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PubMedDate not supplied

Prostate-thyroid axis: prostatic TRH is one of the stimulators of thyroid hormone.

Ventral prostatectomy decreased serum thyroid hormones and histology of the thyroid gland indicate that hypothyroid condition. Co-culture of thyroid gland and ventral prostate stimulates thyroid hormone secretion. In the present study we report prostatic thyrotropin releasing hormone (TRH) is the stimulating factor of thyroid hormone secretion. Mature rat (90 days old) ventral prostate, anterior pituitary and thyroid glands were co-cultured in vitro with or without TRH antibody to assess the direct influence ofprostatic TRH on thyroid hormone secretion. Total thyroxine (T4) and triiodothyronine (T3) were increased significantly in the culture media of ventral prostate, anterior pituitary and thyroid gland when compared with thyroid gland plus anterior pituitary culture media. However, media T4 and T3 concentration decreased significantly in thyroid gland alone; also in thyroid gland plus ventral prostate, thyroid gland plus anterior pituitary and thyroid gland plus anterior pituitary plus ventral prostate were co-cultured with TRH antibody (Ab) in a dose dependent manner. The results suggest that ventral prostatic TRH is one ofthe stimulating factors of thyroid hormone secretion under these in vitro conditions.

Animals↗
PubMed2006

The role of thyroid autoantibodies in the development of thyroid dysfunction in Taiwanese chronic hepatitis C patients with interferon-alpha and ribavirin combination therapy.

To investigate the role of thyroid autoantibodies in the development of thyroid dysfunction among chronic hepatitis C (CHC) patients receiving interferon-alpha (IFN-alpha) plus ribavirin (RBV) combination therapy, 95 Taiwanese naïve patients with baseline euthyroidism were enrolled. They were treated with IFN-alpha2b, 6 million units thrice weekly, plus RBV 1,000-1,200 mg daily for 24 weeks. Thyroid function, anti-thyroglobulin and antiperoxidase autoantibodies were tested at enrollment (M0), at the end-of-treatment (M6) and 6 months after end-of-treatment (M12). The percentages of thyroid autoantibodies were 8.4%, 11.6% and 9.5%, at M0, M6 and M12 respectively. Fourteen (14.7%) patients developed thyroid dysfunction at M6 or M12. Thyroid dysfunction occurred during treatment in five (62.5%) of the eight patients with baseline thyroid autoantibodies, which was significantly higher than nine (10.3%) of 87 patients without baseline thyroid autoantibodies (P = 0.0001). Among 14 patients who developed thyroid dysfunction, four (80.0%) of five patients with baseline thyroid autoantibodies recovered at M12, in contrast to two (25%) of eight without baseline thyroid autoantibodies recovered at M12 (P < 0.05). In conclusion, thyroid autoantibodies, either occurred before or during IFN-alpha plus RBV combination therapy, carry a high prediction of subsequent thyroid dysfunction. There also exists difference in the clinical manifestations of thyroid dysfunction in CHC patients treated with combination therapy.

Adult↗
PubMed1976

Altered thyroidal responsivity to thyrotropin induced by circulating thyroid hormones. A "short-loop" regulatory mechanism?

We studied the effect of thyroid hormone administration on responsivity of murine thyroid to exogenous thyrotropin (TSH) in order to explore the possibility that the thyroid gland might be directly inhibited by its own hormones. In the rat both L-thyroxine (T4) and 3,5,3'-L-triiodothyronine (T3) pretreatment inhibited TSH-induced thyroidal ornithine decarboxylase (ODC) activity in vivo in a dose-related manner (half-maximal inhibition, 1.7 mug/rat and 0.6 mug/rat, respectively). Other structurally related compounds exhibited the following inhibitory potencies compared to T4: T3, 283%; triiodothyroacetic acid, 40%; D-T4, 18%; 3,5-L-diiodothyronine, 9%. Monoiodotyrosine, diiodotyrosine, and iodide were not inhibitory. The full inhibitory effect of T4 or T3 was observed when thyroid hormone was administered from 96 to 12 h before TSH and was also seen in hypophysectomized animals. Pretreatment with T4 or T3 in divided doses over 2 1/2 days inhibited TSH-induced increase in [1-14C]glucose oxidation to 14C02 and [3H] leucine incorporation into protein in rat thyroid. In the mouse T4 or T3 pretreatment (0.25-25 mug daily) caused dose-related inhibition of both thyroidal ODC activity and 131I release induced by TSH in vivo. In mice on a low-iodine diet (LID) but not in animals on a regular diet (RD) NaI pretreatment also blunted TSH-induced thyroidal ODC activation and 131I release. When LID or RD mice were pretreated with 12.5-125 mug of T4 or T3 over 2 1/2 days, TSH-induced in vitro stimulation of thyroid cyclic 3',5'-adenosine monophosphate formation was inhibited in a dose-related manner; NaI pretreatment was inhibitory in the LID mouse only. Prior administration of exogenous TSH blunted the activation of thyroid ODC and thyroid hormone release induced by subsequent TSH administration in rat and mouse. These studies indicate altered thyroid responsivity to TSH under the influence of circulating thyroid hormones and suggest the existence of a "short-loop" negative feedback regulating thyroid function.

Animals↗
PubMed2004

All-trans-retinoic acid treatment inhibits the growth of retinoic acid receptor beta messenger ribonucleic acid expressing thyroid cancer cell lines but does not reinduce the expression of thyroid-specific genes.

Conventional chemotherapy and radiotherapy are ineffective for the treatment of advanced thyroid tumors like poorly differentiated papillary, anaplastic, and medullary thyroid cancer. In the attempt to evaluate the possibility of using retinoic acid (RA) in the treatment of thyroid cancer refractory to conventional therapy, we studied the effect of all-trans-RA treatment on five human thyroid cancer cell lines. We found that WRO and NPA, derived from follicular and poorly differentiated human thyroid carcinoma, respectively, showed a growth inhibition after 25 and 21 d of RA treatment. Both apoptosis and a decrease in DNA synthesis were observed as mechanisms of growth inhibition. In the NPA cell line, a delay of cell-cycle progression has also been observed. On the contrary, we did not observe any recovery of mRNA expression of thyroid-specific genes and in particular of the sodium iodide symporter gene. The lack of recovery of radioiodide uptake after all-trans-RA treatment confirmed the inability to reexpress sodium iodide symporter mRNA. The main difference between the all-trans-RA responding cells (WRO and NPA) and the nonresponding cells [ARO, FRO (derived from human anaplastic thyroid tumors) and TT (derived from human medullary thyroid tumor)] was the basal and all-trans-RA induced RA receptor (RAR)beta mRNA expression. Interestingly, 14 thyroid tumors (10 papillary and four anaplastic) showed a significant lower expression of RARbeta mRNA when compared with normal thyroid tissues. In agreement with this result, only 30% of papillary thyroid carcinomas analyzed were positive for RARbeta protein expression with a degree of expression that was much lower than that found in normal thyroid tissue. In conclusion we found that all-trans-RA treatment can determine a significant in vitro growth inhibition especially in differentiated thyroid tumor-derived cell lines but it seems unable to reinduce the expression of thyroid-specific genes and in particular to reinduce the ability to take up iodine. The growth inhibition is likely due to apoptosis in an early phase and to a decrease of DNA synthesis later. In some cases, a delay of the cell-cycle progression also may be responsible for the growth inhibition. The finding of a basal and RA-induced RARbeta mRNA expression only in cell lines responding to all-trans-RA suggests that the growth inhibition might be mediated by RARbeta.

Cell Line, Tumor↗
PubMed1999

A comparison of recombinant human thyrotropin and thyroid hormone withdrawal for the detection of thyroid remnant or cancer.

Recombinant human TSH has been developed to facilitate monitoring for thyroid carcinoma recurrence or persistence without the attendant morbidity of hypothyroidism seen after thyroid hormone withdrawal. The objectives of this study were to compare the effect of administered recombinant human TSH with thyroid hormone withdrawal on the results of radioiodine whole body scanning (WBS) and serum thyroglobulin (Tg) levels. Two hundred and twenty-nine adult patients with differentiated thyroid cancer requiring radioiodine WBS were studied. Radioiodine WBS and serum Tg measurements were performed after administration of recombinant human TSH and again after thyroid hormone withdrawal in each patient. Radioiodine whole body scans were concordant between the recombinant TSH-stimulated and thyroid hormone withdrawal phases in 195 of 220 (89%) patients. Of the discordant scans, 8 (4%) had superior scans after recombinant human TSH administration, and 17 (8%) had superior scans after thyroid hormone withdrawal (P = 0.108). Based on a serum Tg level of 2 ng/mL or more, thyroid tissue or cancer was detected during thyroid hormone therapy in 22%, after recombinant human TSH stimulation in 52%, and after thyroid hormone withdrawal in 56% of patients with disease or tissue limited to the thyroid bed and in 80%, 100%, and 100% of patients, respectively, with metastatic disease. A combination of radioiodine WBS and serum Tg after recombinant human TSH stimulation detected thyroid tissue or cancer in 93% of patients with disease or tissue limited to the thyroid bed and 100% of patients with metastatic disease. In conclusion, recombinant human TSH administration is a safe and effective means of stimulating radioiodine uptake and serum Tg levels in patients undergoing evaluation for thyroid cancer persistence and recurrence.

Adult↗
PubMed2006

Thyroid-specific enhancer-binding protein/NKX2.1 is required for the maintenance of ordered architecture and function of the differentiated thyroid.

Thyroid-specific enhancer-binding protein (T/ebp)/Nkx2.1-null mouse thyroids degenerate by embryonic day (E) 12-13 through apoptosis whereas T/ebp/Nkx2.1-heterogyzgous mice exhibit hypothyroidism with elevated TSH levels. To understand the role of T/ebp/Nkx2.1 in the adult thyroid, a thyroid follicular cell-specific conditional knockout (KO) mouse line, T/ebp(fl/fl);TPO-Cre, was established that expresses Cre recombinase under the human thyroid peroxidase (TPO) gene promoter. These mice appeared to be healthy and exhibited loss of T/ebp/Nkx2.1 expression in many, but not all, thyroid follicular cells as determined by immunohistochemistry and real-time PCR, thus presenting a T/ebp-thyroid-conditional hypomorphic mice. Detailed analysis of the thyroids from T/ebp(fl/fl), T/ebp(fl/fl);TPO-Cre, and T/ebp(fl/ko) mice, where the latter mouse line is derived from crosses with the original T/ebp/Nkx2.1-heterozygous mice, revealed that T/ebp(fl/fl);TPO-Cre mice can be classified into two groups with different phenotypes: one having atrophic/degenerative thyroid follicles with frequent presence of adenomas and extremely high serum TSH levels, and the other having an altered thyroid structure with reduced numbers of extraordinary dilated follicles consisting of excessive numbers of follicular cells as compared with those usually found in the normal thyroid. The latter phenotype was also observed in aged T/ebp(fl/ko) mouse thyroids. In vitro three-dimensional thyroid primary cultures using thyroids from T/ebp(fl/fl);TPO-Cre, T/ebp(fl/ko), and T/ebp(fl/fl) mice, and the latter treated with recombinant adenovirus with and without Cre expression, demonstrated that only cells from T/ebp(fl/fl) mice without adeno-Cre treatment formed follicular structures. Taken together, these results suggest that T/ebp/Nkx2.1 is required for maintenance of the normal architecture and function of differentiated thyroids.

Alleles↗
PubMed1995

Thyroid cytotoxic antibodies in atrophic and goitrous autoimmune thyroiditis.

It is unknown whether in chronic lymphocytic thyroiditis the goitrous (Hashimoto's thyroiditis) and atrophic forms (primary myxedema) are variants of the same disease or different pathogenic entities. Conventional thyroid-related autoimmune parameters are unable to separate both diseases serologically. It is assumed that cellular and humoral cytotoxic events induce gland atrophy and thus should be detectable more often in non-goitrous than goitrous autoimmune thyroiditis. We determined antibody-dependent cell-mediated cytotoxicity in 67 patients with autoimmune thyroiditis, using a 51chromium-release assay against human thyroid cells. Thyroid volume had been measured by ultrasonography. Other thyroid-specific antibodies, like TSH binding-inhibiting antibodies, TSH function-blocking antibodies, thyroglobulin antibodies and thyroid peroxidase antibodies, were determined. Cytotoxic antibody activity was 20.5% (median, range 0-54.5%) in patients with autoimmune thyroiditis and 8.3% (median, range 0-18.4%) in controls (p < 0.0001). Analysis of cytotoxicity regarding thyroid size showed a high incidence of cytotoxic antibodies in atrophic disease (median thyroid volume 6 ml), where cytotoxic antibodies were detectable in 80% versus 39% (x2 = 9.6; p < 0.0001) in goitrous disease (median thyroid volume 36 ml). The specific lysis of 30% (median; 95% confidence limit 23.9-32.9) in non-goitrous thyroiditis patients was significantly higher than in goitrous patients (16.9%; 95% confidence limit 13.2-20.4) (p = 0.0006).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2000

Efficient evaluation of thyroid nodules by primary care providers and thyroid specialists.

OBJECTIVE: To determine whether primary care providers and thyroid specialists at Gundersen Lutheran Medical Center are evaluating thyroid nodules efficiently by following recently published clinical guidelines. STUDY DESIGN: One-year retrospective chart review. PATIENTS AND METHODS: We reviewed patient records from 1996 and tabulated the use of fine-needle aspiration cytology, radionuclide scanning, and thyroid ultrasonography by 49 primary care physicians evaluating 81 thyroid nodules and by 5 thyroid specialists evaluating 29 thyroid nodules. The results were compared with our previous findings and those recently reported by others. RESULTS: Fine-needle aspiration cytology was widely used by both groups of Gundersen Lutheran healthcare providers. Primary care physicians used imaging studies modestly and generated $106 per patient in unnecessary costs. Thyroid specialists occasionally used radionuclide scanning but did not use thyroid ultrasonography; they generated $41 per patient in unnecessary costs. Overall, the introduction of fine-needle aspiration cytology at our institution has reduced the use of radionuclide scanning from 90% to 12% and the use of thyroid ultrasonography from 30% to 10%. We also found that the frequency of surgery in patients with thyroid nodules fell substantially, yet detection of thyroid cancer in the operative specimens increased from 16% to 43% while the cost of removing a thyroid carcinoma decreased from $64,000 to $25,000. CONCLUSIONS: Fine-needle aspiration cytology, adopted as the initial test for diagnosing thyroid nodules by most of our healthcare providers, has reduced the use of imaging studies far below the frequency reported by others and has substantially decreased the cost of thyroid nodule management.

Adolescent↗
PubMed2001

[Frequency of hypothyroidism after De Quervain thyroiditis and contribution of ultrasonographic thyroid volume measurement].

Subacute thyroiditis conventionally recovers without after-effect. Nevertheless some data relate a 5 to 9% occurrence of final hypothyroidism 6 months after the acute stage. We herein studied end-stage hypothyroidism occurrence and effect of thyroid volume alterations on hormonal course during thyroiditis. Twenty-nine cases of subacute thyroiditis were studied. Final thyroid function remained normal in 15 patients (51%) and undetermined in 5 patients (17%). Final hypothyroidism (TSH: 4.5-14.5 microU/mL) occurred in 9 patients (31%). Mean thyroid volume was increased in acute stage in patients with final normal thyroid function (16.6+/-5.7cm(3)) and decreased by 63% during follow-up; final mean thyroid volume was 6.1+/-1.3cm(3). Mean thyroid volume was normal in acute stage in final hypothyroid patients (10.7+/-3.0cm(3)) and decreased by 72% during follow-up; final mean thyroid volume was 3.3+/-1.1cm(3). End-stage mean thyroid volume was significantly lower in final hypothyroid patients (p<0.05) compared to patients with final normal thyroid function. We conclude that the occurrence of final hypothyroidism is underestimated after subacute thyroiditis. Ultrasonographic follow-up might be helpful in the detection of final hypothyroid-risk patients: thyroid volume not increased in acute stage and lower than 5cm(3) during follow-up is one of the ultrasonographic features of these patients.

Acute Disease↗
PubMedDate not supplied

TV-image analysis based quantification of the proliferative activity and the apoptotic rate in thyroid tumors and thyroiditis.

To analyze the impact of cellular proliferative activity and apoptosis, MIB-1 immunopositivity and the apoptotic rate of normal tissue (n = 20), follicular adenoma (n = 30), follicular carcinoma (n = 32), papillary carcinoma (n = 40), Hashimoto thyroiditis (n = 17) and de Quervain thyroiditis (n = 12) was investigated by means of TV-image analysis. Three-micron sections from paraffin-embedded surgical specimens were investigated. Immunohistochemical reactions were performed using an indirect peroxidase method. For determination of apoptosis the in situ DNA nick-end labeling method (TUNEL) was used. The rate of positive cells was determined using the CM-2 TV-image analysis system (Hund, Wetzlar, Federal Republic of Germany). Forty viewing fields (1.94 mm2) were measured with 20:1 objective mangnification. An average of > 4,400 cells were assessed in each case. The mean MIB-1 immunopositivity was higher in follicular carcinoma (average, 2.30%) than in de Quervain thyroiditis (1.48%), papillary carcinoma (1.26%), Hashimoto thyroiditis (0.97%), follicular adenoma (0.58%) and normal thyroid tissue (0.14%). The apoptotic rates were higher in Hashimoto thyroiditis (4.54%) and de Quervain thyroiditis (3.55%) than in thyroid tumors (0.31%-0.49%) and normal thyroid tissue (0.10%). Calculating the ratio of MIB-1 expression and apoptotic rate, thyroid tumors (12.1-14.6) revealed higher values than normal thyroid tissue (3.6), indicating cell gain. In Hashimoto thyroiditis (1.7) and de Quervain thyroiditis (0.7) the ratio was lower than in normal tissue indicating cell loss. MIB-1 immunohistometry and apoptotic rate quantification present new insights into the proliferative and apoptotic potential of thyroid lesions based on a high number of cells investigated per case. The impact of both methods could be used for the interpretation of diagnostically difficult and inconclusive fine-needle aspirates. However, as there was an overlap of the single values, the results have to be interpreted carefully for diagnostic purposes.

Apoptosis↗
PubMed1994

Ultrasound evaluation of thyroid abnormalities and volume in Chinese adults without palpable thyroid glands.

Typical examination of the thyroid gland involves palpating the patient. If goiter is found, thyroid ultrasonography and/or aspiration cytology is usually performed in addition to assay of thyroid hormones and antibodies. However, palpation may not be sensitive enough to detect thyroid lesions. The purpose of this study was to evaluate the prevalence of thyroid abnormalities detected by ultrasonography in Chinese adults without palpable thyroid glands admitted for health examination. Two hundred and seventy-seven patients (aged 17 to 79 years; mean, 52 years) admitted to National Taiwan University Hospital for health examinations were included in this study. The thyroid was first palpated by a thyroidologist. Goiter was detected in 77 out of 277 patients (27.8%). Two hundred patients who had no palpable goiter underwent thyroid ultrasonography. Thyroid abnormalities were detected in 37 out of 200 patients (18.5%). These included 18 cases of thyroid cyst, 13 cases of solid nodule, and six cases of multiple nodules with ill-defined margins. Patients with thyroid abnormalities were older than those without lesions [59.3 +/- 9.2 years (mean +/- SD) vs 50.1 +/- 12.8 years, p < 0.001]. In addition, we also calculated the thyroid volumes of 163 patients who had neither palpable goiter nor lesions detected by ultrasonography. The thyroid volumes were 7.7 +/- 3.3 mL and positively correlated to the body mass index (BMI, r = 0.17, p < 0.05) and body weight (r = 0.28, p < 0.005). Males (n = 115) had larger thyroid volume than females (n = 48) (8.3 +/- 3.3 vs 6.1 +/- 2.6 mL, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

[The effect of thyroid hormone on thyroid cancer growth].

Differentiated thyroid cancer, like breast cancer, prostatic cancer, and endometrial cancer of the uterus, is well known to be hormone sensitive. Experimental investigations have demonstrated that differentiated thyroid cancer cells have TSH (thyroid-stimulating hormone) receptor on the plasma membrane and that the growth regulation of differentiated thyroid cancer depends upon TSH. Therefore, suppression of TSH with thyroid hormone is rational for the treatment of recurrent thyroid cancer. Recurrent differentiated thyroid cancers reportedly cause regression in response to thyroid hormone administration, but the outcome of adjuvant therapy with thyroid hormone after operation for differentiated thyroid carcinoma is controversial. It is very difficult to analyze the difference in survival rate between the postoperative patient with and without thyroid hormone, because of the excellent postoperative survival rate of differentiated thyroid cancer patients. Further clinical studies and laboratory investigations about TSH suppression in adjuvant therapy for differentiated thyroid cancer are necessary to elucidate the impact of thyroid hormone on survival after operation.

Adult↗
PubMed1989

Relationship between T4, T3 and T4/T3 ratio in thyroid tissue, thyroid and peripheral veins in patients with nontoxic nodular goiter.

The relationship between T4, T3 and T4/T3 ratio in thyroid nodules/paranodular tissues, thyroid and peripheral veins has been investigated in 26 patients with nontoxic nodular goiters; eleven of them were treated with l-thyroxine 150 micrograms daily. A significant correlation between iodothyronine concentrations and T4/T3 [corrected] ratio in paranodular thyroid tissues and thyroid effluents was found in both groups of patients. By contrast, the correlation between these parameters in the nodule and thyroid veins was poor, which implies that the thyroid hormone pattern in the thyroid veins on the side of nodular lesion is predominantly controlled by the release of the hormones from paranodular healthy tissue. A close dependence of the serum T4/T3 ratio on the values of iodothyronines and their ratio in thyroid tissues and thyroid veins was observed in nontreated, but not in treated patients. Conversely, in the latter group, the thyroidal T4/T3 ratio in paranodular tissue, but not in the nodule, was found to be dependent on the serum T4/T3 ratio, suggesting that paranodular thyroid tissue more readily responds to 1-thyroxine-inhibited TSH secretion. The results demonstrate that 1. the serum thyroid hormone pattern under physiological conditions is dependent on the intrathyroidal T4/T3 ratio, and 2. minor alterations in the serum thyroid hormones may secondarily change the thyroidal T4/T3 ratio, presumably by their effect on TSH secretion.

Goiter, Nodular↗
PubMed2002

Pituitary-thyroid axis, thyroid volume and leptin in healthy adults.

OBJECTIVE: Patients with thyroid diseases usually have disturbances relating to body weight and thermogenesis. On the other hand, leptin is involved in the regulation of body weight, food intake and thermogenesis. Some studies have investigated the relationship between leptin and dysthyroid states, but the complex interactions between leptin and pituitary-thyroid axis have led to controversial results. DESIGN: The aims of this cross-sectional study were to investigate the relationship among basal TSH, ultrasonographic thyroid volume and leptin in a group of 268 healthy adults randomly selected from our city, L'Hospitalet de Llobregat, Barcelona, an area free of iodine deficiency. In this euthyroid group, we determined basal TSH, thyroid autoantibodies, leptin concentrations, and thyroid volume by ultrasonography, body anthropometry, and body composition. RESULTS: All subjects were free of goitre and were negative for anti-thyroid antibodies. Basal TSH concentrations were 1.49 +/- 0.8 mU/l in males and 1.67 +/- 0.83 mU/l in females (p = 0.6). Anti-thyroid antibodies were negative in all cases; leptin concentrations were 6.1 +/- 4 ng/ml in males and 16.8 +/- 11.7 ng/ml in females (p = 0.0001). Thyroid volume was 9.8 +/- 4.6 ml in males and 6.5 +/- 2 ml in females (p = 0.001). There were significant correlations among leptin concentrations and anthropometric and body composition variables in both sexes, without correlation with TSH concentrations. There was no significant correlation between anthropometric and body composition variables and thyroid volume in males but there was a correlation in females. In females, there was a positive correlation between leptin and thyroid volume (r = 0.181, p = 0.038). In males, there was a negative correlation between TSH concentrations and thyroid volume (r = - 0.271, p = 0.002). CONCLUSIONS: We did not find any correlation between leptin levels and pituitary-thyroid axis in this control population. The correlation between leptin and thyroid volume in females is probably a consequence that leptin and thyroid volume are regulated in parallel by variables relating to anthropometry and body composition.

Adult↗
PubMed1990

Cytokines, thyroid autoantibody synthesis and thyroid cell survival in culture.

In autoimmune thyroid disease lymphoid cells infiltrating the thyroid gland occur in conspicuous aggregates or as a diffusely distributed population invading the thyroid follicles. Consequently cytokines secreted by activated T cells or macrophages could influence neighbouring thyroid cells as well as other lymphocytes. We have investigated this possibility using recombinant cytokines. Thyroid cell survival was assessed in terms of mitochondrial dehydrogenase activity in monolayers exposed to tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin-1 (IL-1 alpha and beta) and interleukin-2 (IL-2) in the presence or absence of thyroid-stimulating hormone (TSH). Neither TNF-alpha nor IL-2 affected thyroid cell survival, IFN-gamma was usually inhibitory and IL-1 alpha slightly enhanced cell survival in some experiments. However, the effects were small and variable and were not enhanced by potentially synergistic combinations of cytokines, longer periods of exposure, or different culture conditions. In contrast, IFN-gamma, IL-2 and TNF-alpha inhibited the ability of thyroid lymphocytes from patients with Graves' disease and Hashimoto's thyroiditis to synthesize autoantibodies to thyroid peroxidase (TPO) and thyroglobulin (Tg). Comparison of lymphoid populations isolated by digestion and/or mechanical disaggregation indicated that a population of activated B cells, plasma cells and T cells, intimately associated with thyroid cells since they could only be extracted by digestion, was influenced by cytokines. Our studies suggest that in addition to its well-recognized ability to induce MHC class II antigens on thyroid cells, IFN-gamma may inhibit thyroid cell proliferation and TNF-alpha, IFN-gamma and IL-2 may down-regulate thyroid autoantibody synthesis.

Autoantibodies↗
PubMed2005

Risk factors of primary thyroid dysfunction in early infants born to mothers with autoimmune thyroid disease.

AIM: To assess whether the state of maternal thyroid function and the pattern of thyroid alterations during gestation would affect the infants' thyroid function and to evaluate the risk factors affecting early infants' thyroid function by means of multiple logistic regression. METHODS: In a cross-sectional study, 78 neonates born to mothers with Graves disease or Hashimoto thyroiditis were examined and followed clinically and biochemically. Neonates born to healthy mothers during the same period were set as controls. Tests of thyroid function, antithyroid peroxidase antibody (TPOAb), antithyroglobulin antibody (TGAb), anti-TSH receptor antibody (TRAb) and antithyroid-stimulating antibody (TSAb) were performed both in early infants and their mothers. All possible maternal and/or infantile risk factors for thyroid dysfunction during early infancy were analysed by means of multiple-factor logistical regression. RESULTS: The overall prevalence of underlying subtle thyroid abnormalities in these 78 infants was 52.6%, which was significantly higher than that witnessed among infants from healthy mothers (5.4 per thousand, p<0.01). By using multiple logistic regression analysis, the state of maternal thyroid function in gestation, the type of autoimmune thyroid disease during pregnancy and the level of TRAb in the newborn were significantly correlated with the early infants' thyroid dysfunction. CONCLUSION: Maternal autoimmune thyroid disease during pregnancy will affect infant thyroid function. Therefore, appropriate management of maternal autoimmune thyroid disease throughout pregnancy is essential in the prevention of undesirable neonatal outcomes.

China↗
PubMed2004

Id1 gene expression is up-regulated in hyperplastic and neoplastic thyroid tissue and regulates growth and differentiation in thyroid cancer cells.

The Id (inhibitor of DNA binding) proteins are a family of helix-loop-helix (HLH) proteins (Id1, Id2, Id3, and Id4) that lack the basic domain necessary for DNA binding. The Id1 protein enhances cell proliferation and inhibits cellular differentiation in a variety of cell types. We have previously demonstrated that the Id1 gene is up-regulated in papillary and medullary thyroid cancers. In this study we characterized the expression and distribution of the Id1 protein in normal, hyperplastic, and neoplastic human thyroid tissue. We also evaluated the effect of the Id1 gene on thyroid cancer cell growth and markers of thyroid cell differentiation. We used semiquantitative immunohistochemistry to characterize Id1 protein expression in normal, hyperplastic (multinodular goiter and Graves' disease), and neoplastic thyroid tissue from 103 patients. Normal thyroid tissue had the lowest level of Id1 protein expression (P < 0.0001). Anaplastic thyroid cancer had the highest level (vs. benign and malignant thyroid tissues, P < 0.01). Id1 protein expression was higher in malignant thyroid tissue than in hyperplastic thyroid tissue (P < 0.02). We found no significant association between the level of Id1 protein expression and patient age, sex, tumor-node-metastasis stage, tumor size, primary tumor vs. lymph node metastasis, primary tumor vs. recurrent tumors, and extent of tumor differentiation. Inhibiting Id1 mRNA expression in thyroid cancer cell lines using Id1 antisense oligonucleotides resulted in growth inhibition (P < 0.03) and decreased thyroglobulin and sodium-iodine symporter mRNA expression (P < 0.02). In conclusion, Id1 is overexpressed in hyperplastic and neoplastic thyroid tissue and directly regulates the growth of thyroid cancer cells of follicular cell origin, but is not a marker of aggressive phenotype in differentiated thyroid cancer.

Adult↗
PubMed1988

A thyroid cytotoxic antibody that cross-reacts with an eye muscle cell surface antigen may be the cause of thyroid-associated ophthalmopathy.

A hitherto unrecognized thyroid antibody, which reacts with a thyroid cell surface antigen expressed on passaged thyroid cells, was identified in serum from patients with thyroid-associated ophthalmopathy using antibody-dependent cell-mediated cytotoxicity (ADCC) tests. The antibody was detected in 14 of 23 patients with Graves' hyperthyroidism (Gh) and associated ophthalmopathy, in 3 of 4 patients with Hashimoto's thyroiditis (HT) and ophthalmopathy, but in only 1 of 16 patients with Gh without clinically evident eye disease and 4 of 37 patients with HT without eye disease. The ADCC test also was positive in 2 of 30 patients with thyroid cancer, both of whom had had Gh and ophthalmopathy in the past. There was no correlation, in patients with ophthalmopathy, between the levels of the antibody (expressed as percent specific lysis) and the titers of antithyroid microsomal antibody measured using a hemagglutination assay. Based on the results of blocking experiments using mouse monoclonal antibodies against human thyroid peroxidase, now known to be the thyroid microsomal antigen, the corresponding antigen was not thyroid peroxidase. Moreover, the new antigen was expressed on cultured and passaged thyroid cells which do not express the microsomal antigen. In patients with ophthalmopathy there was a close correlation between the degree of lysis of passaged thyroid cells and that of eye muscle cells, and ADCC activity against passaged thyroid cells was absorbed by preincubation of positive serum samples with eye muscle and thyroid cell, but not other cell, monolayers. The reaction of a newly identified cytotoxic thyroid antibody with a shared epitope on eye muscle cells thus appears to be a possible mechanism for the development of ophthalmopathy in patients with Gh and, less often, HT.

Adolescent↗