Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “thyroid”

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 487 records · Page 27Linked to original sources
PubMed2003

Grey-scale analysis allows a quantitative evaluation of thyroid echogenicity in the patients with Hashimoto's thyroiditis.

OBJECTIVE: In the present study we have performed a grey-scale quantitative analysis of thyroid echogenicity in the patients affected by Hashimoto's thyroiditis (HT), obtaining a numerical estimate of the degree of hypoechogenicity associated with the appearance of thyroid dysfunction. MATERIALS AND METHODS: The study group included 89 patients with serum positivity for thyroglobulin (TgAb) and/or peroxidase (TPOAb) antibodies. Ultrasound (US) evaluation of thyroid gland and biochemical assay of serum thyrotropin (TSH), free-thyroxine (FT4) and free-triiodiothyronyne (FT3) were performed in all patients, and in 40 healthy subjects enrolled as control group. Thyroid echogenicity was compared with that of the surrounding neck muscles, using the grey-scale histogram analysis. The echogenicity was expressed in grey-scales (GWE). RESULTS: In HT patients, the mean of thyroid echogenicity was lower when compared to the normal thyroid (61.9 +/- 8.3 GWE vs. 71.9 +/- 3.1 GWE; P = 0.01). In all HT patients the lowest limit of thyroid echo distribution was in the echogenicity range of the surrounding muscle, the overlapping ranging between 3.4% and 95.0% (mean +/- SD 48.4 +/- 20.9%). The extension of like-muscle hypoechogenicity into the thyroid gland was significantly correlated with serum TSH values (r = 0.37; P < 0.001), serum FT4 values (r = -0.60; P < 0.001), and serum TPOAb values (r = 0.31; P = 0.004). Nobody was hypothyroid when the hypoechogenicity was less than 38.0%, whereas hypothyroidism occurred in all cases with hypoechogenicity of more than 68.9%. The receiving operating characteristic curve demonstrated that 48.3% was the best cut-off for identifying hypothyroid patients with sensitivity, specificity and diagnostic accuracy of 88.9%, 86.3% and 87.6%, respectively. CONCLUSIONS: In conclusion, the grey-scale quantitative analysis has provided a measure of thyroid hypoechogenicity associated with the appearance of hypothyroidism during the course of HT. The results of the present study would encourage the application of the computerized grey-scale analysis as complementary tool to US evaluation in the patients affected by HT.

Adult↗
PubMed2002

Hashimoto's thyroiditis shares features with early papillary thyroid carcinoma.

Neoplastic transformation is a multistep process that results in a continuous spectrum from the normal (physiological) state to a fully established neoplasm. The gold standard for diagnosis of papillary thyroid carcinoma is conventional histology, the essential element being the characteristic nuclear features, regardless of whether papillary structures are present or not. However, other criteria are being used increasingly in the diagnosis of neoplasms, including immunohistochemical staining and molecular profile. The RET/PTC gene rearrangement is highly specific for papillary thyroid carcinoma and is associated with the characteristic nuclear features seen in papillary thyroid carcinoma. There is an overlap in the morphological features, immunohistochemical staining pattern, and most importantly, molecular profile between papillary thyroid carcinoma and Hashimoto's thyroiditis. Although considered a 'benign' condition, Hashimoto's thyroiditis almost always harbours a genetic rearrangement that is strongly associated with and is highly specific for papillary thyroid carcinoma. Submicroscopic foci of papillary thyroid carcinoma must be present in Hashimoto's thyroiditis, although the clinical behaviour is still benign. Further studies are required to predict which foci will progress to papillary thyroid carcinoma.

Carcinoma, Papillary↗
PubMedDate not supplied

Thyroid hormone regulation of Xenopus laevis metamorphosis: functions of thyroid hormone receptors and roles of extracellular matrix remodeling.

The regulatory effects of the thyroid hormone on amphibian metamorphosis is mediated by thyroid hormone receptors. Using Xenopus laevis as a model system, we and others have shown that the mRNA levels of thyroid hormone receptors and 9-cis retinoic acid receptors, which form the functional heterodimers with thyroid hormone receptors, are regulated temporally in a tissue-dependent manner so that high levels of their mRNAs are present in an organ when metamorphosis is occurring. By overexpressing thyroid hormone receptors, 9-cis retinoic acid receptors, or both into developing Xenopus embryos, we have shown that both thyroid hormone receptors and 9-cis retinoic acid receptors are required for mediating the effects of thyroid hormone on embryo development and precocious but specific regulation of the genes, which are normally regulated by thyroid hormone during metamorphosis. Analyses of the developmental expression of one class of thyroid hormone response genes, which encode extracellular matrix-degrading metalloproteinases, suggest that extra cellular remodeling plays an important role during tissue remodeling, including cell death (apoptosis) and cell proliferation and differentiation. This effect of extracellular matrix on cell behavior has been supported directly by in vitro primary cell culture experiments, in which intestinal epithelial cells undergo thyroid hormone-induced apoptosis, just like that during natural metamorphosis.

Animals↗
PubMed2001

Thyroid function, thyroid immunoglobulin status, and urinary iodine excretion after enteral contrast-agent administration by endoscopic retrograde cholangiopancreatography.

BACKGROUND AND STUDY AIMS: The aim of this study was to examine the occurrence of clinically relevant changes in thyroid function after enteral administration of contrast agent by endoscopic retrograde cholangiopancreatography (ERCP). PATIENTS AND METHODS: In this study 70 patients without a history of thyroid disease who had not recently undergone thyroid-specific or thyroid-influencing therapy were examined. Patients were examined on two or three occasions using a standardized questionnaire regarding symptoms of hypothyroidism and hyperthyroidism. The parameters of thyroid function (TT3, TT4, FT4, thyroid-stimulating hormone (TSH)) and urinary iodine excretion were measured on day 0 and on day 21 post-ERCP, and in 23 patients additionally on day 42 post-ERCP. Based on ultrasonographic results, four groups differing in thyroid morphology were distinguished. RESULTS: The data show that an average amount of only 4.7 g of enterally applied iodine is associated with a lasting decrease of TSH, especially in patients with enlarged organs with nodular transformation. As far as TT3 is concerned, there was a significant increase in all patient groups; regarding FT4 we only observed a marked increase in the group with enlarged, nodular thyroid glands. There was a notable increase in urinary iodine excretion on day 21, and a further increase on day 42 post-ERCP. Clinical symptoms of hyperthyroidism did not occur. CONCLUSIONS: We conclude that before administration of iodine-containing contrast agent for ERCP in patients without a history of thyroid disease, thyroid ultrasonographic examination, rather than TSH measurements, should be performed, in order to identify patients already at risk for hyperthyroidism before diagnostic enteral contrast-medium application.

Administration, Oral↗
PubMed2002

A thyroid hormone antagonist that inhibits thyroid hormone action in vivo.

We have characterized the newly developed thyroid hormone antagonist NH-3 in both cell culture and in vivo model systems. NH-3 binds Xenopus laevis thyroid hormone receptors directly in vitro and induces a conformation distinct from agonist-bound receptors. Transcriptional activation of a thyroid hormone response element-containing reporter gene is strongly inhibited by NH-3 in a dose-dependent manner. In addition, NH-3 prevents X. laevis thyroid hormone receptors from binding to the p160 family of co-activators GRIP-1 and SRC-1 in a two-hybrid assay. To assess the potency of the compound in vivo, we used induced and spontaneous X. laevis tadpole metamorphosis, a thyroid hormone-dependent developmental process. NH-3 inhibits thyroid hormone-induced morphological changes in a dose-dependent manner and inhibits the up-regulation of endogenous thyroid hormone-responsive genes. Spontaneous metamorphosis is efficiently and reversibly arrested by NH-3 with at least the same effectiveness as the thyroid hormone synthesis inhibitor methimazole. Therefore, NH-3 is the first thyroid hormone antagonist to demonstrate potent inhibition of thyroid hormone action in both cell culture- and whole animal-based assays.

Acetates↗
PubMed2002

Tc-99m-tetrofosmin thyroid scan in patients with low I-131 thyroid uptake.

UNLABELLED: Low 24-hour thyroid uptake of I-131 (I-131 uptake) is a common finding that influences evaluation of the thyroid gland. METHODS: We studied 20 female patients aged 16-82 years with low I-131 uptake. The following causes of reduced I-131 uptake were defined as (A) six cases with subacute thyroiditis, (B) seven cases with T4 suppression therapy, and (C) seven cases with iodinated pharmaceuticals use. Thirty-minute Tc-99m tetrofosmin thyroid scan was performed within 24 hours of the I-131 thyroid study. RESULTS: The results were correlated with neck ultrasound, serum TSH and biopsy histopathological findings. Tc-99m tetrofosmin thyroid scans revealed 10 normal thyroids, five diffuse goiters, four multinodular goitres, and one solitary thyroid nodule. CONCLUSIONS: Our results suggest that Tc-99m tetrofosmin thyroid scans may provide additional information to diagnose thyroid pathology in patients with low 24-hour I-131 uptake.

Adolescent↗
PubMed1991

Asymptomatic autoimmune thyroiditis and thyroid dysfunction in Alport's syndrome. A report of three families.

The purpose of this study was to investigate the significance of serum antithyroid antibodies in Alport's syndrome. Thyroid microsomal and thyroglobulin antibodies were assessed in three families with Alport's syndrome for a total of 11 patients and 17 healthy relatives, as well as in 40 haemodialysis patients and in 40 healthy subjects. Thyroid function tests, including the measurement of serum total thyroxine (TT4), total triiodothyronine (TT3), free thyroxine (fT4) and free triiodothyronine (fT3) concentrations, and thyrotropin-releasing hormone (TRH) stimulation tests were performed in all patients and subjects. Among patients with Alport's syndrome, five (45%) had elevated titres of thyroid microsomal antibodies and eight (73%) had positive titres of thyroglobulin antibodies, whereas only one healthy relative (6%) had circulating antithyroid antibodies. Fine-needle aspiration biopsy of the thyroid demonstrated a lymphocytic infiltration that indicated the existence of asymptomatic autoimmune thyroiditis in all five patients with elevated thyroid microsomal antibody titres. The prevalence of antithyroid antibodies in healthy subjects and in haemodialysis patients was 7.5% and 12.5% respectively. Functional tests demonstrated a thyroid dysfunction in four of five patients with asymptomatic autoimmune thyroiditis. Two patients had evidence of subclinical hypothyroidism. Two other patients, both with end-stage renal failure, showed a blunted TSH response to TRH, increased fT4 and elevated borderline fT3. The present study indicates that elevated titres of serum antithyroid antibodies may be detected in patients with Alport's syndrome. These patients are at risk of developing asymptomatic autoimmune thyroiditis and thyroid dysfunction. Subclinical hypothyroidism and, perhaps, preclinical hyperthyroidism may be found in these patients.

Adult↗
PubMed1992

Thyroid cells in Graves' disease and Hashimoto's thyroiditis stimulate allogeneic T cells when pretreated with phorbol ester.

OBJECTIVE: To assess the capacity of thyroid follicular cells to function as antigen presenting cells, we have examined their ability to stimulate allogeneic T cells. DESIGN: Thyroid follicular cells were pretreated with interferon-gamma or phorbol myristate acetate, washed thoroughly, and their capacity to induce allogeneic T cell proliferation was determined. PATIENTS: Thyroid cells were prepared using thyroidectomy specimens from eight patients with Graves' disease, one with Hashimoto's thyroiditis and two with non-toxic multinodular goitre. MEASUREMENTS: T cell 3H-thymidine incorporation was measured after a 16-hour incubation period with the isotope, 3 days after co-culture of T cells and thyroid cells. RESULTS: Four of the eight thyroid cell preparations from thyroid autoimmunity patients failed to stimulate T cells, although there was a significant, weak stimulation for the whole group (P < 0.05): interferon-gamma pretreatment had no effect on this. Phorbol myristate acetate pretreatment significantly increased the ability of thyroid cells (from both autoimmune and multinodular glands) to stimulate T cells (P < 0.05); this was time and concentration dependent. Cell fixation after PMA treatment did not abolish this stimulatory activity, which could be transferred by supernatants from unfixed cells; exogenous interleukin-1 did not mimic the activity. CONCLUSIONS: Thyroid cells expressing major histocompatibility complex class II molecules only weakly and inconsistently stimulate allogeneic T cells, compared to thyroid cells pretreated with phorbol myristate acetate, a difference which may be due to the expression of an unidentified co-stimulatory signal induced by phorbol ester.

Antigen-Presenting Cells↗
PubMed1975

Free diiodotyrosine effects on protein iodination and thyroid hormone synthesis catalyzed by thyroid peroxidase.

Free diiosotyrosine exerts two opposite effects on the reactions catalyzed by thyroid peroxidase, thyroglobulin iodination and thyroid hormone formation. 1. Inhibition of thyroglobulin iodination catalyzed by thyroid peroxidase was observed when free diiodotyrosine concentration was higher than 5 muM. This inhibition was competitive, suggesting that free diiodotyrosine interacts with the substrate site(s) of thyroid peroxidase. Free diiodotyrosine also competively inhibited iodide peroxidation to I2. 2. Free diiodotyrosine, when incubated with thyroid peroxidase in the absence of iodide was recovered unmodified; in the presence of iodide an exchange reaction was observed between the iodine atoms present in the diiodotyrosine molecule and iodide present in the medium. Using 14C-labelled diiodotyrosine, 14C-labelled non-iodinated products were also observed, showing that deiodination occurred as a minor degradation pathway. However, no monoiodo[14C]tyrosine or E114C]tyrosine were observed. Exchange reaction between free diiototyrosine and iodide is therefore direct and does not imply deiodination-iodination intermediary steps. Thyroglobulin inhibits diiodotyrosine-iodide exchange and vice versa, again suggesting competition for both reactions. These results support, by a different experimental approach, the two-site model for peroxidase previously described by us in this journal. 3. Free diiodotyrosine when present at a very low concentration, 0.05 muM, exerts a stimulatory effect on throid hormones synthesis. The relationship between diiodotyrosine concentration and thyroid hormone synthesis give an S-shaped curve, suggesting that free diiodotyrosine acts as a regulatory ligand for thyroid peroxidase. Evidence is also presented that free diiodotyrosine is not incorporated into thyroid hormones. Therefore, thyroid peroxidase catalyzes only intra-molecular coupling between iodotyrosine hormonogenic residues. 4. Finally, although no direct proof exists that these free diiodotyrosine effects upon thyroglobulin iodination and thyroid hormone synthesis are physiologically significant, such a possibility deserves further investigation.

Animals↗
PubMed1989

Thyroid gland: US screening in middle-aged women with no previous thyroid disease.

To determine the prevalence of thyroid nodules in the healthy population, ultrasonography (US) of the thyroid gland was performed in 101 women aged 49-58 years in an urban area in southern Finland where goiter is not considered endemic. Subjects with any previous thyroid disease were excluded. Thyroid nodules or abnormalities of the echo structure were found in 36 (35.6%) subjects. Seventeen (47.2%) subjects had solitary nodules, 14 (38.9%) had multiple nodules, and five (13.9%) had diffuse abnormalities. Subjects with abnormal findings at US were further examined with fine-needle aspiration biopsy. Clinical examination and blood tests were performed for evaluation of levels of thyroxine, thyroid-stimulating hormone, and thyroid antibodies. One patient had a leukemic thyroid nodule, but no primary thyroid malignancies were found. In most cases, cytologic findings were benign and nonspecific, with a variable amount of degenerative changes. Three atoxic multinodular goiters and two cases of Hashimoto thyroiditis were detected. The results are in accordance with autopsy studies indicating that focal nodular changes of the thyroid gland are common in middle-aged women.

Biopsy, Needle↗
PubMed1994

Immunization against vasoactive intestinal peptide does not affect thyroid hormone secretion or thyroid blood flow.

Vasoactive intestinal peptide (VIP) is present in thyroid parasympathetic nerves. To assess the involvement of endogenous VIP in the regulation of thyroid function, blood levels of thyroid hormones and thyroid blood flows (TBF) were measured after systemic immunization against VIP or after transection of the superior laryngeal nerves in male rats, which reduced the thyroid content of VIP but did not affect blood levels of thyroid hormones or TBF. Anti-VIP monoclonal antibody or anti-VIP serum was used for immunization against VIP in normal rats. In addition, VIP antibody was given to rats fed an iodine-deficient diet for 5 days to examine the involvement of this peptide in iodine deficiency-induced increases in TBF. Effects were measured at different times (90 s, 30 min, 1 h, and 5 days) after immunoneutralization, but none of these treatments changed blood levels of thyroid hormones or TBF in normal or iodine-deficient rats. However, passive immunization against VIP was associated with a high binding capacity of rat plasma to VIP, and this treatment reduced blood levels of prolactin as well as blood flows to the duodenum, stomach, and lung. These findings suggest that the VIP present in thyroid nerves is not involved in maintaining basal thyroid hormone secretion or TBF and that this neuropeptide does not mediate thyroid vascular adjustments to dietary iodine deficiency.

Animals↗
PubMed1997

Thyrotropin regulation by thyroid hormone in thyroid hormone receptor beta-deficient mice.

Thyroid hormone responsive genes can be both positively and negatively regulated by thyroid hormone. TSH is down-regulated by thyroid hormone and rises during thyroid hormone deprivation. Because both thyroid hormone receptor (TR) alpha and beta genes are expressed in the pituitary gland, it is unclear what the relative roles of TR alpha and TR beta are in TSH regulation. Experiments using over expression of artificial genes have yielded conflicting results. The TR beta knock-out mouse that lacks both TR beta1 and TR beta2 isoforms provides a model to examine the role of these receptors in TSH regulation. TR beta deficient (TR beta-/-) and wild-type (TR beta+/+) mice of the same strain were deprived of thyroid hormone by feeding them a low iodine diet containing propylthiouracil and were then treated with different doses of L-T3 and L-T4. Thyroid hormone deprivation rapidly increased the serum TSH level in both TR beta+/+ and TR beta-/- mice, reaching a similar level in the absence of thyroid hormone. In contrast, the decline of serum TSH by treatment with both L-T3 and L-T4 was severely blunted in TR beta-/- mice, and full suppression was not achieved with the maximal L-T3 dose of 25 microg/day x mouse. These data indicate that TR beta is not required for the up-regulation of TSH in thyroid hormone deficiency. However, although TR alpha alone can mediate thyroid hormone induced TSH suppression, TR beta enhances the sensitivity of TSH down-regulation and may be essential for the complete suppression of TSH.

Animals↗
PubMed2004

Retinoic acid and retinoid X receptors are differentially expressed in thyroid cancer and thyroid carcinoma cell lines and predict response to treatment with retinoids.

Therapy for patients with advanced thyroid carcinoma is limited. Clinical and in vitro studies suggest that some patients with advanced thyroid cancer may respond to therapy with retinoic acid. mRNA expression of the six retinoic acid (RAR) and retinoid X receptor (RXR) isoforms (RARalpha, -beta, -gamma and RXRalpha, -beta, -gamma) was measured in four human thyroid cell lines, and protein expression was subsequently measured in 10 thyroid cancer cell lines. Two isoforms, RARbeta and RXRgamma, were differentially expressed in the four cell lines. Comparison of 10 thyroid tumors and matched normal thyroid tissue confirmed differential tumor expression of RARbeta and RXRgamma and lack of the RXRgamma isoform in normal thyroid tissue. Cell lines expressing both RARbeta and RXRgamma demonstrated significant growth suppression when treated with retinoids, whereas cell lines lacking these isoforms were unaffected. Expression of RARbeta, the isoform associated with suppression of tumor growth in other cancer types, was not affected by treatment with retinoids in the thyroid cancer cell lines. LG346 increased apoptosis and decreased cells in the S-phase in an anaplastic carcinoma cell line, suggesting that this retinoid causes growth suppression of these cells by multiple mechanisms. In summary, we identified the RARbeta and RXRgamma isoform to be differentially expressed in thyroid cancer cell lines and tumor tissue. These isoforms seem to predict response to retinoid therapy in thyroid cancer cell lines.

Antineoplastic Agents↗
PubMed1976

Lymphocyte transformation in response to human thyroid extract in patients with subacute thyroiditis.

Seven patients with subacute thyroiditis were studied for evidence of cell-mediated immunity (CMI) to human thyroid extract, as judged from lymphocyte transformation responses, measured by the increase in labeled thymidine uptake in vitro. Significant transformation was observed in lymphocytes from five of the seven patients with active subacute thyroiditis, and in the lymphocytes from only three of 15 patients with Graves disease (x2, P EQUALS 0.036). Repeated studies of lymphocyte transformation were done in four of the patients with subacute thyroiditis, three of whom initially showed abnormal responses. By eight weeks after initial studies, when all patients were in clinical remission without treatment, transformation responses were within the normal range. Thyroid antibodies were absent or present in low titer (is less than 1:100) in sera of patients with subacute thyroiditis, and became undetectable by eight weeks in those patients initially positive. In contrast, significant titers of antithyroid antibodies were frequently present in patients with Graves' disease. The present studies have shown the occurence of CMI to thyroid antigens during the active phase of subacute thyroiditis. The abnormality was transient, however, since it disappeared when the disease had resolved. These findings strongly suggest that the release of thyroid antigen leading tothe development of a cell-mediated immune responses is not in itself sufficient to initiate chronic immunological disease of the thyroid. If, as some have suggested, Hashimoto's disease or Graves' disease are characterized by a permanent disorder of CMI, then in these diseases either the antigenic stimulus is persistent or there exists an intrinsic disorder of immune surveillance.

Acute Disease↗
PubMed1986

Cytolytic T lymphocytes with natural killer activity in thyroid infiltrate of patients with Hashimoto's thyroiditis: analysis at clonal level.

T Lymphocytes from thyroid infiltrates and peripheral blood (PB) of 3 patients with Hashimoto's thyroiditis (HT) were cloned using a microculture system previously shown to allow the clonal expansion of virtually all PB T lymphocytes from normal individuals. The phenotypic and functional features of a total number of 153 clones from thyroid infiltrates and 206 clones from PB were examined and compared with those of 272 clones derived from normal PB and spleens. The majority of clones derived from thyroid infiltrates of patients with HT had the cytotoxic/suppressor (T8+) phenotype, whereas the majority of clones from PB expressed the helper/inducer (T4+) phenotype. In addition, a consistent proportion (25%) of clones derived from PB of one patient had a phenotype (T3+T4-T8-) that was only occasionally found on clones obtained from PB or spleens of normal subjects. Most clones derived from both PB and thyroid infiltrates of the patients with HT had cytolytic activity, assessed by a lectin-dependent cytolytic assay against the murine P815 tumor cell line. The high frequency of cytotoxic T cells in thyroid infiltrates was related to the increased proportion of T8+ cells, whereas enhanced percentages of cytotoxic cell precursors with T4+ and T3+T4-T8- phenotypes primarily accounted for the high frequency of cytolytic T cells in the PB of the same patients. Many cytolytic T cell clones derived from thyroid infiltrates also had natural killer activity against human K562 and MOLT-4 target cells. These data provide the first functional analysis of T lymphocytes infiltrating the thyroid gland in patients with HT and suggest that the high proportions of cytolytic T cell precursors found in both thyroid infiltrates and PB of these patients may be of importance in determining the tissue damage in thyroid autoimmune disease.

Antibodies, Monoclonal↗
PubMed1995

Effect of thyrotropin-releasing hormone on serum thyroid hormones: a study in the patients with untreated and treated Graves' disease and subacute thyroiditis.

In order to investigate the extrapituitary action of TRH on the thyroid, serum T3, T4, and TSH levels after im administration of TRH were analyzed in 63 patients with untreated hyperthyroid Graves' disease, in 60 euthyroid patients with treated Graves' disease, in 8 patients with subacute thyroiditis, and in 140 healthy subjects. TRH administration in the healthy subjects resulted in a significant increase in serum T3 and T4 levels after 2 h. However, in the patients with untreated hyperthyroid Graves' disease, a significant decrease in serum T3 and T4 levels with undetectable TSH was found 2 h after TRH administration. In the patients with subacute thyroiditis, serum T3 levels also significantly decreased after TRH administration. When a decrease in serum T3 and T4 levels after TRH administration in the patients with hyperthyroid Graves' disease was analyzed in terms of thyroid microsomal antibody and thyroglobulin antibody, a decrease in serum T3 and T4 levels was largest in patients with thyroid microsomal antibody and thyroglobulin antibody. In contrast, an increase in serum T3 and T4 levels in response to TRH in the euthyroid patients with Graves' disease was largest in patients without thyroid autoantibodies. It is concluded that TRH acts directly on the thyroid to suppress the thyroid hormone secreting activity in the absence of circulating TSH and that thyroid autoantibodies affect thyroidal response after TRH administration.

Adolescent↗
PubMed1996

Relationship of antibodies to thyrotropin receptors and to thyroid ultrasonographic volume in euthyroid and hypothyroid patients with autoimmune thyroiditis.

It has been reported in hypothyroid patients with Hashimoto's thyroiditis and in patients with primary myxoedema that antibodies (Ab) to the TSH-receptor (R), which inhibit the thyroid gland, decrease both thyroid hormonogenesis and cell growth in vitro. We investigated, in 169 newly diagnosed patients with euthyroid (n = 83) or hypothyroid (n = 86) autoimmune thyroiditis, the relationship between thyroid autoimmunity expression and thyroid ultrasonographic volume or thyroid hormonal status. In patients positive for TSH-receptor (R) antibodies (Ab), negative correlations (P < 0.01) were found between TSH-R Ab levels and free T4 (FT4) values in a euthyroid (r = -0.63), as well as in a hypothyroid (r = -0.54) state, and between TSH-R Ab and total thyroid volume (TTV) values in an euthyroid (r = -0.62) as well as in a hypothyroid (r = -0.53) state. In contrast, no positive correlations were found between TSH levels and FT4 values or TTV levels in patients positive as well as negative for TSH-R Ab in an euthyroid or in a hypothyroid state. These data demonstrate in vivo, that, in contrast to TSH, TSH-R Abs are related to both thyroid hormonal production and volume in euthyroid or hypothyroid patients with autoimmune thyroiditis.

Adolescent↗
PubMed2003

Copper, zinc, and selenium in whole blood and thyroid tissue of people with various thyroid diseases.

We investigated the possible differences among the concentrations of copper, zinc, and selenium, and their mutual relations in the whole blood and thyroid tissue of patients with various thyroid disorders. Trace elements were determined by total-reflection X-ray fluorescence. The mean levels of these metals in blood as well as the mean Cu/Zn, Cu/Se, and Zn/Se ratios in the patients with thyroid cancer were significantly higher that in other patients and the control groups. However, the mean Zn and Se concentrations in the thyroid cancer tissue were significantly lower than in the thyroid tissue of other patients. In addition, the mean Cu/Zn and Cu/Se ratios in the thyroid cancer tissue were significantly higher than in the patients with other thyroid diseases. We confirm that the highest levels of copper and zinc as well as the Cu/Zn, Cu/Se, and Zn/Se ratios in the whole blood of the patients with thyroid cancer may suggest the progression of the proliferation process in the thyroid gland. We suggest that the low concentrations of zinc and selenium in the thyroid tissue confirm their participation in the carcinogenic process.

Adolescent↗