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At least 127 records · Page 7Linked to original sources
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↗
PubMed1999

Involvement of protein kinase Cepsilon (PKCepsilon) in thyroid cell death. A truncated chimeric PKCepsilon cloned from a thyroid cancer cell line protects thyroid cells from apoptosis.

The protein kinase C (PKC) family has been implicated in the regulation of apoptosis. However, the contribution of individual PKC isozymes to this process is not well understood. We reported amplification of the chromosome 2p21 locus in 28% of thyroid neoplasms, and in the WRO thyroid carcinoma cell line. By positional cloning we identified a rearrangement and amplification of the PKCepsilon gene, that maps to 2p21, in WRO cells. This resulted in the overexpression of a chimeric/truncated PKCepsilon (Tr-PKCepsilon) mRNA, coding for N-terminal amino acids 1-116 of the isozyme fused to an unrelated sequence. Expression of the Tr-PKCepsilon protein in PCCL3 cells inhibited activation-induced translocation of endogenous PKCepsilon, but its kinase activity was unaffected, consistent with a dominant negative effect of the mutant protein on activation-induced translocation of wild-type PKCepsilon and/or displacement of the isozyme to an aberrant subcellular location. Cell lines expressing Tr-PKCepsilon grew to a higher saturation density than controls. Moreover, cells expressing Tr-PKCepsilon were resistant to apoptosis, which was associated with higher Bcl-2 levels, a marked impairment in p53 stabilization, and dampened expression of Bax. These findings point to a role for PKCepsilon in apoptosis-signaling pathways in thyroid cells, and indicate that a naturally occurring PKCepsilon mutant that functions as a dominant negative can block cell death triggered by a variety of stimuli.

Amino Acid Sequence↗
PubMed1999

Methimazole and propylthiouracil increase cellular thyroid peroxidase activity and thyroid peroxidase mRNA in cultured porcine thyroid follicles.

Methimazole (MMI) and propylthiouracil (PTU) are common antithyroid drugs for treating hyperthyroidism because the 2 drugs inhibit thyroid peroxidase (TPO)-catalyzed thyroid hormone formation. We studied whether the 2 drugs actually inhibit cellular TPO activity in cultured porcine follicles. Porcine follicles were cultured in the presence of 1 mU/mL thyrotropin (TSH) for 7 days. Then follicles were exposed to MMI or PTU in the presence of 0.1 microM Kl for 2 days. TPO activity was measured in the 100,000 x g-pellet of the thyroid sonicate by the guaiacol oxidation method. Exposure to MMI (1 microM and 10 microM) or PTU (10 microM and 100 microM) for 2 days caused a significant increase in cellular TPO activity; 100 microM MMI inhibited cellular TPO activity. The presence of cyclic adenosine monophosphate (cAMP)-generating system (forskolin) in TSH-free medium increased MMI-mediated TPO activity. Cyclohexamide inhibited MMI-mediated TPO activation, indicating that new protein synthesis is required for increased TPO activity. Reverse transcriptase-polymerase chain reaction (RT-PCR) showed an increase in TPO mRNA by PTU or MMI. In conclusion, MMI and PTU at therapeutic concentrations can increase TPO mRNA and cellular TPO activity, although the 2 drugs inhibit the TPO-H2O2-mediated catalytic reaction.

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↗
PubMed1982

The involvement of the pentose shunt in thyroid metabolism after stimulation with TSH or with immunoglobulins from patients with thyroid disease. 1. The generation of NADPH in relation to stimulation of thyroid growth.

It has been shown previously that both thyrotrophin (TSH), and also immunoglobulins (Ig) derived from patients with goitrous Graves' disease, stimulate DNA-synthesis in guinea-pig thyroid tissue maintained in vitro. Here we describe the use of the same in vitro system and methods of quantitative cytochemistry to test the effect of these substances on the generation of NADPH, which is another indicator of the potential for growth. As could be predicted by its trophic action, TSH stimulated the generation of NADPH by glucose 6-phosphate dehydrogenase. The Ig-fraction from normal subjects depressed this activity. The Ig-fraction from Graves' disease patients with goitres stimulated the generation of NADPH, whereas the Ig from patients with Graves' disease but with minimal enlargement of the thyroid gland behaved like normal Ig. A similar lack of stimulation was found with Ig from patients with Pendred's syndrome, other dyshormonogenetic goitres, and autonomous single adenomas. In all specimens tested, there was good correlation between the amount of DNA-synthesis, measured by Feulgen cytophotometry, and the activity of glucose 6-phosphate dehydrogenase activity that generated NADPH. These results support the concept that there is a distinct type of autoantibody that influences thyroid growth.

Animals↗
PubMed1990

Thyroid function in choriocarcinoma: demonstration of a thyroid stimulating activity in serum using FRTL-5 and human thyroid cells.

Hyperthyroidism is a well recognized complication of gestational trophoblastic tumours (GTT) and may be due to high circulating concentrations of human chorionic gonadotrophin (hCG) or its variants. We have studied 24 clinically euthyroid women with GTT. Eight were biochemically hyperthyroid with low or undetectable serum thyrotrophin (TSH) and had a mean serum hCG of 361.2 x 10(3) IU/l compared to 76.2 x 10(3) IU/l in the other patients (P less than 0.01). Purified hCG stimulated iodide uptake into FRTL-5 cells with 25 x 10(3) IU/l being equivalent in potency to 1 mU/l of thyrotrophin (TSH). Sixteen out of the 24 sera (67%) stimulated iodide uptake when applied to the cells at a 1:10 dilution. Sera from all eight hyperthyroid patients contained thyroid stimulating activity. The mean hCG concentration in the 16 stimulatory sera was 238.2 x 10(3) IU/l compared to 37.1 x 10(3) IU/l in the other eight sera (P less than 0.01). Six men with hCG-secreting testicular tumours were biochemically euthyroid although three of their sera stimulated iodide uptake into FRTL-5 cells. In human thyroid cells the mean cAMP production over 4 h with sera from five healthy controls was 54.2 +/- 1.81 pmol/mg cell protein compared to 67.0 +/- 3.8 pmol/mg protein with sera from five choriocarcinoma patients (P less than 0.02). Serum from patients with gestational trophoblastic tumours contains a thyroid stimulating activity which may be hCG and whose presence correlates with hyperthyroidism.

Adolescent↗
PubMed1994

Thyroid peroxidase prevails over thyroid microsomal and thyroglobulin antibodies in thyroidal and nonthyroidal illnesses.

Autoimmune thyroid disease is usually related to the presence of autoantibodies (TPO, TMA, TGA, TSH-R) in patients' sera. In this study the presence of autoantibodies in the sera of patients with thyroid disease, patients with end-stage renal disease and in several groups of euthyroid subjects have been evaluated (N = 217). The percentages of positive values detected in six groups ranged: 0-47%, 2-94% and 3-100% for TGA, TMA, and TPO, respectively. Autoantibodies were mostly present in the sera of patients with Hashimoto thyroiditis (TPO 100%, TMA 94%, TGA 47%), and sporadically in the control subjects (TPO 4%, TMA 2%, TGA 0%). Authors's results confirm the prevalence of TPO over TGA and TMA in the sera of all investigated groups. The authors did not find changes in ATA levels during methimazole therapy of their patients with Graves' disease. Some of serum autoantibodies were constantly present or absent in spite of remission.

Adolescent↗
PubMed1995

[Problems in thyroid function screening using thyroid stimulating hormone. A case of thyrotoxicosis caused by a thyroid stimulating hormone-secreting pituitary tumor].

UNLABELLED: In a new consensus report from the Danish Society of Internal Medicine a sensitive TSH assay is recommended for screening for thyroid diseases. A patient with thyrotoxicosis, normal serum TSH and a TSH-secreting pituitary adenoma is described. Other reasons for discrepancies between thyroid clinical status and serum TSH are mentioned: Target organ resistance to thyroid hormone, interference in the radioimmunoassay with heterophilic antibodies and insufficient production of TSH because of pituitary disease. IN CONCLUSION: Screening with TSH is acceptable, but if any discrepancy between TSH values and the clinical picture is found, further tests must be made.

Adenoma↗
PubMed1989

[Significance of circulating anti-thyroid stimulating hormone (TSH) receptor antibodies in patients with autoimmune thyroid diseases--thyroid stimulation blocking antibody in patients with Graves' disease].

It is a well-known fact that a thyroid stimulation blocking antibody (TSBAb) may play an important role in primary hypothyroidism. However, it has rarely been reported that TSBAb appears in only a few cases of Graves' disease which became hypothyroidism in their clinical courses. We examined TSBAb in 120 sera from 79 cases with Graves' disease before or while under methimazole (MMI)-treatment. TSBAb value was expressed as the percentage inhibition of TSH-stimulated cAMP response of porcine thyroid cells by the patient's IgG. TSBAb was positive in 9 cases (11.4%) of 79 cases of Graves' disease. In 6 of the 9 cases, TSBAb was detected at the untreated period. In the other 2 of the 9 cases, it was detected during the exacerbation related with their pregnancy. It was difficult to control Graves' disease in all 9 cases. These results suggest that TSBAb appears not only in primary hypothyroidism but also even in the hyperthyroid state of Graves' disease, and that the combination of TSAb and TSBAb may regulate the pathogenesis of Graves' disease.

Adult↗
PubMed1999

Augmentation of thyroid-stimulating antibody-stimulated cyclic adenosine monophosphate response by polyethylene glycol, polyvinyl alcohol, and dextran; highly sensitive porcine thyroid cell thyroid-stimulating antibody assay.

Previously, we reported that 5% polyethylene glycol (PEG) (6000) augmented thyroid-stimulating antibody (TSAb)-stimulated cyclic adenosine monophosphate (cAMP) production in porcine thyroid cell (PTC) assay. This augmentation by PEG was specific to TSAb-stimulation. In this study we examined the effects of nonionic hydrophilic polymers such as PEG, polyvinyl alcohol (PVA), and dextran (DEX) on TSAb-stimulated cAMP production. We demonstrated that graded doses of PEG, PVA, and DEX augmented TSAb-stimulated cAMP productions; the prominent augmentations were observed with 5% PEG (20,000), 5% PEG (6000), 6% PEG (4000), 10% PVA, 14% DEX T-250, and 14% DEX T-70. PVA did not augment thyrotropin (TSH)-stimulated cAMP synthesis. Five percent PEG (20,000), 14% DEX T-250, and 14% DEX T-70 augmented TSH-stimulated cAMP synthesis very slightly. PEG, PVA, and DEX had no effects on the cAMP synthesis stimulated by GTPgammaS, forskolin, or pituitary adenylate cyclase activating polypeptide (PACAP), which stimulated adenylate cyclase. We also demonstrated that PEG, PVA, and DEX augmented the cAMP responses stimulated by small amounts (50 microL) of sera from Graves' patients; small amounts (50 microL) of sera could be used instead of purified immunoglobulin G (IgG). This may simplify the TSAb assay. We developed a highly sensitive simplified TSAb assay. PEG weakly augmented TSAb binding to isolated TSH receptor (thyrotropin-binding inhibitor immunoglobulin [TBII] increased slightly). The mechanisms of the augmentations of TSAb-stimulated cAMP productions by PEG, PVA, and DEX is not simply explained by increased binding of TSAb to the receptors. Some factors that enhance TSAb action at the receptor site are suggested.

Animals↗
PubMed1982

Catecholamine-thyroid hormone interactions: II. Thyroid hormone and platelet MAO activity in patients with thyroid disorders.

Platelet monoamine oxidase (MAO) activity and serum thyroxine indices were determined in 62 children and adolescents currently undergoing medical treatment for various thyroid disorders. The platelet MAO activity of these patients was similar to that of control and contrast groups previously reported, and there were no differences when patients were grouped according to specific thyroid disorders. Estimated free thyroxine and total thyroxine levels were generally in the upper normal or slightly elevated range and were not significantly related to MAO activity.

Adolescent↗