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PubMed1998

Clonal analysis helps to differentiate aberrant thyroid tissue from thyroid carcinoma.

A rare case of multiple aberrant of thyroid tissues in the tongue and lymph nodes of the bilateral neck was studied by immunohistochemistry and molecular clonal analysis to determine whether these tissues represent aberrant ectopic thyroid or metastases of a thyroid carcinoma. The thyroid tissues in the tongue and lymph nodes were all of polyclonal origins, consistent with ectopic thyroid in the tongue and bilateral cervical lymph nodes, rather than malignant thyroid tissues. This case shows that molecular clonal analysis can be used to distinguish aberrant thyroid from metastases of thyroid carcinoma.

Adult↗
PubMed2006

Thyroid hemiagenesis: clinical significance in the patient with thyroid nodule.

Thyroid hemiagenesis is a rare abnormality in which one thyroid lobe fails to develop. Most of the patients diagnosed have an associated thyroid disease. We report the case of a 32-year-old woman who presented with a left thyroid mass which had been gradually increasing in size over a period of two years. A thyroid scan revealed the absence of the right thyroid lobe and isthmus, and a hypoactive nodule was evident in the lower pole of the left lobe. Ultrasonography confirmed the right lobe and the isthmus agenesis. The operative findings confirmed hemiagenesis of the right lobe and nodular hyperplasia in the left lobe. The purpose of this report is to present a patient with hemiagenesis of the thyroid gland who concomitantly had nodular hyperplasia; we also stress the importance of pre-operative differentiation between benign lesions and malignancy in order to aid critical decision making and to facilitate preservation of thyroid function if possible.

Adult↗
PubMed1987

Thyroid cancer among young women related to prior thyroid disease and pregnancy history.

We conducted an epidemiologic case-control study of thyroid cancer in women aged 40 and under to test the hypothesis that endogenous hormones may relate to the development of this disease, since the only known cause of thyroid cancer, ionizing radiation, does not account for the striking female over male excess. When compared to neighbour controls women with thyroid cancer more often had a history of benign hyperplastic thyroid disease (Relative Risk (RR) = 14.5; P less than 0.01) and more often had ever been pregnant (RR = 2.1; P = 0.04). Both these findings were consistent with findings of previous studies. After eliminating women with a history of hyperplastic thyroid disease from the analysis we found a strong association with miscarriage as the outcome of the first pregnancy (RR = 11.5; P less than 0.01), and we suspect that this factor may be another indicator of thyroid abnormality. An independent and increasing risk was observed with an increase in the total number of pregnancies after excluding women with prior thyroid disease and those whose first pregnancy ended in a miscarriage. The RR for 4 or more pregnancies was 6.3 (P = 0.03). Prior exposure to radiation therapy was not an important factor in our study of young women; this suggests that the emphasis in future studies of thyroid cancer must shift to study other types of risk factors.

Abortion, Spontaneous↗
PubMed2004

Detection and molecular characterisation of thyroid cancer precursor lesions in a specific subset of Hashimoto's thyroiditis.

Hashimoto's thyroiditis (HT) represents the most common cause of hypothyroidism and nonendemic goiter, but its clinical and pathological heterogeneity opens the question if this disease should be more properly considered as a spectrum of different thyroid conditions rather than as a single nosological entity. In this study, we analysed 133 cases of HT for the expression of galectin-3, a lectin molecule involved in malignant transformation, apoptosis and cell cycle control. An unexpected expression of galectin-3 was demonstrated in a subset of HT together with the presence of HBME-1, c-met and cyclin-D1 that are also involved in malignant transformation and deregulated cell growth. Furthermore, a loss of allelic heterozygosity in a specific cancer-related chromosomal region was demonstrated in some HT harbouring galectin-3-positive follicular cells, by using laser capture microdissection. On the basis of the morphological and molecular findings we identified four subsets of HT: (a) HT with classic features of chronic autoimmune thyroiditis; (b) HT associated to hyperplastic/adenomatous lesions; (c) HT harbouring thyroid cancer precursors; (d) HT associated to unequivocal thyroid microcarcinomas. Our findings provide a well-substantiated morphological and molecular demonstration that HT may include a spectrum of different thyroid conditions ranging from chronic autoimmune thyroiditis to thyroiditis triggered by specific immune-response to cancer-related antigens.

Chromosome Mapping↗
PubMed2001

Toxic multinodular goitre in a patient with generalized resistance to thyroid hormone who harbours the R429Q mutation in the thyroid hormone receptor beta gene.

The association of resistance to thyroid hormone (RTH) due to a receptor defect with toxic multinodular goitre or with carcinoma of the thyroid has not been previously reported. Previous histopathological studies of the thyroid gland in patients with RTH have revealed changes similar to multinodular goitre, probably due to continuous stimulation by TSH. We report here a case of generalized resistance to thyroid hormone associated with a multinodular goitre, which became toxic. The patient was a 46-year-old Japanese woman who noticed a goitre although she had no symptoms of thyrotoxicosis. Initial examination revealed elevated serum thyroid hormone levels and a normal TSH level. Ultrasonography disclosed a multinodular goitre with cystic lesions. Three years later, the patient complained that the goitre had become larger and that she had developed symptoms of thyrotoxicosis such as palpitation and hyperhydrosis. Progressive hyperthyroxinaemia with relatively suppressed TSH, increased radioiodine uptake and negative anti-TSH receptor antibodies led to the diagnosis of toxic multinodular goitre. Subtotal thyroidectomy was performed, and pathological examination revealed a micropapillary carcinoma within the multinodular goitre. Occurrence of thyroid carcinoma should be considered in RTH because its incidence is high in multinodular goitre. Molecular examination revealed the R429Q mutation in the thyroid hormone receptor beta gene, which is one of the mutations usually manifesting as the pituitary resistance phenotype. That thyrotoxic manifestations appeared only during toxic stage of multinodular goitre in this case suggests that the phenotype of this type of mutation can be dependent on the amount of thyroid hormone.

Amino Acids↗
PubMed2002

Thyroid dysfunction: reproduction and postpartum thyroiditis.

Thyroid function during pregnancy is characterized by changes in circulating thyroid hormone concentrations related to alterations in thyroxine binding globulin (TBG), human chorionic gonadotropin (hCG), and iodine status. The immunology of normal pregnancy shows a reduction in antibody titer during gestation and an increase in T helper-2 (TH2) immune responses. Thyroid dysfunction may cause menstrual disturbances in hyper- and hypothyroidism but less marked disturbances of sexual function in men. Fertility is reduced in hypo- and hyperthyroid females. Accumulating evidence suggests a strong association between the presence of thyroid antibodies and fetal loss, although the data relating to recurrent abortion are not so convincing. Asymptomatic maternal gestational hypothyroidism may occur in up to 2.5% of women; studies have shown a significant impact of this condition in causing a decrease of child IQ, suggesting that screening for maternal hypothyroidism with intervention may be justified. Postpartum thyroid disease occurs in 5 to 9% of women and thyroid dysfunction postpartum is seen in 50% of thyroid peroxidase antibody positive (TPO Ab+ve) women. There is a significant rate of hypothyroidism in long-term follow-up of women who have transient postpartum thyroid dysfunction.

Autoantibodies↗
PubMed1993

New animal models for human autoimmune thyroid disease. Xenografts of human thyroid tissue in severe combined immunodeficient (SCID) and nude mice.

We have been employing two mouse models for the study of human thyroid xenografts from patients with autoimmune thyroid disease (AITD). The first mouse strain is that of the athymic "nude" mouse which accepts human thyroid xenografts, but the passenger lymphocytes are lysed in this model over several weeks; in the second model, the severe combined immunodeficient (SCID) mouse, both the xenograft and its lymphocytes survive. The AITD thyroid xenograft returns to normal function and morphology in the nude mouse over several weeks whereas the same AITD thyroid xenografts undergo aggravation of their lesions in the SCID mouse. Normalized ("cleansed") thyroid tissue in the nude mouse, now bereft of the passenger lymphocytes, can be removed and then re-xenografted into SCID mice. There it will remain normal unless autologous peripheral blood mononuclear cells are added, whereupon the AITD lesion will be reproduced. Autologous "irrelevant" muscle tissue having undergone the same process will not show such lesions. There is thus no evidence for a primary thyroid cell disturbance in AITD, the abnormality appearing to be only in the immune system. Moreover peripheral blood mononuclear cells appear to contain sufficient memory cells to be able to mount an immune assault on the autologous normalized thyroid tissue (to which they had been previously sensitized) but not on irrelevant autologous (muscle) tissue.

Animals↗
PubMed1992

Acute thyroid dysfunction (thyroiditis) after therapy with interleukin-2.

Interleukin-2 (IL-2) is frequently incorporated in antineoplastic therapy: While the effect of interferon on the thyroid has been extensively studied the impact of other cytokines on thyroid function is less well understood. We monitored the thyroid function in six patients who received IL-2 in combination with tumor necrosis factor-alpha (TNF) or alpha-Interferon (alpha IFN). Hyperthyroxinemia with suppressed TSH developed within the first four weeks of IL-2 administration; during this phase, there was no technetium or iodine uptake by the thyroid gland. During the following few weeks, serum thyroxine decreased and serum TSH rose, consistent with the development of primary hypothyroidism; during this phase, thyroidal isotope incorporation was normal. All hypothyroid patients received thyroxine replacement therapy upon documentation of hypothyroidism; in several cases thyroxine was successfully discontinued after 2-3 months. None of the patients had detectable antithyroidal antibodies and none experienced thyroid-related pain, although two patients developed thyroid enlargement. We conclude that IL-2 administration is associated with the development of transient, subacute, painless thyroiditis. The frequency and severity of this complication requires further elucidation through systematic, prospective study.

Adult↗
PubMed1989

Generalized resistance to thyroid hormone associated with a mutation in the ligand-binding domain of the human thyroid hormone receptor beta.

The syndrome of generalized resistance to thyroid hormone is characterized by elevated circulating levels of thyroid hormone in the presence of an overall eumetabolic state and failure to respond normally to triiodothyronine. We have evaluated a family with inherited generalized resistance to thyroid hormone for abnormalities in the thyroid hormone nuclear receptors. A single guanine----cytosine replacement in the codon for amino acid 340 resulted in a glycine----arginine substitution in the hormone-binding domain of one of two alleles of the patient's thyroid hormone nuclear receptor beta gene. In vitro translation products of this mutant human thyroid hormone nuclear receptor beta gene did not bind triiodothyronine. Thus, generalized resistance to thyroid hormone can result from expression of an abnormal thyroid hormone nuclear receptor molecule.

Alleles↗
PubMed2002

Thyroid-stimulating hormone induces interleukin-18 gene expression in FRTL-5 cells: immunohistochemical detection of interleukin-18 in autoimmune thyroid disease.

Interleukin (IL)-18 is a cloned cytokine that was identified originally as a factor having potent interferon (IFN)-gamma-inducing activity on Kupffer cells. First, we analyzed IL-18 gene expression by reverse transcription-polymerase chain reaction (RT-PCR) in rat thyroid FRTL-5 cells and human thyroid tissue samples. The expression of IL-18 mRNA in FRTL-5 cells was enhanced by thryoid-stimulating hormone (TSH) in a dose-dependent manner. 8-Bromo-cyclic adenosine monophosphate (cAMP) also increased in IL-18 mRNA levels. Furthermore, TGCT clones that exhibited an increase in intracellular cAMP accumulation showed an increased IL-18 mRNA signal when compared to controls. Taken together, these data suggested that the effect of TSH on IL-18 gene expression was mediated by activating protein kinase A. Treatment of FRTL-5 cells with the antithyroid drug, methimazole (MMI), suppressed this stimulatory action of TSH on IL-18 gene expression. Next, we examined IL-18 expression in human thyroid tissue derived from patients with autoimmune thyroid diseases (ATD). RT-PCR and immunohistology demonstrated that human thyroid follicular cells expressed IL-18. Especially in thyroid tissue from a patient with Hashimoto's thyroiditis, expression was more diffuse and extensive, generally observed in close relation to a lymphocytic infiltrate. Also, IL-18 protein was distributed in the same follicles that express Fas-L and HLA-DR. This study is the first to demonstrate the detection of IL-18 in the thyroid gland. The frequent expression of IL-18 in thyrocytes suggests that IL-18 itself might be a secreted immunomodulator in ATD.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1999

Gender, clinical findings, and serum thyrotropin measurements in the prediction of thyroid neoplasia in 1005 patients presenting with thyroid enlargement and investigated by fine-needle aspiration cytology.

One thousand five euthyroid patients (870 females and 135 males, mean age 47 years), who presented with thyroid enlargement were evaluated by fine-needle aspiration cytology (FNAC) of the thyroid as the first-line investigation. The final cytological or histological diagnosis was determined after surgery (n = 312) or clinical follow-up for a minimum period of 2 years (range 2-14 years, mean 6.7 years). Goiter type was assessed clinically and was classified as diffuse in 147, multinodular in 247, or solitary nodule in 611. The overall sensitivity and specificity of the procedure in the detection of thyroid neoplasia was 88% and 89%, respectively. Males who presented with thyroid enlargement had significantly higher rates of malignancy (p = 0.007) and neoplasia (benign + malignant) (p = 0.002) than females, as did subjects with solitary nodule compared with diffuse or multinodular goiters (malignancy p = 0.001, neoplasia p < 0.001). Subjects with normal thyrotropin (TSH) (>0.4 mU/L) at presentation had a nonsignificantly increased risk of thyroid neoplasia (p = 0.07) and malignancy, in contrast to those with low TSH (<0.4 mU/L). We confirmed FNAC of the thyroid to be an accurate test in the detection of thyroid neoplasia. Gender and goiter type at presentation both contribute significantly to the prediction of the diagnosis of thyroid neoplasia.

Adolescent↗
PubMed2000

Growth factor-expressing mast cells accumulate at the thyroid tissue-regenerative site of subacute thyroiditis.

The localization and biological roles of the multifunctional cell type mast cells remain unclear in subacute thyroiditis that is characterized by both epithelioid granuloma formation and thyroid tissue repair. We examined their immunolocalization with tryptase of a mast cell marker, using the biopsy specimens from 12 cases. In the epithelioid granuloma, no mast cells were detected in any of the cases, although a small number of them (4.6 +/- 2.4) were seen at the fibrous stroma around the granuloma in all cases. By contrast, in all cases, increased mast cells (28 +/- 7.2) localized at the thyroid tissue-regenerative site where both thyroid folliculogenesis and angiogenesis take place. To elucidate possible roles of mast cells in the disease, we also examined their immunoexpressions of vascular endothelial cell growth factor (VEGF), basic fibroblast growth factor (bFGF), platelet-derived growth factor-BB (PDGF), transforming growth factor-beta1 (TGF-beta1) and epidermal growth factor (EGF), which affect thyroid folliculogenesis and angiogenesis. In all 12 cases, mast cells displayed all of these growth factors in a manner not specific to the infiltrating site. The data suggest that growth factor-expressing mast cells may play crucial roles in the thyroid tissue repair of subacute thyroiditis, modulating thyroid folliculogenesis and angiogenesis; and that the multifunctionality of the cells may be partly dependent on their expressions of various growth factors.

Acute Disease↗
PubMed1988

Carcinomatous involvement of the thyroid presenting as subacute thyroiditis.

Carcinomatous involvement of the thyroid is a most unusual cause of hyperthyroidism and thyroiditis, with only a few cases reported in the literature. The authors present a 35-year-old woman with signs, symptoms, and laboratory findings of hyperthyroidism, and subacute thyroiditis that was due to extensive replacement of the thyroid gland by adenocarcinoma (shown by fine needle aspiration). After chemotherapy with vincristine and cisplatin, the swelling of the thyroid resolved, thyroidal uptake of radioactive iodine increased, and mild hypothyroidism developed. Despite the improvement in her thyroid status, she died from progressive malignancy. This case illustrates the value of fine needle aspiration cytology where doubt exists in the diagnosis of thyroid disorders.

Adenocarcinoma↗
PubMed1981

Feasibility of low doses of I-131 for thyroid ablation in postsurgical patients with thyroid carcinoma.

The feasibility of using low doses of I-131 (30 mCi) for ablation of thyroid remnants following surgery for papillary and follicular thyroid carcinoma was examined in 21 patients. Six weeks following near-total thyroidectomy and three days following intramuscular thyroid-stimulating hormone (10 IU), patients were given 30 mCi of I-131 and scans were performed 24 to 72 hours later. Remaining thyroid tissue was identifiable in the thyroid bed in 19 patients, and two patients also had evidence of cervical metastases. Patients with metastases received an additional 100 mCi of I-131. Follow-up I-131 scans were performed at nine to 15-month intervals in ten patients who initially received 30 mCi of I-131, and only one patient showed complete ablation of the residual thyroid tissue, whereas the remaining nine patients had persistent uptake of I-131 in the same regions in which the uptake was seen in the initial postoperative scans. One of the nine patients had evidence of a cervical metastasis as well. It is therefore apparent that total or near-total thyroidectomy rarely removes all thyroid tissue and that an "out-patient" dose of I-131 is not adequate for ablation of postoperative thyroid remnants.

Adenocarcinoma↗
PubMed2000

Thyroid transcription factor-1, thyroglobulin, cytokeratin 7, and cytokeratin 20 in thyroid neoplasms.

Thyroid transcription factor-1 (TTF-1), a member of the NKx2 family of homeodomain transcription factors, is a mediator of thyroid-specific transcription of the thyroglobulin (TG) gene. The combined immunohistochemical profile of TTF-1, TG, cytokeratin 7 (CK7), and cytokeratin 20 (CK20) in neoplasms of the thyroid gland and their metastases to other sites has not been defined previously. Formalin-fixed tissue of 43 thyroid tumors, including 31 carcinomas and 12 adenomas, and 16 metastasic lesions were immunostained using monoclonal antibodies to TTF-1, TG, CK7, and CK20. Immunoreactivity of the primary tumors (adenomas and carcinomas) for TTF-1 was seen in 32 cases (74%), TG 32 (74%), and CK7 34 (79%), whereas none (0%) showed positivity for CK20. The distribution of reactivity in the 31 carcinomas for TTF-1, TG, and CK7, respectively was papillary (8/8), (8/8), and (8/8); poorly differentiated (6/7), (4/7), and (6/7); oncocytic (Hürthle) cell (2/6), (6/6), and (4/6); follicular (4/4), (3/4), and (3/4); medullary (1/2), (0/2), and (1/2). One of four anaplastic carcinomas was focally immunoreactive showing positivity for TTF-1 only. Of the six follicular adenomas, five were positive for TTF-1, six for TG, and six for CK7. Among the six oncocytic cell adenomas, five were reactive for TTF-1, five for TG, and all six for CK7. Twelve (75%) of the 16 metastatic tumors were positive for TTF-1, 10 (63%) for TG, 15 (94%) for CK7, and none (0%) for CK20. In summary, TTF-1 and TG are demonstrable by immunohistochemistry in the majority of thyroid neoplasms. Compared with TG, an antibody to TTF-I is a similarly sensitive marker for thyroid tumors. Moreover, TTF-1 is a more sensitive marker for poorly differentiated carcinomas and metastasis. In most cases, its nuclear pattern of immunoreactivity facilitates interpretation. Thyroid tumors are CK7+/CK20-. The panel of antibodies for TG, TTF-1, CK7, and CK20 is useful when the thyroid origin of a metastatic tumor is a consideration.

Adenoma↗
PubMed1987

Lymphocytic choriomeningitis virus can persistently infect thyroid epithelial cells and perturb thyroid hormone production.

Although viral infection has been suspected as the cause of some thyroid disorders, there has been limited data to support this contention seriously. Now we report the first evidence that lymphocytic choriomeningitis virus can persist in the thyroid gland, particularly thyroid epithelial cells in which thyroglobulin (Tg) the precursor of thyroid hormone, is synthesized. Concomitant with the infection of these cells is a significant reduction in Tg mRNA and in the level of circulating thyroid hormones. Another virus (lactate dehydrogenase virus) that causes persistent infection but does not replicate in the thyroid gland failed to alter levels of circulating thyroid hormones. These observations in an experimental model support the hypothesis that viruses may account for some thyroid disorders in man.

Animals↗
PubMed1976

Evidence that mouse thyroid stimulator does not stimulate the human thyroid gland.

Thyroid 131I uptake and human thyroid stimulator (HTS) level were measured in 20 untreated thyrotoxic patients who also showed mouse thyroid stimulator (MTS) ACtivity. The correlation between thyroid uptake and HTS level was highly significant (P less than 0-005), the coefficient, r, being 0-66, comparable with the value 0-68 obtained in a previous study of patients not showing MTS. Thus, the presence of widely varying amounts of MTS does not impair the close correlation existing between HTS level and thyroid 131I uptake in thyrotoxic people. There was no correlation between MTS level and thyroid 131I uptake (r = 0-11, n.s.). It is concluded that MTS, a potent stimulator of the thyroid glands of mice, guinea pigs and monkeys, does not stimulate the human thyroid gland.

Animals↗
PubMed1992

The role of thyroid stimulating antibody (TSAb) in the thyroid function of patients with post-partum hypothyroidism.

OBJECTIVE: We investigated the association between thyroid function and the biological activities of thyroid stimulating antibodies (TSAb) and thyroid stimulation blocking antibodies (TSBAb) in patients with post-partum hypothyroidism. DESIGN: A prospective study. PATIENTS: We studied 25 patients with post-partum hypothyroidism who visited our thyroid clinic during the period from 1985 to 1990. MEASUREMENTS: We measured TSH binding inhibitory immunoglobulin (TBII) and TSAb activity at the initial presentation of each of the 25 patients. Women found to have elevated TSAb activity were followed up. Upon finding negative TSAb activity along with positive TBII activity in the serum at the initial presentation, we measured TSBAb activity. Women found to have elevated levels of TSBAb at the initial presentation were also followed up. RESULTS: Elevated TBII activity was found in six of the 25 patients, as was high TSAb activity (205-2651%, normal 55.0-145.0%) in five of these six and in one other patient at the initial presentation. Markedly elevated TSBAb activity (89%) was found in one TBII positive patient. We were able to follow up serially five TSAb positive patients and the TSBAb positive patient over periods ranging from 11.5 to 26.5 months post-partum. The maximal value of TSAb activity was observed at the initial presentation in all TSAb positive patients, following which the activities gradually decreased. One of these patients developed Graves' hyperthyroidism associated with high TSAb activity (1223%) at 10.5 months post-partum. One of the other patients was restored to euthyroid with elevated TSAb activity (279%), but thereafter developed hypothyroidism in conjunction with the disappearance of TSAb activity at 26.5 months post-partum. In the other two patients, normalization of thyroid function was observed with elevated TSAb activity. Thereafter, thyroid function remained within the normal range even with the disappearance of TSAb activity. In the other patient, normalization of thyroid function was observed at 11.5 months post-partum, 3 months after the disappearance of TSAb activity. In the TSBAb positive patient, TSBAb activity decreased to 21% by 17.5 months post-partum associated with normalization of thyroid function. CONCLUSION: The present study demonstrates the presence of elevated levels of TSAb activity in some patients with post-partum hypothyroidism. In these patients, Graves' hyperthyroidism may be induced by TSAb activity, and hypothyroidism may reoccur with the disappearance of the TSAb activity. Furthermore, post-partum hypothyroidism may be due to increased TSBAb activity in some patients.

Antibodies↗