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PubMed1997

Demonstration of fragments with thyroid stimulating activity from thyroid stimulation blocking antibodies-IgG molecules by papain digestion.

OBJECTIVES: Thyroid stimulation blocking antibodies (TSBAb) inhibit TSH action and may have a role in the pathogenesis of hypothyroidism. In order to study the relationship between blocking and stimulating activities we have examined the biologically active fragments in TSBAb-IgG molecules after papain digestion. DESIGN: Both thyroid stimulating (TS) activity (cAMP production in thyroid cells) and TSH binding inhibitory (TBI) activity (determined by TSH receptor assay) in sera from patients with primary hypothyroidism were examined after digestion with papain-Sepharose in the presence of cysteine. The digested IgG was separated into unbound (UF) and bound (BF) fractions on a Protein A-Sepharose column. Each fraction was then gel-filtrated on a Sephadex G-100 column. RESULTS: TS activity was found within one hour after hydrolysis in 5 out of 7 antibodies, then gradually decreased after more prolonged incubation. Both TS and TBI activities in the UF and the BF from Protein A were found in Feb (Mr 50 kD) and the second protein peak (Fc with trace amounts of Fab), respectively. The biological activity in the second protein peak was suggested as being derived from Fab fraction, because the activity bound to the anti-F(ab')2 column. However, the first peak (undigested IgG) in the BF had neither TS nor TSB activity. The TS activity in the retarded fraction (less than Mr 20 kD) in the UF gradually increased with prolonged digestion. CONCLUSIONS: The conversion of Thyroid stimulation blocking antibodies activity to thyroid stimulating activity by papain digestion suggests that the inherent thyroid stimulating activity located in the Fab portion of the IgG molecule is unmasked by papain cleavage. We also suggest that the thyroid stimulating activity in the retarded fraction in the unbound fraction may be released from hydrolysis of the Fab portion of the IgG molecule.

Antibodies, Blocking↗
PubMed2001

Thyroid function in the newborn in relation to maternal thyroid status during labour in a mild iodine deficiency endemic area in Sudan.

OBJECTIVES: Data on neonatal and maternal thyroid function during labour in a mild iodine deficiency endemic area are lacking. The current study focuses on elucidating the thyroid function during labour, in a group of pregnant women who live in an area of mild iodine deficiency in Sudan compared to that observed in their corresponding newborns. MEASUREMENTS: Serum concentrations of TSH, thyroglobulin (Tg), triiodothyronine (T3) and free thyroxine (FT4) were investigated during labour in a group of mothers and their neonates residing in an area with mild iodine deficiency in Sudan (n = 76 mother-newborn pairs). DESIGN: Maternal blood samples were taken on two occasions: first, during the third trimester of pregnancy (weeks 32-39); and, second, just before delivery. Cord blood samples were obtained by a doctor or a trained midwife during delivery. RESULTS: The median concentrations (and interquartile ranges) of neonatal TSH, Tg, T3 and FT4 were 6.8 (4.7-12.4) mU/l, 61 (40.2-98.2) microg/l, 0.9 (0.8-1.2) nmol/l and 14.2 (13.4-15.9) pmol/l, respectively. The corresponding levels for the mothers during labour were 2.3 (1.9-3.2) mU/l, 33 (15.0-56.8) microg/l, 2.6 (2.0-2.9) nmol/l and 11.4 (10.3-13.3) pmol/l, respectively. The median neonatal serum concentrations of TSH, Tg and FT4 were significantly higher than the corresponding maternal levels (P < 0.0001, P < 0.0001, P < 0.0001, respectively). In contrast, the median maternal serum concentration of T3 was significantly higher than that of the neonates (P < 0.0001). When the different neonatal thyroid parameters were compared with each other, significant correlations were observed between TSH and FT4 (r = 0.4, P = 0.001); Tg and T3 (r = -0.3, P = 0.04) and Tg and FT4 (r = 0.5, P = 0.0001). Women with Tg concentrations above 20 microg/l showed a higher median TSH concentration and lower median FT4 concentration than those with Tg concentrations below 20 microg/l (P < 0.001, P < 0.001, respectively). Nevertheless, the thyroid function of neonates born of mothers with elevated Tg was similar to that of neonates born of mothers with low Tg levels. No significant changes had occurred in the thyroid function parameters between the third trimester of pregnancy and during the time of labour. The thyroid function indicators of the babies born by vaginal delivery did not differ significantly from those of the babies born by Caesarian section. CONCLUSIONS: The study suggests that, in areas with mild iodine deficiency, neonates may be at the limit of decompensation as evidenced by their enhanced TSH and Tg levels as well as increased T4 compared to their mothers. This finding must not create a false sense of well-being and points rather to the urgency of iodine supplementation of mothers even in areas with mild iodine deficiency, as in this part of Sudan. The mode of delivery, whether by spontaneous vaginal delivery or Caesarian section, did not seem to affect the thyroid function of the newborn.

Adult↗
PubMed2003

Risk factors for and prevalence of thyroid disorders in a cross-sectional study among healthy female relatives of patients with autoimmune thyroid disease.

OBJECTIVE: Autoimmune thyroid disease (AITD) is a common disorder especially in women, and both genetic and environmental factors are involved in its pathogenesis. We wanted to gain more insight into the contribution of various environmental factors. Therefore, we started a large prospective cohort study in subjects at risk of developing AITD, for example healthy female relatives of AITD patients. Here we report on their baseline characteristics. SUBJECTS: Only first- or second-degree female relatives of patients with documented AITD were included. MEASUREMENTS: Smoking habits, oestrogen use, pregnancy history and iodine exposure were assessed by questionnaires, and correlated to the thyroid function and antibody status. RESULTS: Of 803 subjects, 440 came from families with more than one patient with documented AITD. Of these families, 33% had documented cases of both Graves' disease and Hashimoto's thyroiditis. Although the subjects were in self-proclaimed good health, 3.6% were found to have hypothyroidism (overt disease in 1.3%) and 1.9% had hyperthyroidism (overt disease in 0.4%). These patients were older than the euthyroid subjects and were mostly positive for thyroid peroxidase (TPO) antibodies. Oestrogen use was associated with a lower rate of hyperthyroidism [relative risk (RR) 0.169; 95% confidence interval (CI) 0.06-0.52], whereas having been pregnant was associated with a higher relative risk for hyperthyroidism (RR 6.88; 95% CI 1.50-30.96). Of the 759 euthyroid subjects, 24% had TPO antibodies. Smoking and oestrogen use were negatively correlated with the presence of TPO antibodies. In the euthyroid subjects, TPO antibody titre correlated positively with TSH levels (r = 0.386; P < 0.001). CONCLUSIONS: The high prevalence of evidence for autoimmune thyroiditis at baseline supports the importance of genetic factors in its pathogenesis. The co-occurrence of Hashimoto's thyroiditis and Graves' disease within one family suggests a common genetic basis for these diseases. Oestrogen use is associated with a lower risk, and pregnancy with a higher risk for developing hyperthyroidism. The positive correlation between TPO antibody titres and TSH levels in euthyroid subjects suggests that TPO antibodies are indeed a marker of future thyroid failure.

Adolescent↗
PubMedDate not supplied

Palpable parathyroid adenomas presenting as clinical solitary thyroid nodules and cytologically as follicular thyroid neoplasms.

BACKGROUND: A palpable parathyroid mass, in a patient with primary hyperparathyroidism, is presumed to be parathyroid carcinoma until proven otherwise, with other less common causes including parathyroid cysts and adenomas. These parathyroid pathologies can be more difficult to interpret with concomitant thyroid disease. METHODS: A retrospective review was undertaken of a series of three patients with palpable parathyroid adenomas mimicking thyroid nodules. RESULTS: Two of three patients had preoperative biochemical evidence of primary hyperparathyroidism. Sestamibi scanning confirmed the presence of parathyroid pathology in one case. Fine-needle aspiration cytology revealed probable follicular neoplasms of the thyroid in all three cases. Only one of three parathyroid adenomas was diagnosed at neck exploration; the others were diagnosed at subsequent histopathology. CONCLUSION: Parathyroid and thyroid disease often occur simultaneously. Concomitant parathyroid pathology should be considered, even in the absence of biochemical and radiological evidence, at neck exploration for thyroid disease. Macroscopic identification of parathyroid disease at neck exploration can be difficult when within the thyroid gland capsule. Cytology and imaging of parathyroid adenomas may, on occasion, mimic follicular thyroid neoplasms.

Adenocarcinoma, Follicular↗
PubMed1996

Mild resistance to thyroid hormone with a truncated thyroid hormone receptor beta.

Recent studies have revealed mutations in the thyroid hormone receptor beta (TR beta) gene as a cause of the most cases of the thyroid hormone resistance syndrome. We have identified a novel nonsense mutation in codon 449 in the 3' end of exon 10 in the TR beta gene in a 16-year-old male patient with generalized resistance to thyroid hormone who also had familial thyroxine binding globulin deficiency. Receptor protein generated from this gene is thought to be 13 amino acid deficient at carboxy-terminus. Resistance to thyroid hormone was mild at least when the patient was evaluated. The patient was eumetabolic in the presence of elevated plasma-free thyroid hormone levels, and both thyrotrope and peripheral tissues responded to triiodothyronine (T3) administration. This mildness of resistance is in contrast to severe resistance to thyroid hormone in two previously reported cases with truncated receptors in which 16 amino acids or 11 amino acids were deficient at C-terminus. Thus, truncation of C-terminus of thyroid hormone receptor beta does not uniformly produce sever resistance.

Adolescent↗
PubMed2003

Influence of iodide and iodolactones on thyroid apoptosis. Evidence that apoptosis induced by iodide is mediated by iodolactones in intact porcine thyroid follicles.

Iodine induced thyroid involution is caused by apoptosis rather than necrosis. This effect of iodide on apoptosis of thyroid epithelial cells may be not a direct one but mediated by iodinated derivatives i.e. of polyunsaturated fatty acids, especially of iodolactones, which have previously shown to inhibit thyroid cell proliferation. We studied the influence on apoptosis of iodide (2 microM and 20 microM) and iodolactone (0.05 microM and 0.5 microM), with and without TSH (1 mU/ml), using a well characterized ex vivo- culture system of intact porcine thyroid follicles in three-dimensional culture. Apoptosis and necrosis was evaluated by electron-microscopy. Stimulation with 2 and 20 microM iodide rapidly induced a rate of apoptosis (4 - 6 %) comparable to about 40-fold lower doses of delta-iodolactone (0.05 microM and 0.5 microM). Addition of TSH (1 mU/ml) caused a slight but not significant further increase of the incidence of apoptotic cells. The rate of necrotic thyroid epithelial cells (1 - 2 %) was similar in all experiments. As delta-iodolactone in very low concentrations--comparable to iodide in higher concentrations--not only inhibits growth but also induces apoptosis, it has to be supposed that the effect of iodide is mediated by this iodinated compound. However, further experiments are necessary to confirm this hypothesis. In addition it could be demonstrated, that apoptosis is a very rapid and limited process in intact follicles. This also may explain, why iodine supplementation even in high doses does not lead to thyroid atrophy but only normalisation of thyroid size. These results confirm that apoptosis is an important regulated and limited mechanism in goiter involution.

Animals↗
PubMed1987

Lowering of T3 and rise in reverse T3 induced by hyperglucagonemia: altered thyroid hormone metabolism, not altered release of thyroid hormones.

Recently we reported that hyperglucagonemia induced by glucagon infusion causes a decline in serum T3 and a rise in reverse T3 in euthyroid healthy volunteers. These changes in T3 and rT3 levels were attributed to altered T4 metabolism in peripheral tissues. However, the contribution of altered release of thyroid hormones by the thyroid gland could not be excluded. Since the release of thyroid hormones is inhibited in primary hypothyroidism and is almost totally suppressed following L-thyroxine replacement therapy, we studied thyroid hormone levels for up to 6 hours after intravenous administration of glucagon in subjects with primary hypothyroidism who were rendered euthyroid by appropriate L-thyroxine replacement therapy for several years. A control study was conducted using normal saline infusion. Plasma glucose rose promptly following glucagon administration demonstrating its physiologic effect. Serum T4, Free T4, and T3 resin uptake were not altered during both studies. Glucagon infusion induced a significant decline in serum T3 (P less than 0.05) and a marked rise in rT3 (P less than 0.05) whereas saline administration caused no alterations in T3 or rT3 levels. Thus the changes in T3 and rT3 were significantly different during glucagon study when compared to saline infusion. (P less than 0.01 for both comparisons). Since, the release of thyroid hormones is suppressed by exogenous LT4 administration in these subjects; we conclude that changes in serum T3 and rT3 observed following glucagon administration reflect altered thyroid hormone metabolism in peripheral tissues and not altered release by the thyroid gland.

Adult↗
PubMed1999

The value of thyroid peroxidase immunohistochemistry for preoperative fine-needle aspiration diagnosis of the follicular variant of papillary thyroid cancer.

BACKGROUND: With the use of May-Grunwald-Giemsa staining, cytologic features of the follicular variant of papillary thyroid cancers (FVPTCs) on thyroid fine-needle aspiration (FNA) often resemble those of hyperplastic and adenomatous nodules. Detection of reduced staining after thyroid peroxidase (TPO) immunohistochemistry with monoclonal antibody MoAb47 has been shown to be a helpful diagnostic marker. The purpose of this study was to assess the value of TPO immunohistochemistry for the diagnosis of FVPTC. METHODS: Of 3505 patients with adequate FNA samples, 1576 patients underwent surgical procedures. Histologic examination of the surgical specimen demonstrated papillary thyroid cancer in 227 cases, including 42 FVPTCs (18%). The diagnostic accuracy of standard thyroid FNA and TPO immunohistochemistry, which we use routinely, was compared in these 42 FVPTCs. RESULTS: Standard FNA allowed accurate diagnosis of malignancy in 32 of the 42 FVPTCs and in 170 of the 185 typical papillary thyroid cancers. TPO-immunohistochemistry staining was accurate in all 42 FVPTCs and in 182 of 185 typical PTCs. CONCLUSIONS: FVPTC is a frequent source of false-negative results on standard thyroid FNA. This study shows that TPO immunostaining accurately demonstrates malignancy in these tumors.

Adolescent↗
PubMed2005

Relation of thyroid disfunction, thyroid autoantibodies, and renal function.

Fifty-eight patients with thyroid dysfunction were included, comparing 27 healthy subjects to evaluate the relationship between thyroid autoimmunity, thyroid functional status, and renal function. Regardless of clinical status, hypothyroidism was defined as T3-T4 upper limit of normal, and hyperthyroidism was defined as T3-T4>normal limits and TSH <0.1 mcU/mL. In all participants, serum antithyroperoxidase level, serum antithyroglobulin level, creatinine clearance (CC), and urinary albumin excretion rate (UAER) in 24-h urine collections were measured. Of 85 persons, 41 patients ages 20 to 71 years (median; 44) had hypothyroidism, 17 patients ages 22 to 56 years (median; 32) had hyperthyroidism, and 27 subjects ages 20 to 67 years (median; 50) were normal. Regarding thyroid autoantibody positiveness, the positive group had a higher UAER than the negative group (30.2 mg/day, 20.8 mg/day, respectively; p=0.05). In hypothyroid patients, UAER was significantly higher than in hyperthyroid patients and control subjects (30.1 mg/day, 11.8 mg/day, 10.5 mg/day, respectively; p<0.001). In the hypothyroid population, with regard to UAER and CC, we could not find a significant difference between the thyroid autoantibody positive and negative groups. In view of CC, hypothyroid patients had significantly lower CC than the hyperthyroid group (79.0 mL/ min, 86.5 mL/min, respectively; p<0.01). A careful control of the renal function in thyroid diseases should be evaluated. Renal dysfunction seems to be secondary to hypothyroidism rather than thyroid autoimmunity.

Adult↗
PubMed1992

Analysis of the TSH receptor gene structure in various thyroid disorders: DNA from thyroid adenomas can have large insertions or deletions.

We examined the structure of the TSH receptor gene in various thyroid disorders by a restriction fragment length polymorphism (RFLP) study with a cloned human TSH receptor cDNA as a probe. Southern blot analysis of DNAs in peripheral white blood cells obtained from normal individuals revealed a single band in each of several restriction enzyme digestions, indicating that the TSH receptor gene is a single copy gene in the human genome. Although RFLPs were not detected in peripheral blood cells and thyroid tissues in patients with Graves' disease, thyroid carcinomas, or subacute thyroiditis, significant RFLPs were found in 2 of 6 patients with adenoma in all restriction enzyme digestions examined. Moreover, these RFLPs were heterozygous and adenoma specific, and these additional bands in adenoma were amplified in both cases. We conclude that there are no major abnormalities in the structure of the TSH receptor gene in patients with Graves' disease, thyroid carcinoma, or subacute thyroiditis, although there may be a possibility of point mutations, small insertions, or deletions that cannot be detected by RFLP studies, and that there are large insertions or deletions in the region, including the TSH receptor gene, in some patients with thyroid adenoma.

Blotting, Southern↗
PubMed1998

Increase of thyroid stimulating activity in Graves' immunoglobulin-G by high polyethylene glycol concentrations using porcine thyroid cell assay.

Cyclic adenosine monophosphate (cAMP) production during a 5-hour incubation using porcine thyroid cells (PTC) was stimulated significantly more by polyethylene glycol (PEG) 22.5% precipitated fractions (ppt frs) than by PEG 12.5% ppt frs from almost all Graves' sera. However, the thyrotropin (TSH) binding inhibition (TBI) activities of the PEG 12.5% and 22.5% ppt frs using porcine thyroid membranes were similar, and did not change in the 5-hour incubation. When the PEG 12.5% ppt fr from Graves' serum and the PEG 22.5% ppt fr from normal human serum (NHS) were coincubated, cAMP production was also stimulated as much as by the PEG 22.5% ppt fr from Graves' serum. When purified thyroid stimulating antibody (TSAb)-immunoglobulin G (IgG) and the PEG 22.5% ppt fr from NHS were coincubated, increased cAMP production was also observed, whereas bovine thyrotropin (bTSH) did not produce this effect. When purified TSAb-IgG and PEG solutions were coincubated, maximum increases in cAMP production (approximately 10-fold) with 5% PEG were found, whereas no increase was observed using bTSH. The stimulatory effect of high PEG concentrations on thyroid stimulating activity was observed by TSAb-IgG in salt-free or salt-containing medium (<0.15 mol/L NaCl concentration) but not by either TSAb-IgG conjugated to protein A-sepharose 4B or the inactivated TSAb-IgG by the treatment of 70 degrees C for 10 minutes. No stimulatory action by PEG was found with the thyroid stimulating substances such as GTPgammaS, forskolin, or pituitary adenylate-cyclase activating polypeptide (PACAP). The increased thyroid stimulating activity of Graves (IgG) at high PEG concentrations suggests the existence of some factors influencing the ability of TSAb to stimulate thyroid cells, although the exact mechanism remains to be clarified.

Animals↗
PubMed1998

Thyrotropin suppression and disease progression in patients with differentiated thyroid cancer: results from the National Thyroid Cancer Treatment Cooperative Registry.

The ideal therapy for differentiated thyroid cancer is uncertain. Although thyroid hormone treatment is pivotal, the degree of thyrotropin (TSH) suppression that is required to prevent recurrences has not been studied in detail. We have examined the relation of TSH suppression to baseline disease characteristics and to the likelihood of disease progression in a cohort of thyroid cancer patients who have been followed in a multicenter thyroid cancer registry that was established in 1986. The present study describes 617 patients with papillary and 66 patients with follicular thyroid cancer followed annually for a median of 4.5 years (range 1-8.6 years). Cancer staging was assessed using a staging scheme developed and validated by the registry. Cancer status was defined as no residual disease; progressive disease at any follow-up time; or death from thyroid cancer. A mean TSH score was calculated for each patient by averaging all available TSH determinations, where 1 = undetectable TSH; 2 = subnormal TSH; 3 = normal TSH; and 4 = elevated TSH. Patients were also grouped by their TSH scores: group 1: mean TSH score 1.0-1.99; group 2: mean TSH score 2.0-2.99; group 3: mean TSH score 3.0-4.0. The degree of TSH suppression did not differ between papillary and follicular thyroid cancer patients. However, TSH suppression was greater in papillary cancer patients who were initially classified as being at higher risk for recurrence. This was not the case for follicular cancer patients, where TSH suppression was similar for all patients. For all stages of papillary cancer, a Cox proportional hazards model showed that disease stage, patient age, and radioiodine therapy all predicted disease progression, but TSH score category did not. However, TSH score category was an independent predictor of disease progression in high risk patients (p = 0.03), but was no longer significant when radioiodine therapy was included in the model (p = 0.09). There were too few patients with follicular cancer for multivariate analysis. These data suggest that physicians use greater degrees of TSH suppression in higher risk papillary cancer patients. Our data do not support the concept that greater degrees of TSH suppression are required to prevent disease progression in low-risk patients, but this possibility remains in high-risk patients. Additional studies with more patients and longer follow-up may provide the answer to this important question.

Adenocarcinoma, Follicular↗
PubMed1997

Identification of rapid turnover transcripts overexpressed in thyroid tumors and thyroid cancer cell lines: use of a targeted differential RNA display method to select for mRNA subsets.

The mRNAs of transiently expressed proteins such as cytokines and proto-oncogenes are commonly subject to rapid transcriptional activation and degradation. Transcript turnover is determined in part by association of certain proteins with consensus AU-rich motifs (AUUUA) in the 3'-untranslated region of the transcripts. Here we report a modification of differential RNA display (DRD) to detect differentially expressed rapid turnover mRNAs containing AU-rich motifs from thyroid cancer tissues and cell lines. RNA of normal and thyroid cancer tissues was differentially displayed using a 3'anchor primer to the poly(A) tail and an arbitrary 5'primer incorporating an AUUUA sequence. The appropriateness of the strategy was established by its ability to display known early response genes, such as c- fos, using partially degenerate primers. To test whether the novel cDNAs isolated coded for transcripts subject to rapid turnover, they were used as probes for Northern blots of RNA from clonal human thyroid carcinoma cell lines treated for varying periods with either cycloheximide or actinomycin D. A number of novel differentially expressed cDNA fragments were isolated from human papillary thyroid carcinoma tissues, among them a cDNA with zinc finger motifs and homology to other zinc finger proteins. Using this fragment to probe a cDNA library, a full-length cDNA (ZnF20) was isolated that was 4333 bp in length and contained an open reading frame of 1029 amino acids. The ZnF20 cDNA hybridized to multiple transcripts in a thyroid cancer cell line (8.0, 4.5 and 2 kb) that increased after cycloheximide treatment and decayed <2 h after addition of actinomycin D. The ZnF20 mRNA was overexpressed in three of six thyroid papillary carcinomas as compared with paired normal thyroid tissue controls. The data presented here support the use of a targeted DRD approach for the isolation of rapid turnover mRNAs, many of which may be interesting candidate oncogenes.

Amino Acid Sequence↗
PubMed1985

Characterization of a monoclonal antibody to hog thyroid peroxidase and its use for immunohistochemical localization of the peroxidase in the thyroid gland.

A monoclonal antibody (30.1.2) to hog thyroid peroxidase was produced, purified, and characterized. The IgG of 30.1.2 formed an immune complex with the peroxidase in a 1:2 or 1:1 molar ratio depending on the IgG to antigen ratio in the incubation mixture. Immune complex formation did not inhibit the peroxidase activity, which was actually activated 2-fold in the 1:1 complex. Studies of the binding of the conjugate of the IgG or its Fab' with horseradish peroxidase to untreated and acetone-treated thyroid microsomes showed that the IgG conjugate could bind to only a very small portion of the total binding sites (thyroid peroxidase) present in untreated microsomes even after prolonged incubation. The binding of the Fab' conjugate to untreated microsomes, on the other hand, increased as the incubation time was increased, reaching 40% of the total sites after 20 h of incubation. These findings indicated that thyroid peroxidase is localized on the inner surface of the microsomal membranes and that the Fab' conjugate, but not the IgG conjugate, can slowly penetrate through the membrane barrier to reach the peroxidase. Immunohistochemical experiments using the Fab' conjugate as a probe revealed that most thyroid peroxidase in the thyroid gland is located in the endoplasmic reticulum and perinuclear cisternae of the follicular cell, although a small amount could occasionally be detected in the apical membrane including microvilli. In contrast to previous reports, no thyroid peroxidase could be found in other cellular structures such as Golgi apparatus and apical vesicles by the immunohistochemical technique employed.

Animals↗
PubMed1991

Autoantibody stimulation of the human thyrotropin receptor: regulation of adenylate cyclase activity, thyroglobulin and thyroid peroxidase mRNA levels in primary cultures of Graves' thyroid tissue.

The effects of immunoglobulin preparations from hyperthyroid Graves' disease patients on primary cultures of thyroid cells have been studied at the mRNA level. Autoantibodies to the thyrotropin (TSH) receptor from these patients, which had been initially characterized by their ability to stimulate adenylate cyclase and inhibit the binding of radiolabelled TSH to thyroid membrane preparations, were studied for their effects on thyroglobulin and thyroid peroxidase mRNA levels. Incubation of thyroid cells with TSH receptor autoantibodies from different Graves' disease patients for 48 h led to time- and dose-dependent increases in the levels of thyroid peroxidase and thyroglobulin mRNA in primary cultures of thyrocytes. The incomplete correlation between G protein-linked adenylate cyclase activation and thyroid mRNA elevation indicates the possibility of the involvement of alternative second messenger pathways in the regulation of thyroid cell function and differentiation.

Adenylyl Cyclases↗
PubMed1985

Diagnostic value of a single serum thyroglobulin determination on and off thyroid suppressive therapy in the follow-up of patients with differentiated thyroid cancer.

To assess the significance of a single serum thyroglobulin (Tg) determination on and off thyroid suppressive therapy, serum Tg measurements have been performed in 349 serum samples from 82 patients with differentiated thyroid cancer. All samples were collected after total thyroidectomy with or without subsequent ablation of residual thyroid tissue by radioiodine. One hundred and fifty-three samples were obtained while the patients were on thyroid suppressive therapy and 196 after withdrawal of medication. The results of serum Tg assays were analysed in relation to the presence or absence of residual or metastatic thyroid tissue, as assessed by clinical and laboratory evaluation, including 131I whole body scan. In patients with thyroid residue but no metastases, undetectable serum Tg (false negative results) occurred in 45% of cases off therapy and in 92.9% of cases during therapy. In the presence of metastases no undetectable serum Tg result was found in patients off therapy, while four (6.9%) out of 58 samples from patients with bone and/or lung metastases and seven (31.8%) out of 22 samples from patients with lymph node metastases alone were undetectable (falsely negative) during suppressive therapy. Serum Tg was undetectable in sera from patients with no evidence of thyroid residue or metastatic disease in all but one (1.7%) of 59 samples on and three (5.4%) of 56 samples off suppressive therapy. These Tg results were confirmed to be truly rather than falsely positive, since evidence of metastatic disease was obtained by whole body scan after the administration of therapeutic doses of 131I.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1992

Localized primary amyloid tumor of the thyroid developing in the course of Hashimoto's thyroiditis.

A case of localized primary amyloid tumor of the thyroid gland developing in the course of Hashimoto's thyroiditis was studied using histochemistry, immunohistochemistry and electron microscopy. The patient was diagnosed as having Hashimoto's thyroiditis by histological examination of the thyroid and by the presence of a high titer of serum thyroglobulin and thyroid microsomal antibodies. In addition, the thyroid gland exhibited multiple nodular deposits of amyloid which were resistant to prior incubation with potassium permanganate. The amyloid deposits were surrounded by numerous histiocytes and multinucleated giant cells which contained small amyloid droplets in their cytoplasm. However, no amyloid deposits were observed in the walls of blood vessels. Immunohistochemistry showed that the amyloid was strongly positive for amyloid P component, IgG and kappa light chains. Ultrastructurally, the amyloid was composed of straight fibrils with a diameter of 7 to 10 nm. Histiocytes extended slender cytoplasmic processes in a radial fashion into amyloid fibrils, which exhibited a highly organized star-like pattern. This was considered to be an extremely rare case of localized primary amyloidosis of the thyroid, in which IgG, especially kappa light chains (AL), was present as a precursor protein.

Aged↗
PubMed2005

Thyroid-stimulating hormone receptor levels and binding affinity in the thyroid gland of growth-retarded mice.

Growth-retarded (grt/grt) mice are congenitally primary hypothyroid. Our previous study indicated that thyroid-stimulating hormone (TSH) responsiveness was defective in the grt/grt thyroid gland. We now report additional studies of impaired grt/grt thyroid function. Semiquantitative RT-PCR confirmed that TSH receptor (TSHR) mRNA expression in the grt/grt thyroid was significantly decreased compared with +/+ thyroids. Scatchard analysis revealed that grt/grt and +/+ mice have only one type of TSH binding site. grt/grt thyroids had fewer TSH binding sites, although this did not apparently affect the affinity of TSH for its receptor. The present data suggest that reduced TSHR levels or defects in TSHR signaling could be one of the possible defective sites in the grt/grt thyroid gland.

Animals↗