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PubMed1988

Human orbital tissue and thyroid membranes express a 64 kDa protein which is recognized by autoantibodies in the serum of patients with thyroid-associated ophthalmopathy.

A 64 kDa protein has been identified in the membrane fraction of human eye muscle, orbital connective tissue and thyroid, by testing sera of patients with thyroid-associated ophthalmopathy in SDS-polyacrylamide gel electrophoresis and Western blotting. Antibodies to this membrane antigen seem characteristic of the early stage of ophthalmopathy. In the thyroid this newly recognized protein seems different from previously known membrane antigens. A thyroid antibody reactive with a 64 kDa membrane antigen in eye muscle could explain the very frequent association of ophthalmopathy with autoimmune thyroid disease.

Adult↗
PubMed1982

Studies on the cyclic AMP response to thyroid stimulating immunoglobulin (TSI) and thyrotropin (TSH) in human thyroid cell monolayers.

Studies were conducted on the cultured human thyroid cell bioassay for thyroid stimulating immunoglobulin (TSI) and thyrotropin (TSH). In confirmation of the data of Kasagi, et al.,15 incubation of human thyroid cells in Hank's balanced salt solution deficient in NaCl increased the sensitivity of the c-AMP response to bovine TSH by approximately one order of magnitude. Half-maximal stimulation was attained at approximately 0.1 mU bTSH/ml. The effect of NaCl in the medium was greater with stimulation by TSI greater than hTSH greater than bTSH. In contract to incubations in NaCl(+)medium, with NaCl(-) medium most (70%-80%) of the c-AMP produced was released into the medium; this proportion remaining relatively constant over a wide range of bTSH and hTSH concentrations. At TSI concentrations higher than 3mg/ml efflux of c-AMP into the medium was significantly diminished. Stimulation by cholera toxin and prostaglandin E of thyroid cell c-AMP generation was not enhanced in NaCl(-) medium, in contrast to stimulation by TSH and TSI. The presence of 10(-4)m cycloheximide in NaCl(+) medium enhanced the c-AMP response to physiological concentrations of TSH. As with NaCl(-) medium, cycloheximide increased the sensitivity but not the maximum response of the c-AMP response to TSH. However no additivity was observed with NaCl(-) medium and cycloheximide. Human thyroid cells obtained from patients with Graves' disease are relatively insensitive to TSI stimulation. In NaCl(-) medium, however, the sensitivity of these cells to TSI stimulation is sufficient to enable them to be utilized in the TSI assay. The present state of the TSI assay is discussed.

Alprostadil↗
PubMed1987

Desensitization of the thyroid cyclic AMP response to thyroid stimulating immunoglobulin: comparison with TSH.

Studies were conducted to examine the characteristics of thyroid cell cAMP stimulation by thyroid stimulating immunoglobulins (TSI) and to compare the cAMP response to TSI and TSH in desensitized human thyroid cells. In terms of cAMP production, preexposure (eight hours) of the cells to TSI induced a desensitization very similar to TSH-induced desensitization: both TSH- and TSI-desensitized cells showed a normal response to cholera toxin and forskolin stimulation; TSH and TSI desensitization was interchangeable in that desensitization by either stimulator affected the action of the other; the time of recovery from either TSH and TSH desensitization was identical; the cycloheximide (10(-4) mol/L) prevented both TSI- and TSH-induced desensitization; preexposure of the cells to iodine, which affects mainly the adenylate cyclase catalytic unit, or to epinephrine, which activate the inhibitory regulatory protein Ni by the alpha 2-adrenergic stimulation, induced a similar inhibition of the subsequent stimulation by both TSH or TSI. The remarkable similarities between TSH and TSI in stimulating and desensitizing thyroid cells strongly support the concept that TSI activates thyroid adenylate cyclase by interacting with the TSH receptor and not through an allosteric mechanism.

Cells, Cultured↗
PubMed1991

Hepatic UDP-glucuronyltransferase(s) activity toward thyroid hormones in rats: induction and effects on serum thyroid hormone levels following treatment with various enzyme inducers.

Induction of hepatic UDP-glucuronyltransferase(s) (hUDP-GT(s] activity toward thyroid hormones and the relationship between the activity and the serum thyroid hormones or the thyroid stimulating hormone (TSH) level were examined in male Sprague-Dawley rats after four consecutive ip doses of various hepatic enzyme inducers at 75-150 mg/kg/day. hUDP-GT activity toward thyroxine (T4; hUDP-GT-T4) was induced by treatment with beta-naphthoflavone, 3-methylcholanthrene (3-MC), polychlorinated biphenyls, or pregnenolone-16 alpha-carbonitrile. However, no significant induction was observed for isosafrole administration and in the cases of phenobarbital and 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane slight decreases were found. The induction profile of hUDP-GT-T4 for these inducers was approximately the same as that of hUDP-GT activity toward triiodothyronine (T3; hUDP-GT-T3), indicating that these two thyroid hormones (T4 and T3) are glucuronidated by the same hUDP-GT(s). Moreover, the induction profile of both hUDP-GT-T4 and hUDP-GT-T3 was similar to that of hUDP-GT toward 1-naphthol, but not chloramphenicol, suggesting that T4 and T3 belong to the so-called group-1 substrates which are preferentially glucuronidated by hUDP-GT(s) inducible by treatment with 3-MC. Decreases in serum T4 levels clearly correlated with an increase in hUDP-GT-T4 activity, indicating that serum T4 levels are directly affected by hUDP-GT-T4 activity. However, no direct correlation between decrease in thyroid hormone levels and compensatory increase in TSH levels was found.

Animals↗
PubMed1991

Human thyrotropin receptor gene: expression in thyroid tumors and correlation to markers of thyroid differentiation and dedifferentiation.

Human thyrotropin (TSH) receptor steady-state transcript levels were analyzed by Northern blot analysis in thyroids of patients with thyroid carcinoma, with hyperfunctioning adenoma and in normal controls. In control tissue and benign tumors expression levels of TSH receptor mRNA were high whereas in anaplastic carcinomas no normal TSH receptor mRNA was detected. In papillary and follicular tumors it varied from normal to markedly reduced levels. Thyroid peroxidase (TPO) and thyroglobulin (Tg) mRNA were strongly expressed in normal tissue and in hyperfunctioning adenomas but were completely lost in all anaplastic tumors. In papillary tumors expression of TPO and Tg mRNA varied from normal to a complete loss of expression of either TPO, Tg or both. Tg and TPO steady-state expression did not correlate to TSH receptor transcript levels. C-myc mRNA was highly expressed in anaplastic carcinomas, very variable in normal controls and in differentiated thyroid tumors and low in hyperfunctioning adenomas. In summary, TSH receptor mRNA is persistently expressed in all differentiated thyroid tissues and tumors but lost in undifferentiated carcinomas. Its persistence far along the transformation pathway further supports the concept that this gene which inserts the thyrocytes in the physiological regulatory network is almost constitutively expressed in this cell.

Adolescent↗
PubMed1995

Effect of thyroid stimulating hormone on the development and progression of rat thyroid follicular cell tumors.

Time course changes in cell proliferative activity of thyroid focal hyperplastic and tumorous lesions as well as blood thyroid-related hormones in male F344 rats initiated with N-bis(2-hydroxypropyl)nitrosamine (DHPN: 2800 mg/kg body weight, single s.c. injection) were examined following chronic administration of 0.1% sulfadimethoxine (SM) in the drinking water for 1, 4, 8, 12 and 16 weeks and at the end of a subsequent 4-week recovery period. Serum thyroid stimulating hormone (TSH) levels increased rapidly from week 1 of SM treatment, reaching a peak at week 8, and then decreased gradually with prolongation of treatment period, although remaining significantly elevated as compared with the corresponding controls at all time points up to week 16. Follicular cell hyperplasias and adenomas of the thyroid occurred from week 4 and carcinomas from week 8. All of these lesions showed high cell proliferative activities corresponding to high serum TSH levels during the early stage, but the levels in hyperplasias and adenomas decreased rapidly with prolongation of SM treatment. After the recovery period, serum TSH levels had returned to below the normal range and cell proliferation in follicular hyperplasias and adenomas had stopped or was very low. Some carcinomas demonstrating invasive growth also showed remarkable decreases in the cell proliferative activity. The results of our study strongly suggest that a high serum TSH level plays an important role in the early stage of thyroid tumorigenesis and that some tumors exhibiting invasive growth are still dependent on TSH stimulation.

Animals↗
PubMed2006

Thyroid hormone in hypopituitarism, Graves' disease, congenital hypothyroidism, and maternal thyroid disease during pregnancy.

Although measurement of serum thyroid-stimulating hormone (TSH) is the single best test to diagnose thyroid disorders and monitor treatment, there are certain situations in which the TSH level cannot be used as a guideline. In the diagnosis of children with hypopituitary hypothyroidism, TSH is often "inappropriately" normal. Treatment is aimed at adjusting the l-thyroxine dose to maintain the serum free thyroxine (T4) in the upper half of the normal range for age. In children with Graves' disease, serum TSH can be suppressed for several months after a euthyroid state is restored, so the clinician must rely on serum free T4 and triiodothyronine (T3) levels. Up to 30% of infants and 10% of children with congenital hypothyroidism have a mildly elevated TSH level despite other indications that the thyroid hormone dosage is correct. Such resistance to thyroid hormone at the pituitary gland diminishes with age. Pregnancy is another condition in which serum TSH levels are altered (slightly lower); in this situation, it is the result of elevated human chorionic gonadotropin levels that cross-react with the TSH receptor. This alteration must be taken into account when diagnosing or treating maternal thyroid disorders during pregnancy.

Clinical Laboratory Techniques↗
PubMed1981

Thyroid suppression and stimulation testing: The place of scanning in the evaluation of nodular thyroid disease.

In the past, T3 suppression testing was often required to confirm the presence of autonomous thyroid function in patients with borderline clinical and laboratory findings suggestive of hyperthyroidism or in euthyroid patients with the stigmata of Graves' disease. Similarly, TSH stimulation testing was used to document the presence of "low thyroid reserve" in patients with borderline clinical and laboratory findings suggestive of hypothyroidism. The current availability of radioimmunoassays for triiodothyronine (T3) and thyrotorpin (TSH) plus the ability to evalate pituitary responsiveness by performing a TRH stimulation test permits a definitive diagnosis to be made in the majority of borderline situations without recourse to the more cumbersome suppression and stimulation tests. Suppression and stimulation thyroid scanning retain a unique position in the evaluation of localized areas in increased uptake of radionuclide (hot nodules), especially in patients who are euthyroid. Proof that such nodules are autonomously functioning thyroid adenomas (AFTN) greatly decreases the possibility that they represent malignant thyroid tumors. Suppression and stimulation scanning have a more limited role in the evaluation of patients with hyperthyroidism arising in a multinodular goiter, where TSH stimulation scanning may help to differentiate between toxic multinodular goiter and Graves' disease arising in a preexisting goiter.

Diagnosis, Differential↗
PubMed1995

Follicular thyroid cells of autoimmune thyroiditis may coexpress ICAM-1 (CD54) and its natural ligand LFA-1 (CD11a/CD18).

The leukocyte functional associated antigen-1 (LFA-1)-intercellular adhesion molecule-1 (CD11a-CD18/CD54) intercellular adhesion system plays a crucial role in several immunologic phenomena, including adhesion between lymphocytes and epithelial cells. In previous studies evidence for CD54 expression on thyroid follicular cells in Hashimoto's thyroiditis was provided. In this study we evaluated the possible expression of CD11a and CD18 antigens on thyrocytes of patients with Hashimoto's thyroiditis and on thyrocytes of patients with Graves' disease and simple goiter as controls; we used both alkaline phosphatase immunostaining and indirect immunofluorescence on cryostatic tissue sections. The results showed that LFA-1 (both CD11a and CD18) positivity on thyroid follicles may occur in glands of patients with Hashimoto's disease, with a pattern very similar to that of CD54: this was observed in five of seven specimens. Conversely, no positivity was observed in tissues from patients with Graves' disease or goiter: notably, isolated follicular cells from Graves' goiter tissues are induced in culture to express CD54, but not LFA-1. Using double-staining techniques, we were able to show that in specimens from patients with Hashimoto's disease, the same follicular structures coexpressed LFA-1 and CD54. Such a coexpression of the two ligands further emphasizes the possible role of this adhesion system in the pathogenesis of epithelial damage, through bidirectional interactions between thyroid epithelial cells and infiltrating LFA-1 or CD54-positive mononuclear cells.

Adult↗
PubMed1999

Thyroid-specific enhancer-binding protein/thyroid transcription factor 1 is not required for the initial specification of the thyroid and lung primordia.

Targeted disruption of the homeobox gene T/ebp (Ttf1) in mice results in ablation of the thyroid and pituitary, and severe deformities in development of the lung and hypothalamus. T/ebp is expressed in the thyroid, lung, and ventral forebrain during normal embryogenesis. Examination of thyroid development in T/ebp homozygous null mutant embryos revealed that the thyroid rudiment is initially formed but is eliminated through apoptosis. Absence of T/EBP expression in the lung primordium does not activate apoptosis since a lung tissue, albeit dysmorphic, is nevertheless formed in T/ebp-/- embryos. These results demonstrate that T/EBP is not required for the initial specification of thyroid or lung primordia, but is absolutely essential for the development and morphogenesis of these organs.

Animals↗
PubMed1988

Thyroid nodules and thyroid cancer--diagnostic aspects.

The clinical evaluation of patients with thyroid nodules is a common problem confronting the clinician. The vast majority of such nodules are benign, but concern that such a thyroid swelling may harbour malignancy demands prompt and accurate diagnosis. Furthermore, it is clear that properly treated differentiated thyroid carcinoma is associated with an excellent prognosis. The objective of investigating patients presenting with thyroid nodules is to define the small number of malignancies with minimum inconvenience to the patient in the most cost-effective way. There are no laboratory tests which reliably differentiate benign from malignant disease. The traditional approaches of radionuclide and ultrasound scanning have been shown to be poorly specific in the diagnosis of malignancy, resulting in many unnecessary operations for benign lesions. These tests have been replaced in many centres by fine needle aspiration cytology, with surgery for abnormal cytological findings alone. This technique is easily performed in an out-patient clinic and is well tolerated; accuracy in the diagnosis of thyroid neoplasia of up to 97% can be achieved.

Humans↗
PubMed2005

Mutant-selective thyromimetics for the chemical rescue of thyroid hormone receptor mutants associated with resistance to thyroid hormone.

The thyroid hormone receptors (TRs) are ligand-dependent transcription factors that control the expression of multiple genes involved in development and homeostasis in response to thyroid hormone (triiodothyronine, T3). Mutations to TRbeta that reduce or abolish ligand-dependent transactivation function are associated with resistance to thyroid hormone (RTH), an autosomal dominant human genetic disease. A series of neutral alcohol-based compounds, based on the halogen-free thyromimetic GC-1, have been designed, synthesized, and evaluated in cell-based assays for their ability to selectively rescue three of the most common RTH-associated mutations (i.e., Arg320 --> Cys, Arg320 --> His, and Arg316 --> His) that affect the basic carboxylate-binding arginine cluster of TRbeta. Several analogues show improved potency and activity in the mutant receptors relative to the parent compound GC-1. Most significantly, two of these mutant-complementing thyromimics show high potency and activity with a strong preference for the mutant receptors over wild-type TRalpha(wt), that is associated with the cardiotoxic actions of T3. The compounds were evaluated in reporter gene assays using the four common thyroid hormone response elements, DR4, PAL, F2 (LAP), and TSH, and show activities and selectivites consistent with their unique potential as agents to selectively rescue thyroid function to these RTH-associated mutants.

Acetates↗
PubMed1999

A pooled analysis of case-control studies of thyroid cancer. IV. Benign thyroid diseases.

OBJECTIVE: To obtain more precise estimates of the association between thyroid cancer and benign thyroid diseases and to elucidate the role of potential confounders or effect modifiers. METHODS: The original data from 12 case-control studies from the United States, Asia, and Europe were pooled. Based on 2,094 women and 425 men with cancer of the thyroid and, respectively, 3,248 and 928 control subjects, odds ratios (ORs) and the corresponding 95% confidence intervals (CIs) were obtained by conditional regression models, conditioning on study and age at diagnosis, and adjusting for age and radiotherapy. RESULTS: A history of hypothyroidism was not associated with cancer risk (pooled ORs = 0.9, 95% confidence interval, CI: 0.7-1.3 in women and 1.7, 95% CI: 0.3-11.7 in men). ORs for hyperthyroidism were 1.4 (95% CI: 1.0-2.1) in women and 3.1 (95% CI: 1.0-9.8) in men. In women, however, risk was lower in the absence of or after allowance for history of goiter. Pooled ORs for a history of goiter were 5.9 (95% CI: 4.2-8.1) in women and 38.3 (95% CI: 5.0-291.2) in men. Risk for a history of benign nodules/adenomas was especially high (OR = 29.9, 95% CI: 14.5-62.0, in women; 18 cases versus 0 controls in men). The excess risk for goiter and benign nodules/adenomas was greatest within 2-4 years prior to thyroid cancer diagnosis, but an elevated OR was present 10 years or more before cancer. CONCLUSIONS: Goiter and benign nodules/adenomas are the strongest risk factors for thyroid cancer, apart from radiation in childhood.

Adenoma↗
PubMed2000

Effect of oral iodized oil on thyroid size and thyroid hormone metabolism in children with concurrent selenium and iodine deficiency.

OBJECTIVES: To determine the efficacy of oral iodized oil in goitrous children who are both selenium (Se) and iodine deficient; to investigate if Se status modifies the response of iodine deficient, goitrous children to oral supplementation with iodized oil. DESIGN: A longitudinal intervention trial. SETTING: Two rural villages in the western Côte d'Ivoire. SUBJECTS: 51 goitrous non-anemic schoolchildren with both iodine and Se deficiency. INTERVENTION: Each child received an oral dose of 0.4 ml iodized poppyseed oil containing 200 mg of iodine. They were followed for 1 y with measurements of urinary iodine (UI), thyrotropin (TSH), thyroxine (T4), and thyroid volume by ultrasound. RESULTS: At baseline all children were goitrous and Se deficient; median UI was 29 microg/l and mean serum Se (s.d.) was 14.8 (10.7) microg/l. After receiving iodized oil, thyroid volume decreased significantly vs baseline at 10, 15, 30 and 50 weeks (P<0.001). At 50 weeks mean percentage change in thyroid volume from baseline was-46.6% and only five children remained goitrous. Median TSH values at 5, 10, 15, 30 and 50 weeks were reduced significantly (P<0.001) compared to baseline. Among individual children the severity of Se deficiency predicted the degree of response to iodized oil. Baseline serum Se and percentage change in thyroid volume from baseline at 50 weeks were strongly correlated (r2=0.554). Baseline Se and percentage decrease in TSH from baseline at 30 weeks were also well-correlated (r2=0.467). CONCLUSION: Although more severe Se deficiency partially blunts the thyroid response to iodine supplementation, oral iodized oil is an effective method for iodine repletion in goitrous children who are Se deficient. SPONSORSHIP: The Swiss Federal Institute of Technology, Zürich, the Foundation for Micronutrients in Medicine, Rapperswil, Switzerland, and the Thrasher Research Fund, Salt Lake City, USA.

Body Mass Index↗
PubMed1998

IL-10 expression in thyroid glands: protective or harmful role against thyroid autoimmunity?

IL-10 is a cytokine which not only suppresses cellular immunity but also stimulates the humoral response. In certain animal models of autoimmunity, IL-10 exerts a protective effect against autodestruction. This study was to ascertain whether there could be a role for IL-10 in human autoimmune thyroid disease. Total RNA was extracted from snap-frozen thyroid blocks from surgical specimens. Five 'normal', five multinodular, six Graves and two Hashimoto thyroids (one euthyroid and one hypothyroid) were studied. Approximately 7 microg of total RNA from each gland were reverse transcribed with oligo-dT primers. Pre-plateau semiquantitative polymerase chain reaction (PCR) was performed with specific IL-10 primers. PCR products were run on a 1-5% agarose gel, blotted onto a N-hybond nylon membrane, hybridized with a specific internal probe labelled with gamma-32P-ATP and autoradiographed. Statistical analysis of densitometric values showed significantly higher IL-10 levels in the autoimmune than in the non-autoimmune glands. In situ hybridization and immunohistochemistry showed that the IL-10 message was located within the infiltrating lymphomononuclear cells. Histological analysis revealed that the autoimmune thyroids with the highest IL-10 levels were characterized by relevant degrees of B and T cell infiltration and also exhibited the greatest percentage of spontaneous HLA class II expression on thyrocytes. IL-10 and neutralizing anti-IL-10 antibodies were not able to regulate in vitro spontaneous or interferon-gamma (IFN-gamma)/phytohaemagglutinin (PHA)-induced HLA class II on thyrocytes. We conclude that in active autoimmune thyroiditis, in addition to the well documented production of Th1 cytokines, Th2-related lymphokines can be detected simultaneously. It can be envisaged that in this condition the role of IL-10 might be directed to the stimulation of B cell proliferation and antibody production rather than to the suppression of proinflammatory cytokine release.

Adult↗
PubMed1999

Anti-CD44 treatment does not prevent the extravasation of autopathogenic T cells to the thyroid in experimental autoimmune thyroiditis.

The hyaluronic acid binding glycoprotein CD44 is expressed on a wide variety of cells, and by mediating interactions between cells and extracellular matrices promotes the movement of cells from the circulation into organs. Recent reports have described the effects of an antibody specific for CD44 (IM7) that has beneficial effects in two murine models of autoimmune disease. Both experimental allergic encephalomyelitis (EAE) and collagen-induced arthritis were ameliorated by treatment with IM7, which was considered to be acting by preventing the homing of lymphocytes to the relevant inflammatory sites, namely the central nervous system and the synovium, respectively. In this study the same anti-CD44 antibody was used to try to prevent leucocytic infiltration of the thyroid in the murine model of Hashimoto's thyroiditis, experimental autoimmune thyroiditis (EAT). We report that, in contrast to the previous findings, this antibody had an exacerbating effect on thyroiditis induced by immunization of mice with mouse thyroglobulin (MTg) and complete Freund's adjuvant (CFA). Thyroid infiltrates lasted longer and showed increased severity compared with untreated or control antibody-treated mice. Antibody responses to MTg were unaffected by antibody treatment. The data suggest that simple rules cannot be drawn that predict the potential broad therapeutic use of anti-CD44 reagents, presumably due to differences in the cellular phenotypes and the dynamics of their movement into inflammatory sites during different disease processes.

Animals↗
PubMed1985

Thyroidal thyroxine and triiodothyronine in autonomously functioning thyroid nodule and paranodular tissue.

Thyroidal thyroxine (T4), triiodothyronine (T3), thyroglobulin (Tg) and T4/T3 ratio were investigated in nodular and paranodular tissue from 16 patients with autonomously functioning thyroid adenomas. The concentration of T4 and T3 in the nodule were 97.7 +/- 20.5 (Mean +/- SE) and 10.2 +/- 2.4 micrograms/g wet weight (w.w.). Both iodothyronines were significantly lower in paranodular tissue (22.6 +/- 4.8 and 1.45 +/- 0.32 micrograms/g w.w., respectively), but with disproportionately decreased T3 which resulted in T4/T3 ratio (25.4 +/- 6.4) higher than in adenoma tissue (11.2 +/- 1.6). In patients with high normal or supranormal serum T3 concentration, thyroidal concentration of T3 in adenoma tissue was higher (15.6 +/- 5.0 vs. 6.3 +/- 1.2 micrograms/g w.w.) and T4/T3 ratio lower (8.05 +/- 2.1 vs. 13.2 +/- 1.9) than in patients with normal serum T3. The results suggest that thyroid release of T3 from adenoma is relatively higher than T4 in patients with autonomously functioning thyroid nodules and increased peripheral T3.

Adenoma↗
PubMed1986

Similar triiodothyronine releasing activity of thyroid stimulating antibodies in human and porcine thyroid slices.

In an approach to addressing species specificity of thyroid stimulating antibodies (TSAb) stimulation of T3 release by Graves' sera was comparatively studied in human and porcine thyroid slices. A high sensitivity and specificity was found for the T3 bioassay independently on the use of human or porcine thyroid. Moreover, activity indices of the individual sera in both tissues were significantly correlated to each other and to circulating hormone levels in untreated disease. In conclusion, we suppose a lack of functionally relevant differences between target antigens, brought about probably by the TSH receptor itself and other membrane components, in human and porcine thyroid. Thus, for clinically applicable T3 releasing bioassay porcine thyroid may be alternatively used. In addition, this bioassay renders the advantage of reflecting the activity of disease.

Adult↗