for those women without thyroid disease. When specific cancer sites were studied, excess numbers of deaths were observed from breast cancer in women with nontoxic nodular goiter (SMR = 1.6, 95% CI 1.0-2.6) and from lymphatic and hematopoietic cancer in women with nontoxic nodular goiter (SMR = 2.4, 95% CI 1.2-4.3) and thyroid adenoma (SMR = 2.7, 95% CI 1.1-5.2). An increase in thyroid cancer risk was observed in women with thyroid adenoma (SMR = 11.7, 95% CI 1.3-42.1) but was based on only two deaths. In hyperthyroid women, statistically significant increases in the number of deaths were observed from pancreatic cancer (SMR = 2.6, 95% CI 1.4-4.3) and respiratory cancer (SMR = 2.2, 95% CI 1.3-3.5), but not breast cancer (SMR = 1.3, 95% CI 0.8-1.8). When the data were stratified by the time between the onset of thyroid symptoms and death, a nonsignificant excess number of cancer deaths was observed in hyperthyroid women who died 20 or more years after their symptoms began.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenoma↗

Autoantibodies to insulin are present in sera of patients with autoimmune thyroid disease.

It has been clinically suspected that patients with autoimmune thyroid disease are at an increased risk of developing other autoimmune diseases later in life. To determine the presence and potential importance of a more generalized deregulation of immune response in patients with Grave's disease and Hashimoto's disease, sera from 33 patients with Graves' disease and 16 patients with Hashimoto's disease were screened for the presence of anti-insulin antibodies and anti-insulin-receptor antibodies. An enzyme-linked immunosorbent assay was used to identify the presence of IgG against human insulin. The optical density indicating the presence of IgG against insulin in sera from patients with Graves' disease averaged .172 +/- .024 (mean +/- SE; range .010-.802), compared to the mean normal value of .098 +/- .0009 (range .012-.238) in 33 control subjects. Ten of 33 patients with Graves' disease had values greater than .200, whereas control sera values were less than .200 in all but one case (P less than .005, Graves' sera vs. controls). The sera from patients with Hashimoto's disease had a mean optical density of .110 +/- .016, with 15 of 16 values between .010 and .200. These values were not significantly different from controls with an insulin-binding inhibition assay. Anti-insulin-receptor antibodies were not detected in any of 33 patients with Graves' disease, and cytoplasmic islet cell antibodies were not detected in sera from seven patients with Graves' disease who had insulin-binding antibodies. These data support the hypothesis that the immunologic response in autoimmune thyroid disease may be more heterogeneous and polyclonal than previously believed.

Autoantibodies↗

Immunological aspects of autoimmune thyroid disease.

There is considerable evidence to indicate that autoimmune thyroid diseases (both Graves disease and Hashimoto thyroiditis) are primary disorders of the lymphoid system. Evidence is now available to indicate that both cell-mediated and humoral immune factors are important in the pathophysiological expression of these conditions. The basic genetic defect in these disorders now appears to be the presence of a specific defect in suppressor T lymphocytes, which in turn permits the survival and expansion of a randomly appearing "forbidden" clone of thyroid-directed, organ-specific, helper T lymphocytes. These then cooperate with already present groups of appropriate B lymphocytes, which in turn produce humoral immunoglobulins directed against the thyroid. There appear to be subtle genetic differences that distinguish between Graves disease and Hashimoto thyroiditis, leading to their different expressions. Indeed, subtle genetic differences between different groups of patients with Graves disease may reveal whether there is a complete defect in immunoregulation (thus preventing any immunological remission) or a partial defect in immunoregulation, in which case the possibility of remission does exist. The role of stress in precipitating hyperthyroidism may be via stress-related physiological effects on partially defective suppressor T lymphocytes.

Antibody Formation↗

The genetics of the autoimmune thyroid diseases.

AIM: To understand the modern approach to finding the genes responsible for complex diseases when compared to simple Mendelian inheritance. To define the autoimmune thyroid diseases as we now understand them and introduce the concept of disease heterogeneity. To review the evidence for a genetic contribution to autoimmune thyroid disease as opposed to environmental factors and to be aware of new information generated from recent studies concerning the role of HLA, immune modulators, and new loci of interest providing susceptibility to the autoimmune thyroid diseases.

Autoimmune Diseases↗