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At least 109 records · Page 6Linked to original sources

PubMed1979

Evidence that both long-acting thyroid stimulator and long-acting thyroid stimulator-protector stimulate the human thyroid gland.

Thyroid-stimulating immunoglobulins were prepared from two potent sera, one contained long-acting thyroid stimulator (LATS) and the other contained both LATS and LATS-protector (LATS-P). The potencies of the immunoglobulin G (IgG) preparations were estimated in the McKenzie assay. The accumulation of cyclic AMP in mouse thyroid lobes was stimulated only by LATS--IgG; LATS-P--IgG was inactive. In contrast, both LATS-IgG and LATS-P--IgG were equally effective in slices of human thyroid.

Animals↗

PubMed1989

High potential to tumor necrosis factor alpha (TNF-alpha) production of thyroid infiltrating T lymphocytes in Hashimoto's thyroiditis: a peculiar feature of destructive thyroid autoimmunity.

T lymphocytes present in thyroid infiltrates of 6 patients with Hashimoto's thyroiditis (HT) and of 4 patients with Graves' disease (GD) were analyzed at clonal level and their profiles of mitogen-induced lymphokine secretion were characterized. Production of interleukin-2 (IL-2), interleukin-4 (IL-4), interferon-gamma (IFN-gamma) was measured in culture supernatants of a total number of 332 T cell clones (TCC) from HT, of 269 TCC from GD infiltrates and of 266 control TCC derived from normal lymphoid tissues. No significant difference was found in the ability to produce IL-2 between TCC from HT or GD infiltrates and control TCC. The proportion of HT- or GD-derived TCC able to produce IL-4 was extremely low (4 and 5%, respectively) in comparison with controls (19%). In contrast, the proportion of interferon-gamma (IFN-gamma)-producing (IFN-P) TCC derived from either HT (87%) or GD (80%) infiltrates was much higher (p less than 0.0005) than that found in controls (59%). In addition, most of IFN-P TCC from either HT or GD usually released higher amounts (p less than 0.002) of IFN-gamma than did control clones. No significant difference was found between GD infiltrates and controls in the proportions of TCC able to secrete TNF-alpha (39% and 47%, respectively), whereas the proportion of TNF-alpha-producing (TNF-P) TCC derived from HT (78%) was significantly higher (p less than 0.0001). In addition, most of both CD8 and CD4 TCC from HT released higher amounts of TNF-alpha than did TNF-P clones from controls or GD. These data suggest that T cells present in autoimmune thyroid infiltrates share a number of functions, such as high production of IFN-gamma, but differ with regard to their ability to secrete TNF-alpha, which is peculiar of most T cells present in the thyroid of HT patients.

Antigens, Differentiation, T-Lymphocyte↗

PubMed1988

Seronegative Hashimoto thyroiditis with thyroid autoantibody production localized to the thyroid.

A patient without serologic evidence of an autoimmune disorder had a thyroidectomy for neck compression caused by her goiter. Histologic examination of the gland revealed pathologic changes compatible with Hashimoto disease, and lymphocytes isolated from her thyroid gland were transformed into lymphoblastoid cells in vitro by Epstein-Barr virus in the presence of cyclosporine. These cells produced antibodies against thyroglobulin, thyroid microsome, thyrocyte membrane, and thyrotropin, whereas lymphoblastoid cells produced from the patient's peripheral blood lymphocytes showed no antithyroid activity. Several human monoclonal antibodies were produced from the intrathyroidal lymphocytes by fusion with the SHM-D33 heteromyeloma, and the resulting cell lines produced antibodies with high-affinity binding specific for thyroid antigens. These studies show that lymphocytes capable of producing antithyroid antibodies can be present in the thyroid glands of patients with Hashimoto disease without evidence of a peripheral immune response, thus indicating that Hashimoto disease can exist as an organ-restricted autoimmune disorder.

Adipose Tissue↗

PubMed1988

Pituitary-thyroid interaction: effects of thyroid hormone, non thyroidal illness and various agents on TSH secretion.

Recent developments in thyroid hormone metabolism have helped to understand the complex events which characterize the regulation of TSH secretion. Plasma T3 concentration as well as intrapituitary T3 generation from T4, exert a profound effect on TSH synthesis and release. Pituitary Type II deiodinase differs from Type I deiodinase found in other tissue such as liver and kidney, and in fact different conditions such as hypothyroidism and hyperthyroidism affect these enzymes in opposite direction. Thyroid hormones exert other effects on the pituitary such as increased synthesis of substance P, increased synthesis of GH, and decreased TRH receptors, TRH also modifies its own receptors in the pituitary and exerts modulatory effects on TSH molecule. Patients with non thyroidal illness may display TSH molecules with decreased biological activity. Various agents used in every day praxis may alter TSH and thyroid secretion. The physician must be aware of changes in order to avoid diagnostic pitfalls.

Animals↗

PubMed1985

Thyroid iodine content and serum thyroid hormone levels in autoimmune thyroiditis: effect of iodide supplementation.

The relationship between thyroid iodine content (TIC) measured by x-ray fluorescence and serum TSH, T4, and T3 levels was investigated under iodide supplementation (0.5 mg/day for 1 to 9 mo). In five euthyroid control patients, whose TIC ranged from 2.5 to 14 mg, the TIC increased from 1.5 to 4 mg after 4 wk of treatment and had a tendency to plateau when the treatment was pursued. No significant changes in serum T4, T3, and TSH levels have been observed in these control subjects. Fourteen patients with autoimmune thyroiditis with low TIC (0-5 mg) were also studied. In six patients, the TIC increased significantly (3-10 mg over initial value after 3-7 mo of treatment). In parallel, there was a significant increase in serum T4 levels (35-150% over initial value) while T3 levels were modified in only two patients. In five patients serum TSH level decreased and was two- to seven-fold lower than before treatment whatever was its initial value; however, the spectrum of changes varied among patients from slight increase to a complete normalization of hormonosynthesis. In the eight other patients, iodide supplementation aggravated the thyroid disorders during the first months of treatment. The thyroid hormone blood levels dropped significantly in six patients (percent decrease below initial value: 20-100%) and was unchanged in the two others. An increase in the TSH blood level (X2-6) was observed in all patients except one. Concomitantly, the iodine stores were progressively depleted in three patients, unchanged in three and increased in two. When iodide treatment was pursued, an escape from this organification block was observed in two patients.

Adult↗

PubMed1983

Influence of thyroid substitution therapy and thyroid autoantibodies on the value of serum thyroglobulin in recurring thyroid cancer.

The study was performed to evaluate the influence of thyroxine substitution therapy and the presence of thyroglobulin antibodies (TgAb) on the usefulness of serum thyroglobulin (Tg) measurements in the follow-up of patients treated for well differentiated thyroid carcinoma. Seventy-two consecutive patients with differentiated thyroid cancer and eight with medullary carcinoma as well as controls were studied on one or more occasions and blood was drawn for measurement of serum Tg, TgAb, TSH and thyroid hormones. In 23 patients the hormonal substitution was withdrawn and 3-4 weeks later new blood samples and a 131I scintigraphy was performed. Eighteen patients were shown to have recurrence or metastases. Four of these had TgAb, two had normal Tg values, and the remaining 12 had extremely elevated levels. Those with TgAb and normal Tg values all had high Tg levels off thyroxine substitution. The 54 patients without evidence of recurrence had low levels of serum Tg except for one with highly elevated values. Based on the results from this and other studies is concluded that serum Tg is an important adjunct in the follow-up of patients with well differentiated thyroid carcinoma, but certain limiting factors have to be taken into account, i.e., the radicality of surgery, the sufficiency of the substitution, the presence of TgAb and the method for measurement of Tg.

Adolescent↗

PubMed1996

Dominant-negative mutant thyroid hormone receptors prevent transcription from Xenopus thyroid hormone receptor beta gene promoter in response to thyroid hormone in Xenopus tadpoles in vivo.

We describe a dominant-negative approach in vivo to assess the strong, early upregulation of thyroid hormone receptor beta (TR beta) gene in response to thyroid hormone, characteristic of the onset of natural and thyroid hormone-induced amphibian metamorphosis, 3,3',5-Triiodo-thyronine (T3) treatment of organ cultures of premetamorphic Xenopus tadpole tails coinjected in vivo with the wild-type Xenopus TR beta (wt-xTR beta) and three different thyroid responsive element chloramphenicol acetyltransferase (TRE-CAT) reporter constructs, including a direct repeat +4 (DR +4) element in the -200/+87 fragment of the xTR beta promoter, resulted in a 4- to 8-fold enhancement of CAT activity. Two human C-terminal TR beta 1 mutants (delta-hTR beta 1 and Ts-hTR beta 1), an artificial Xenopus C-terminal deletion mutant (mt-xTR beta), and the oncogenic viral homology v-erbA, none of which binds T3, inhibited this T3 response of the endogenous wt-xTR in Xenopus XTC-2 cells cotransfected with the -1600/+87 xTR beta promoter-CAT construct, the potency of the dominant-negative effect of these mutant TRs being a function of the strength of their heterodimerization with Xenopus retinoid X receptor gamma. Coinjection of the dominant-negative Xenopus and human mutant TR beta s into Xenopus tadpole tails totally abolished the T3 responsiveness of the wt-xTR beta with different TREs, including the natural DR +4 TRE of the xTR beta promoter.

Amino Acid Sequence↗

PubMed1989

Differential effects of methylmercuric chloride and mercuric chloride on the histochemistry of rat thyroid peroxidase and the thyroid peroxidase activity of isolated pig thyroid cells.

This study was designed to characterize the interaction of CH3HgCl or HgCl2 with thyroid peroxidase (TPO). Two types of experiments were performed. First, the thyroids from rats that were given 5.6 mg/kg/day of either CH3HgCl or HgCl2 for 2 weeks by intubation were subjected to histochemical treatment and then to electron microscopy. TPO activities in all cell compartments were inhibited by HgCl2 but not by CH3HgCl. Morphological observation showed that taller epithelia were induced by HgCl2, whereas flattened epithelia forming large follicles were induced by CH3HgCl. The serum thyrotropin level was substantially lowered by CH3HgCl but was unchanged by HgCl2. Second, the guaiacol oxidation by TPO in isolated and ruptured pig thyroid cells was spectrophotometrically monitored in the presence of either CH3HgCl or HgCl2. The TPO was not inhibited by CH3HgCl but was inhibited by HgCl2. These results indicated that CH3HgCl induced a hypothyroid state without affecting TPO, whereas HgCl2 inhibited TPO and induced a hypertropic state owing to compensation for loss of enzyme activity, and that the lack of inhibitory activity of CH3HgCl was not due to the inability to penetrate the cells. Therefore, there appeared to be a differential interaction of organic and inorganic forms of mercurials with the thyroid.

3,3'-Diaminobenzidine↗

PubMed1990

Alterations of serum concentrations of thyroid hormones and sex hormone-binding globulin, nuclear binding of tri-iodothyronine and thyroid hormone-stimulated cellular uptake of oxygen and glucose in mononuclear blood cells from patients with non-thyroidal illness.

Nuclear tri-iodothyronine (T3) binding and thyroid hormone-stimulated oxygen consumption and glucose uptake were examined in mononuclear blood cells from patients with non-thyroidal illness (NTI) in which serum T3 was significantly (P less than 0.05) depressed (0.62 +/- 0.12 (S.D.) nmol/l) compared with healthy control subjects (1.45 +/- 0.30 nmol/l). Neither serum TSH nor sex hormone-binding globulin differed from that of the control group. Nuclear T3 binding capacity was increased (P less than 0.05) in patients with NTI (10.1 +/- 3.0 fmol/100 micrograms DNA) compared with controls (2.5 +/- 0.9 fmol/100 micrograms DNA). Unstimulated glucose uptake was increased in cells from patients with NTI (2.03 +/- 0.49 mmol/l per mg DNA per h, P less than 0.01) compared with controls (1.13 +/- 0.20 mmol/l per mg DNA per h). Thyroxine-stimulated glucose uptake (stimulated glucose uptake--unstimulated glucose uptake) was increased in cells from patients with NTI (2.06 +/- 1.67 mmol/l per mg DNA per h, P less than 0.01) compared with controls (0.26 +/- 0.12 mmol/l per mg DNA per h), and T3-stimulated glucose uptake was also increased in cells from patients with NTI (1.34 +/- 0.81 mmol/l per mg DNA per h, P less than 0.05) compared with controls (0.24 +/- 0.10 mmol/l per mg DNA per h). In contrast, neither unstimulated nor thyroid hormone-stimulated oxygen consumption differed. We conclude that both increased nuclear T3 binding and increased thyroid hormone-induced glucose uptake may represent counter-regulatory mechanisms which tend to maintain intracellular homeostasis.

Adult↗

PubMed1987

Detection of thyroid-stimulating antibodies in thyroid diseases, employing rat thyroid fragment perifusion.

The technique of perifusing rat thyroid fragments was used to investigate the presence of thyroid-stimulating antibodies (TSAb) in the sera of 48 patients. Response to IgG was measured by determining the mean rate of release of T4 (R) during a 30-min perifusion and the secretion peak (Imax) by means of samples taken every 5 min. Values found to be above the mean + 2 SD of the control values of R or Imax were considered to be positive. TSAb were found in all the 17 patients with untreated Graves' disease (GD) and in the 2 treated with antithyroid drugs, but not in the 3 who had undergone surgery or 131I treatment or in the 2 on corticosteroid treatment. TSAb were also found in 2 out of 3 patients with untreated nodular toxic goiter (UNTG) and in 6 out of 8 with diffuse nontoxic goiter (DNG) but at lower levels. In the untreated GD group, R and Imax correlated significantly with the corresponding IgG concentrations (from 90 to 800 micrograms/ml), suggesting TSAb activity which can be compared from one patient to another. TSAb activity did not correlate with thyroid function tests in any group. In all the groups it induced an early secretion peak followed by a decreasing response throughout the stimulation period, as was previously found with 65 mIU/ml TSH. The specificity of this technique was verified by five different control methods: the perifusion technique was checked by using KRBG buffer alone; sera were studied from a group of healthy controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Hyperthyroidism with potent thyroid-stimulation-blocking antibodies and negative thyroid-stimulating antibodies after subtotal thyroidectomy for Graves' disease with follicular thyroid carcinoma.

A 39-year-old woman with Graves' disease associated with follicular thyroid carcinoma underwent subtotal thyroidectomy. TSH-binding inhibitor immunoglobulins (TBII) were positive, whereas thyroid-stimulating antibodies (TSAb) and thyroid-stimulation-blocking antibodies (TSBAb) were both negative before the operation. After the operation, TBII markedly increased above the pretreatment value. TSBAb became positive 3 months after the operation and then their activity increased, while TSAb remained negative after the operation. Subtotal thyroidectomy may have influenced the development of TSBAb in this patient. Irrespective of these findings, the patient became hyperthyroid again several months after the operation.

Adenocarcinoma↗

PubMed1991

Studies of CD4+ (helper/inducer) T lymphocytes in autoimmune thyroid disease: demonstration of specific induction in response to thyroid peroxidase (TPO) in vitro and its relationship with thyroid status in vivo.

We have studied by flow cytometric analysis the antigen specific activation of CD4+ (helper/inducer) T lymphocytes by purified human thyroid peroxidase (TPO). Peripheral blood mononuclear cells were obtained from 26 patients with Graves' disease (GD), 16 with Hashimoto's thyroiditis (HT), 7 with nontoxic nodular goiter (NG), and 14 normal subjects (N). Cells were cultured for 7 days in the presence or absence of TPO at final concentrations of 3, 30, and 300 ng/mL. When harvested, cells were reacted with an FITC-conjugated anti-CD4 and a PE-conjugated anti-HLA-DR murine monoclonal antibodies. The percentage of HLA-DR+ CD4+ cells (activated CD4+ cells) was determined by a flow cytometer. In the absence of TPO, CD4+ cells had been activated without any specific stimulant. This is known as the autologous mixed lymphocyte reaction (AMLR). In the AMLR, CD4+ cells from GD and HT were less activated compared to those from NG and N. Results of TPO-specific activation were expressed as an incremental increase of activated CD4+ cells (II) (percentage of activated CD4+ cells cultured with TPO minus percentage of activated CD4+ cells cultured without TPO). II of N, GD, HT, and NG were 0.37 +/- 0.21, 2.20 +/- 0.45,** 2.0 +/- 0.66,* and 0.35 +/- 0.27 (mean +/- SEM), respectively (**p less than 0.01; *p less than 0.05 vs N). When patients were further subdivided, the highest mean II was found in patients with hyperthyroid GD (p less than 0.01), followed by euthyroid HT (p less than 0.05) and euthyroid GD (p less than 0.05), however there was no significant difference between hypothyroid HT and N. In conclusion (1) AMLR reactivity of CD4+ cells from GD and HT was impaired, (2) however, CD4+ cells from both GD and HT were significantly more induced by TPO compared to N, and (3) this induction depends, in part, on the in vivo thyroid status.

Adolescent↗

PubMed1984

[Thyroid functions in nonthyroidal illness: specific changes in serum levels of thyroid hormones related in illness and the correlation between thyrotropin and free thyroid hormones in patients with nonthyroidal illnesses].

In order to assess the thyroid function of patients with nonthyroidal illness, 292 patients with nonthyroidal illness were employed in the present study. These patients were then subdivided into 6 groups according to their original illness. The groups consisted of patients with malignant illnesses (19 males and 10 females; mean age of 59.7 yr.), with chronic hepatitis (14 males and 8 females; mean age of 55.2 yr.), with liver cirrhosis (5 males and 6 females, mean age of 60.4 yr.), with uremia who had been receiving constant hemodialysis 2 approximately 3 times per week (52 males and 38 females; mean age of 48.1 yr.), with diabetes mellitus (50 males and 43 females; mean age of 52.3 yr.) and with cerebrovascular accident (21 males and 26 females; mean age of 74.9 yr.). In addition, 34 healthy persons (15 males and 19 females; mean age of 41.6 yr.) were also employed as controls. Because the differences between mean ages in these groups were significant, the relationship between age and thyroid function was examined. Significant positive correlations between age and total thyroxine (TT4) (r = 0.19; p less than 0.01), and reverse triiodothyronine (rT3) (r = 0.175; p less than 0.01) were found. A negative correlation was also found between age and total triiodothyronine (TT3) (r = 0.231; p less than 0.01). The serum levels of rT3 were elevated in patients with neoplasma and liver cirrhosis but significantly low in patients with uremia. These characteristic findings were correlated with the severity of each original disease such as % motarity, serum levels of cholinesterase, blood urea nitrogens and the blood sugar control in the diabetics. In these circumstances, multiple correlation analyses were performed in order to assess whether there might exist a negative feedback mechanism between thyrotropin and FT4/FT3. The highest partial correlation coefficient was obtained between thyrotropin and FT4. It might, therefore, be concluded that in patients with a nonthyroidal illness, decreased levels of serum thyroid hormones indicate not only the severity of the illness but also the supposed presence of a hypothyroid state.

Adult↗

PubMed1975

Thyroid metabolism in the recessive sex-linked dwarf female chicken. 1. Age related changes in thyroid hormone synthesis and circulating thyroid hormone levels.

Age related changes in the levels of circulating thyroid hormones as well as the type of hormones synthesized in the thyroid glands from normal and sex-linked recessive dwarf, female chickens were studied. The impact of the presence of the dwarf gene on the parameters measured was minimal but significant alterations in the types of hormones produced in the thyroid gland with increasing age were observed. As the birds approached sexual maturity, the synthesis of triiodothyronine increased sharply such that the ratio of triiodothyronine (T3): tetraiodothyronine (T4) was approximately 15:1. This was in contrast to the T3:T4 ratio of younger birds which was approximately 0.7:1.0. This shift in hormone synthesis was reflected in relatively more circulating T3 in laying hens when compared with younger birds. It was also noted that four week old dwarf birds had higher circulating T3 values than those found for the normals.

Age Factors↗

PubMed1995

Self-thyroid epithelial cell (TEC)-reactive CD8+ T cell lines/clones derived from autoimmune thyroiditis lesions. They recognize self-thyroid antigens directly on TEC to exhibit T helper cell 1-type lymphokine production and cytotoxicity against TEC.

Self-thyroid epithelial cell (TEC)-reactive CD8+ and CD4+ T cell lines were established by culturing T cells that infiltrate in autoimmune thyroiditis lesions. We investigated the properties of CD8+ T cell lines and clones in comparison with previously characterized CD4+ T cell lines/clones. Although the recognition of self-Ag by anti-TEC CD4+ T cell lines/clones required the cooperation of syngeneic spleen cells as APC, a representative CD8+ line (N4C) was stimulated with syngeneic TEC in the absence of APC. Precise analysis of MHC restriction using N4C-derived clones revealed that CD8+ clones recognize self-Ag on TEC in the context of class I MHC molecules. Most CD8+ clones were also found to express TCR with V beta specificities that were different from those observed for anti-TEC CD4+ clones. N4C cells produced IL-2, IFN-gamma, and TNF-alpha beta, but not IL-4 and IL-5 after stimulation with TEC, thus exhibiting the profile of lymphokine production similar to that expressed by CD4+ Th1 on one hand, but on the other, they showed the functional property that has not been observed for anti-TEC CD4+ clones. Namely, they elicited appreciable levels of cytolytic effects on syngeneic TEC in a short-term (4-h) 51Cr release assay. Thus, these results indicate that self-TEC-reactive CD8+ T cell lines/clones recognize Ag directly on TEC in a class I MHC-restricted way so as to exhibit various functions including the Th1-like profile of lymphokine production and anti-TEC cytolysis. The results are also discussed in terms of the nature of self-Ag presented with class I MHC molecules on TEC, as well as the potential roles of anti-TEC CD8+ T cells in the pathogenesis of thyroiditis.

Animals↗

PubMed1995

[Estimation of anti-thyroid peroxidase autoantibody (TPOAb) and anti-thyroglobulin autoantibody (TgAb) in patients with various thyroid disease--comparison between histopathological findings and serological results in patients with Hashimoto's thyroiditis].

We compared and evaluated titers of AMC (anti-microsome antibody), and ATG (anti-thyroglobulin antibody) by passive gelatin-agglutination and by radioimmunoassay in 170 sera from 129 patients with various thyroid diseases and 41 normal subjects. The results of conventional ATG and TgAb by RIA correlated (r = 0.731) and those of conventional AMC and TPOAb correlated well (r = 0.907), with discrepancies mostly limited to sera with low antibody titers. Five patients with Hashimoto's thyroiditis showed positive results in AMC, whilst negative in TPOAb. These sera had positive ATG autoantibody and preincubation with thyroglobulin inhibited the agglutination reaction of AMC tests, suggesting ATG producing false positive results in AMC assay. The prevalences of positive TgAb rates were higher than (p < 0.001) ATG in patients with Hashimoto's disease (96.6% vs 50.0%) and Graves' disease (76.9% vs 46.1%). However, the prevalences of positive TPOAb were not different from AMC (Hashimoto's disease 75.9% vs 81.0%: Graves' disease 80.8% vs 76.9%). In patients with Hashimoto's thyroiditis, our study demonstrates the results of TgAb by RIA reflects the pathological findings and the diagnostic sensitivity increases by using in combination with TPOAb.

Adult↗

PubMed1983

Effects of substance P on thyroidal cyclic AMP levels and thyroid hormone release from canine thyroid slices.

A neuropeptide, substance P (1-50 microM) caused a prompt but transient rise in tissue cyclic AMP levels and also increased the release of thyroid hormones from canine thyroid slices. While norepinephrine markedly inhibited the stimulation by TSH of such parameters as reported previously, substance P had no effect. These results suggest that substance P may play a regulatory role in thyroid gland functions in a manner different from norepinephrine.

Animals↗

PubMed1991

Anti-thyroid peroxidase antibodies in sera from healthy subjects and from patients with chronic thyroiditis: differences in the ability to inhibit thyroid peroxidase activities.

A significant percentage (6.4%) of healthy subjects was found to contain anti-thyroid peroxidase (TPO) antibodies in their sera. However, in contrast with IgG from sera of patients with chronic thyroiditis, IgG from sera of healthy subjects did not inhibit TPO activities both in guaiacol and iodide assays. In addition, anti-TPO antibodies from healthy subjects did not block the inhibition of enzyme activities by anti-TPO antibodies from patients. These findings suggest that anti-TPO antibodies from healthy subjects do not bind to the epitopes relating to substrate-combining sites of TPO. Thus, the specificities of anti-TPO antibodies in healthy subjects may differ from those in cases of chronic thyroiditis.

Adult↗