Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “thyroiditis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources
PubMed2005

[Differentiated thyroid carcinoma in previously manifested autoimmune thyroid disease].

Autoimmune thyroid diseases are frequently associated with differentiated thyroid carcinomas. The role of autoimmune phenomena in the origin and clinical course of coexisting papillary and follicular carcinomas is still controversial. In Graves' patients, the prevalence of palpable thyroid nodules is 15.8%, and by using ultrasonography, the prevalence increases to 33.6%. Since the malignancy rate of palpable thyroid nodules in Graves' patients is 16.9%, approximately threefold higher than in general population, it seems that a thyroid nodule diagnosed in Graves' patients is at higher risk for malignancy. In addition, radioiodine therapy for Graves' disease was found to be associated with increased incidence of thyroid cancer in some studies. These studies however, were not able to confirm the carcinogenic effect of radioiodine therapy since the late growth of occult carcinomas could not be excluded. The frequency of the association of Hashimoto's thyroiditis and differentiated thyroid carcinomas is approximately 30%. The presence of coexistent Hashimoto's thyroiditis does not affect the diagnostic evaluation and management of papillary thyroid cancer. The frequent presentation of differentiated thyroid carcinomas in Graves' disease and Hashimoto's thyroiditis opens the possibility that some mutual pathogenethic mechanisms might be involved in the development of these diseases.

Adenocarcinoma, Follicular↗
PubMed1989

Distribution of calcitonin- and somatostatin-containing cells in thyroid lymphoma and in Hashimoto's thyroiditis.

Eleven cases of thyroid lymphoma were studied by the immunoperoxidase avidin-biotin technique with calcitonin and somatostatin rabbit antisera. In 6 cases of non-Hodgkin lymphoma, in thyroid tissue residual to the lymphomatous infiltration, the C cell density was markedly increased and clustering was often observed; the C cells often took part in the follicular lining, frequently with polar distribution; these elements displayed a strong positivity for calcitonin, while the number of somatostatin-containing cells was lower and the staining less intense. In the only case of Hodgkin's lymphoma of the thyroid gland the staining was negative; in other 4 cases of non-Hodgkin lymphoma no residual thyroid tissue was found and the staining was also negative. As Hashimoto's thyroiditis is often associated with thyroid lymphoma, 13 cases of Hashimoto's thyroiditis were also studied; no C cells were observed and both stainings were negative. These data show that an increase in the C cell number may be a hallmark of thyroid lymphoma and that hyperplastic C cells show an intensive positivity for calcitonin. On the other hand, C cell hyperplasia is not present in Hashimoto's thyroiditis, in spite of the close association with thyroid lymphoma. Furthermore, we provide evidence that somatostatin-containing cells are present both in normal thyroid glands and in thyroid lymphoma.

Calcitonin↗
PubMed2026

Thyroid-joint crosstalk: a systematic review and meta-analysis of thyroid autoimmunity and dysfunction in juvenile idiopathic arthritis.

BACKGROUND: Recent observational studies outlined the concomitant presence of autoimmune diseases in children with juvenile idiopathic arthritis (JIA), including endocrine autoimmunity. Despite the growing evidence of thyroid involvement in JIA, available data are heterogeneous and fragmented. We aimed to systematically review the available evidence on the prevalence of thyroid autoantibody positivity and thyroid dysfunction in patients with JIA. METHODS: PubMed/Medline, Cochrane, and Scopus databases were approached to identify studies reporting data on thyroid autoantibody positivity and dysfunction in children with JIA. RESULTS: A total of 15 studies were included in the final analysis, encompassing 19 015 children with JIA (13 225 females, 69.6%) with a weighted mean age of 8.0 years (range 1.8-21 years). The pooled prevalence estimates of antithyroid antibody positivity and thyroid dysfunction were 0.04 (95% CI: 0.03-0.05) and 0.04 (95% CI: 0.03-0.08), respectively. The risk difference for thyroid autoantibody positivity between children with JIA and controls was 0.08 (95% CI: 0.02-0.14). Possible risk factors were analyzed: the presence of family history for thyroid autoimmune disease (odds ratio - OR 3.91, 95% CI 1.86-8.25), concurrent Antinuclear Antibodies (ANA) positivity (OR 1.62, 95% CI 1.13-2.31), and older age (MD 2.10 years, 95% CI 1.32-2.89) were associated with thyroid autoantibody positivity and/or thyroid dysfunction in children with JIA. No significant difference emerged for the specific JIA form. CONCLUSION: Thyroid dysfunction may be detected in children with JIA, with a significant risk difference in comparison to healthy controls. Specific clinical characteristics, such as family history, ANA positivity, and older age at JIA onset, may suggest which patients should benefit from thyroid autoantibody screening.

Humans↗
PubMed2006

[Cytofluorometric analysis of chosen markers of apoptosis CD95/CD95L (Fas/FasL) in thyroid tissues from young patients with Graves' disease and Hashimoto's thyroiditis].

BACKGROUND: Apoptosis, one of the forms of programmed cell death, is a physiologic process of cell death that is central to normal development and occurs in response to a variety of physiologic and pathophysiologic stimuli. In the thyroid, abnormal apoptotic activity may be involved in a variety of diseases such as Hashimoto thyroiditis and Graves disease. The aim of this study was to estimate the expression of chosen apoptotic molecules CD95 (Fas) and CD95L (FasL) on the surface of thyroid follicular cells in application of mouse monoclonal antibodies #64 which recognized B antigen regions of thyroid peroxidase (TPO) and infiltrating inflammatory cells. MATERIAL AND METHODS: The investigation was performed on thyroid cells isolated from surgically treated thyroid tissues of 15 patients with Graves' disease (GD), 15 patients with a nontoxic multinodular goiter (NTMG) and 15 aspirates obtained by FNAB from patients with Hashimoto thyroiditis (HT). The thyrocytes were identified by an indirect method: in the first stage we added mouse monoclonal autoantibodies specific for TPO (mAb #64) regions and in the second stage we conjugated this complex with rabbit anti-mouse antibodies IgG (Fab')2 with FITC. In the next step the cellular suspension was completed with suitably well-chosen two-colour monoclonal antibodies marked (PE or PerCP) (Becton Dickinson) directed against suitable apoptotic (Fas/FasL) molecules. All investigations were performed by flow cytometry using Coulter EPICS XL apparatus. RESULTS: The percentages of thyroid cells were estimated with expression of region B antigenic TPO in reference to individual apoptotic molecules. The analysis of Fas and FasL expression in thyroid tissues revealed significantly increased percentage of intrathyroidal T cells with CD95+ (p<0.005, p<0.001), CD95L+ (p<0.02, p<0.01) and both CD95/CD95L (ns, p<0.05) expression in comparison to percentages of T cells in patients with HT and NTMG. In addition, on the surface of thyroid follicular cells in patients with GD (p<0.01, p<0.01) and NTMG (p<0.001, p<0.004) we observed a lower percentage of thyrocytes with CD95 and CD95L molecules than in cases with HT. The expression of both apoptotic molecules on thyroid cells was higher (18%) in patients with HT in comparison to the percentages of positive cells in patients with GD (p<0.02, p<0.002) and NTMG, 8% and 1%, respectively. CONCLUSIONS: We conclude that alterations in the expression of death receptors and their ligands on the surface of thyroid follicular cells may play a role in the regulation of apoptosis in thyroid autoimmune disorders.

Adolescent↗
PubMed1998

Cyclin D1 and Cyclin E expression in malignant thyroid cells and in human thyroid carcinomas.

Evidence of the involvement of cyclin gene alterations in human cancer is growing. In this study, we sought to determine the pattern of expression of cyclin D1 and cyclin E in normal and malignant thyroid cells. Quiescent rat thyroid cells in culture, induced to synthesize DNA by thyrotropin (TSH), expressed cyclin D1 gene after 6 hr and cyclin E gene with a peak at 18 hr from the stimulus; K-ras-transformed rat thyroid cells, which grew without addition of hormones necessary for normal cell proliferation, expressed elevated levels of cyclin D1 and cyclin E, compared with normal differentiated thyroid cells. Human benign and malignant thyroid tumors and their relative normal tissues were then analyzed. Neither major genetic alterations nor amplifications for cyclin D1 and cyclin E genes were found by Southern blot analysis in genomic DNAs extracted from all types of thyroid tumors. Moreover, statistical analyses of densitometric values from Northern blots did not show increased levels of cyclin D1 and E mRNAs in the tumor samples, compared with normal thyroid. Immunohistochemical analyses of formalin-fixed paraffin-embedded sections of tissues with specific antibodies revealed a prevalent cytoplasmic cyclin E staining in the thyroid tissues analyzed. Cyclin D1, instead, was present in the cytoplasm of normal thyroids and adenomas, but in 31% of thyroid papillary carcinomas analysed, it was overexpressed, with a localization in the nucleus. Our in vivo observations suggest that unlike cyclin E, elevated nuclear cyclin D1 expression defines a subset of thyroid papillary carcinomas, and might be a contributory factor to thyroid tumorigenesis.

Animals↗
PubMed1993

Transfer of experimental autoimmune thyroiditis by in situ perfusion of thyroids with immune sera.

The role of autoantibodies in the pathogenesis of autoimmune thyroiditis (AT) still remains poorly understood. Serum transfer experiments in experimental AT (EAT) and spontaneous AT (SAT) animal models frequently did not succeed or only resulted in minor thyroid lesions. The inconsistent results may have arisen because of technical problems inherent in serum transfer, the major of which is to obtain high enough concentrations of autoantibodies over long enough periods at the potential site of tissue injury. An attempt was made to circumvent this hurdle by repeated in situ perfusions of the rabbit thyroid via the superior thyroid artery. In situ perfusion of rabbit thyroids with high-titered homologous sera reactive with saline thyroid extract indeed led to thyroiditis characterized by granular deposits of rabbit IgG and C3 in the thyroid follicular basal laminae, cellular infiltrates consisting of mononuclear cells and granulocytes, destruction of the thyroid follicular architecture, and focal fibrosis. Perfusion with control sera lacking thyroid-reactive antibodies did not lead to thyroid lesions. These results demonstrate that humoral antibodies can induce severe AT comparable to actively induced thyroiditis.

Animals↗
PubMed1993

Increased binding capacity of receptors for the epidermal growth factor in benign thyroid nodules and thyroid malignancies.

To determine the role of epidermal growth factor (EGF) receptors in thyroid tumorigenesis, EGF binding was compared in membranes from malignant and from benign thyroid tumors. Surgical specimens were obtained from 28 patients with thyroid carcinomas (3 papillary, 13 follicular, 6 undifferentiated, and 6 medullary carcinomas) and from 30 patients with benign thyroid tumors (15 scintigraphically functional and 15 nonfunctional nodules). In 30 cases normal tissue adjacent to the tumor was also obtained. EGF binding was seen to be increased not only in thyroid carcinomas but also in benign thyroid tumors, particularly in functional thyroid adenomas. The highest EGF binding was found in undifferentiated carcinomas. A direct comparison of the EGF binding characteristics in tumor and adjacent normal thyroid tissue revealed that the increased binding of EGF is due mainly to an increase in the number of binding sites rather than an alteration in receptor affinities. EGF binding capacities were 18.4 +/- 16.7 fmol/mg protein in thyroid carcinomas and 10.5 +/- 5.2 fmol/mg in the corresponding normal tissue (P < 0.05, Kd 0.84 +/- 0.26 nM, n = 11). In autonomously functioning thyroid adenomas binding capacities were 14.2 +/- 8.2 fmol/mg in the nodules and 8.9 +/- 4.8 fmol/mg in normal tissue (P < 0.01, Kd 0.73 +/- 0.62 nM, n = 15). In conclusion, EGF receptor levels are increased not only in malignant thyroid tumors but also in well-differentiated benign thyroid nodules.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2000

Occurrence of Riedel's thyroiditis in the course of sub-acute thyroiditis.

Riedel's Thyroiditis is an uncommon form of chronic thyroiditis characterized by an invasive fibrosclerosis of the gland, often involving surrounding tissue. The relationship of Riedel's Thyroiditis to other forms of thyroiditis is not clear. We presented a 47 year-old woman first diagnosed with sub-acute thyroiditis based on clinical findings and laboratory results. Eight months later, she had a thyroidectomy operation due to an enlargement of the thyroid gland and symptoms of compression. Histopathologic evaluation showed that she had Riedel's Thyroiditis, but there were some histopathologic findings of sub-acute thyroiditis as well. Until now, there has only been one case reported in which Riedel's Thyroiditis was diagnosed in a patient with a history of sub-acute thyroiditis in the literature. Although aetiology of Riedel's Thyroiditis is unknown, it may develop in the course of sub-acute thyroiditis.

Acute Disease↗
PubMed1985

The aging thyroid. Relationship between elevated serum thyrotropin level and thyroid antibodies in elderly patients.

The relationship of thyroid antibodies and the serum level of thyrotropin in older adults (over age 60) was studied to determine whether thyroid antibodies were a good clue to thyroid failure in elderly persons. Of those with thyroid failure, evidenced by clearly elevated serum thyrotropin values (more than 10 microU/ml), 67 percent had positive antimicrosomal antibody levels, a prevalence much greater (p less than 0.001) than that among those of comparable age with normal thyroid function (18 percent). Nevertheless, one third (33 percent) had thyroid failure without positive antimicrosomal antibody levels; this was true whether or not a low serum thyroxine value was present. Furthermore, of those with positive antimicrosomal antibody levels, most (68 percent) did not have thyroid failure. Thus, although positive antimicrosomal antibody levels occurred more often in elderly patients with thyroid failure than in those with normal thyroid function, a sizable fraction of those with thyroid failure did not have positive antimicrosomal antibody levels. Hence, measurement of thyroid antimicrosomal antibodies is not a good test of early thyroid failure in older patients; direct demonstration of a clearly elevated serum thyrotropin value is a better approach.

Adult↗
PubMed2004

[Thyroid hormone levels and thyroid dysfunction of French adults participating in the SU.VI.MAX study].

Abnormal thyroid function has important public health consequences. However, the various degrees of thyroid dysfunction remain unsettled. The SU.VI.MAX cohort provided a unique opportunity to conduct a cross-sectional study of abnormal thyroid function in a large representative population of 11256 men and women representing the geographic distribution of the French continental adult population. Thyroid status was measured, in fasting blood samples, at baseline in 1994-1995. Serum thyrotropin (TSH) levels (abnormal < 0.4 mU/l or > or =4.0 mU/l) and free thyroxine (fT4) were both performed in duplicate on the same sample. Subjects with previous or present thyroid diseases or who were taking thyroid hormones or antithyroid drugs (n=920) were excluded (8.1%). Thus, the final study group consisted of 10346 subjects, 4121 men aged 45-60 years (mean +/-SD) (51.8+/-4.7 yrs), 2641 women aged 35-44 years (40.6+/-2.8 yrs), and 3584 women aged 45-60 years (51.4+/-4.4 yrs). Median (2.5th and 97.5th percentiles) for TSH (mU/l) were 1.52 (0.20-4.54) for men, 1.78 (0.22-5.54) for women aged 35-44 years, and 1.96 (0.22-6.80) for women aged 45-60 years. The TSH distribution of women was shifted to the right compared with men. Arithmetic mean fT4 (+/-SD) was 10.7+/-1.7 ng/l (13.8 +/-2.2 pmol/l) for men and 10.9+/-1.8 ng/l (14.0+/-2.3 pmol/l) for women. The prevalence of abnormal TSH values in men, and in women (35-44 yrs and 45-60 yrs) were TSH<0.4 mU/l 7.0%, 5.3% and 4.4%; TSH 4.0-9.9 mU/l 4.0%, 7.2% and 11.1% and TSH > or =10.0 mU/l 0.2%, 0.4% and 0.7%, respectively. Geometric mean serum TSH and arithmetic mean serum fT4 concentrations showed significant overall inter-regional differences for men and women (p<0.0001). There was also an inter-regional difference in the prevalence of thyroid dysfunction for men (p=0.003), and for the older group of women (i.e. > or =45 yrs) (p=0.04) exclusively. Over the age of 45 years, the women: men ratio for unrecognized elevated TSH levels (> or =4.0 mU/l) was 2.82, whereas it was 0.64 for low TSH levels (<0.4 mU/l). In summary, abnormal TSH values and thyroid dysfunction were more prevalent in women than men, increased with age and were significantly associated with environmental factors. A high prevalence of identified thyroid diseases in the French population was confirmed by the high number of subjects in this study with laboratory evidence of abnormal biochemical thyroid function. Further studies are needed to determine the geographical determinants of thyroid dysfunctions, especially regional differences in iodine intakes, and to assess the long-term adverse effects of biochemical thyroid dysfunction on all-cause morbidity.

Adult↗
PubMed1996

Thyroid-stimulating hormone promotes the secretion of vascular endothelial growth factor in thyroid cancer cell lines.

BACKGROUND: Vascular endothelial growth factor (VEGF) is a vascular endothelial cell-specific mitogen secreted by some cancer cells and is a major regulator of angiogenesis. Because thyroid-stimulating hormone (TSH) promotes growth and progression of thyroid cancers, we postulated that TSH may increase the production and secretion of VEGF by thyroid cancer cells. METHODS: We examined primary cultures of normal human thyroid (NT 1.0), medullary thyroid cancer (MTC 1.1), and cell lines derived from the papillary (TPC-1), follicular (FTC-133), and Hürthle cell (XTC-1) thyroid cancer. We quantified the concentration of VEGF in conditioned medium by means of enzyme-linked immunosorbent assay. RESULTS: Cell lines derived from thyroid secrete VEGF. Basal VEGF secretion was similar in normal and thyroid cancer cells, except XTC-1, which has high basal secretion (p < 0.01). All thyroid cancer cells secrete significantly more VEGF than normal thyroid cells after TSH (10 mIU/ml) stimulation (p < 0.05). TSH stimulated secretion of VEGF in FTC-133 (8.2 ng/dl versus 18.8 ng/dl), TPC-1 (5.5 ng/dl versus 26.9 ng/dl), and MTC 1.1 (5.9 ng/dl versus 13.4 ng/dl) cell lines (p < 0.01), but not in NT 1.0 (8.4 ng/dl versus 9.9 ng/dl) and XTC-1 (25.4 ng/dl versus 31.2 ng/dl) cells. CONCLUSIONS: These results suggest that VEGF secretion is constitutively activated in some thyroid cancers and that VEGF secretion is stimulated by TSH; thus TSH may promote growth in some thyroid cancers by stimulating VEGF secretion and angiogenesis.

Endothelial Growth Factors↗
PubMed2005

Thyroid hormones directly activate the expression of the human and mouse uncoupling protein-3 genes through a thyroid response element in the proximal promoter region.

The transcription of the human UCP3 (uncoupling protein-3) gene in skeletal muscle is tightly regulated by metabolic signals related to fatty acid availability. However, changes in thyroid status also modulate UCP3 gene expression, albeit by unknown mechanisms. We created transgenic mice bearing the entire human UCP3 gene to investigate the effect of thyroid hormones on human UCP3 gene expression. Treatment of human UCP3 transgenic mice with thyroid hormones induced the expression of the human gene in skeletal muscle. In addition, transient transfection experiments demonstrate that thyroid hormones activate the transcription of the human UCP3 gene promoter when MyoD and the TR (thyroid hormone receptor) were co-transfected. The action of thyroid hormones on UCP3 gene transcription is mediated by the binding of the TR to a proximal region in the UCP3 gene promoter that contains a direct repeat structure. An intact DNA sequence of this site is required for thyroid hormone responsiveness and TR binding. Chromatin immunoprecipitation assays revealed that the TR binds this element in vivo. The murine Ucp3 gene promoter was also dependent on MyoD and responsive to thyroid hormone in transient transfection assays. However, it was much less sensitive to thyroid hormone than the human UCP3 promoter. In summary, UCP3 gene transcription is activated by thyroid hormone treatment in vivo, and this activation is mediated by a TRE (thyroid hormone response element) in the proximal promoter region. Such regulation suggests a link between UCP3 gene expression and the effects of thyroid hormone on mitochondrial function in skeletal muscle.

Animals↗
PubMed1999

Coexistent Hashimoto's thyroiditis with papillary thyroid carcinoma: impact on presentation, management, and outcome.

BACKGROUND: This study was performed to assess the relationship between Hashimoto's thyroiditis and the development, presentation, management, and outcome of papillary thyroid carcinoma. METHODS: Two complementary analytic methods were used. The clinical study was a retrospective case-control study, including patients seen with papillary thyroid carcinoma presenting during a 12-year period. We also used a systematic literature review to identify suitable reports and meta-analysis to statistically combine published results. RESULTS: The prevalence of Hashimoto's thyroiditis is significantly higher in patients with papillary thyroid cancer (odds ratio, 1.89; 95% CI, 1.02-3.50). These patients typically have a dominant nodule, 44% of which are discovered incidentally on routine examinations. Fine-needle aspiration has a sensitivity of 91% for the identification of papillary cancer. The prognostic variables at the time of a diagnosis of papillary cancer and the approach to management are not altered by the presence of coexistent Hashimoto's thyroiditis. In addition, the rate of surgical complications was not higher in patients with coexistent Hashimoto's disease. Meta-analysis suggested a positive correlation between Hashimoto's disease and disease-free survival (r = 0.09; 95% CI, 0.05-0.12) and overall survival (r = 0.11; 95% CI, 0.07-0.15). CONCLUSIONS: There is an increased prevalence of Hashimoto's thyroiditis in patients with papillary thyroid carcinoma. The presence of coexistent Hashimoto's thyroiditis does not affect the diagnostic evaluation or management of papillary thyroid cancers. The survival of patients who have papillary thyroid cancers may be superior in coexistent Hashimoto's thyroiditis.

Adult↗
PubMed2006

Thyroid ultrasound in diabetic patients without overt thyroid disease.

PURPOSE: To assess thyroid volume and to evaluate possible lesions in the gland structure using thyroid ultrasound in patients with diabetes mellitus type 1 (DM1) and 2 (DM2) without overt thyroid disease. MATERIAL AND METHODS: Consecutive adult patients with DM2 (n = 98) and DM1 (n = 30) without overt thyroid disease referred to our department because of poorly controlled disease and/or diabetic complications were prospectively analyzed. Thyroid volumes, gland echogenicity, thyroid nodules incidence, and TSH levels were compared with control groups (n = 50 and 38) and matched according to sex and age. RESULTS: Significant increases in median thyroid volume were observed in both subjects with DM1 (17.3 cm3, interquartile range (IR) 13.9-21.6 cm3 versus 14.4 cm3, IR 11.3-18.3 cm3; P < 0.05) and DM2 (20.5 cm3, IR 14.9-27.1 cm3 versus 14.1 cm3, IR 11.3-18.3 cm3; P < 0.001) in comparison to their control groups. Moreover, in the population of type 2 diabetics, thyroid nodules (OR 2.37, 95% CI 1.14-4.93), parenchymatous goiter (OR 5.40, 95% CI 1.20-24.30), and all kinds of thyroid goiter according to the WHO definition (OR 4.18, 95% CI 2.02-8.66) were remarkably more frequent. In our patients, reduced (but within normal range) TSH level occurred in DM1 (median 0.97 mIU/l, IR 0.61-1.58 mIU/l versus median 1.66 mIU/l, IR 0.76-2.09 mIU/l; P < 0.05). The presence of a negative linear correlation between thyroid volume and TSH concentration was noticed in patients with DM2 (RS = -0.38, P < 0.01). CONCLUSION: In individuals with DM1 and DM2 treated for poorly controlled disease and/or diabetic complications, thyroid volumes were significantly higher than in the normal population. Moreover, nodular thyroid structure and parenchymatous goiter occurred more frequently in these type 2 diabetic patients.

Adult↗
PubMed2000

Review of thyroid cancer cases among patients with previous benign thyroid disorders.

A previous register linkage study showed an increased risk of thyroid cancer among patients previously discharged from a hospital with a diagnosis of a benign thyroid disorder. In this study, we have reviewed all available medical records, first to validate the earlier result and second to describe the symptomatology of patients with a history of benign thyroid disorder prior to the cancer diagnosis. The previous study identified 189 patients with a benign and subsequent malignant thyroid disorder. Medical records were obtainable for 156 of these patients and were reviewed. For 104 patients, benign and malignant thyroid diseases were metachronous (a clearly separated disease history of the benign and malignant diseases), and for 48 patients synchronous. In 4 cases, thyroid cancer could not be confirmed. Among patients with metachronous thyroid disorders, all major benign thyroid disorders were represented including hot nodules, diffuse and multinodular toxic and nontoxic goiter. Symptoms preceding diagnosis of thyroid cancer included growth of goiter/nodules, globulus, stridor, hoarseness, and metastasis. No major differences were found among patients with metachronous and synchronous benign and malignant thyroid disorder, apart from the fact that all metastases were found among metachronous cases. This study confirmed the conclusion that patients with a previous history of goiter or nodules have an increased risk of thyroid cancer. However, thyroid cancer still occurs too infrequently to warrant screening in all patients with a previous history of goiter or nodules.

Goiter↗
PubMed2001

Thyroid transcription factor-2 gene expression in benign and malignant thyroid lesions.

Thyroid transcription factor-2 (TTF-2) is a recently cloned thyroid-specific gene and is central to the development and differentiation of the thyroid follicular cell. Information regarding transcript levels in normal and diseased adult human thyroids is lacking. We have investigated TTF-2 gene expression in various thyroid pathologies and assessed its potential in preoperative diagnosis of thyroid nodular disease, which is a common clinical problem. We have used reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization (ISH) and detected TTF-2 transcripts in 60% of 125 samples of adult human thyroids tested by RT-PCR (64% of 35) or ISH (59% of 90). In normal thyroid tissues TTF-2 transcript levels are low, 18 of 36 were weakly positive and 18 of 36 negative when tested by ISH. In the benign lesions, TTF-2 transcripts were detected either by RT-PCR or ISH in 8 of 8 Graves disease; 3 of 7 Hashimoto's; 2 of 2 follicular hyperplasia; 15 of 21 follicular adenoma; 11 of 13 multinodular goiters and 0 of 1 hyalinizing trabecular adenoma. In the malignant thyroid lesions, TTF-2 transcripts were detected in 8 of 18 follicular cancers; 0 of 2 anaplastic carcinoma, and 11 of 17 papillary cancers. Compared with normal thyroids, transcripts were more abundant in 24% of thyroid lesions tested by ISH. In conclusion, we report for the first time on TTF-2 gene expression in normal and diseased adult human thyroids.

Adult↗
PubMed2003

Familial aggregation of autoimmune thyroiditis in first-degree relatives of patients with juvenile autoimmune thyroid disease.

Several studies have shown aggregation of autoimmune thyroiditis in families by estimation of thyroid antibodies. However, the prevalence by concurrent estimation with fine-needle aspiration cytology (FNAC) and thyroid antibodies has not been previously reported. We therefore studied 222 first-degree relatives (group 1) of 71 index cases diagnosed as lymphocytic thyroiditis on FNAC and 81 family members (group 2) of 23 goitrous children diagnosed as colloid goiter on FNAC for comparison. Successful FNAC conducted in 122 group 1 subjects revealed lymphocytic thyroiditis in 51 (42%), whereas lymphocytic thyroiditis was diagnosed in only 5 goitrous subjects (13%) in group 2. Among group 1 subjects with FNAC-proven lymphocytic thyroiditis, antithyroid peroxidase (TPO) antibodies were found in 35 (67%), while in anti-TPO antibody positive goitrous relatives of group 1, lymphocytic thyroiditis was found in 36 (78%). Eight new cases of overt hypothyroidism and 45 new cases of subclinical hypothyroidism were diagnosed among group 1 subjects. Our study suggests: (1). familial clustering of autoimmune thyroiditis; (2). if only FNAC or thyroid antibodies is used for diagnosis of autoimmune thyroiditis in children, 22%-33% of cases are likely to be missed; and (3). serum thyrotropin (TSH) should be offered to all first-degree relatives of patients with juvenile autoimmune thyroiditis.

Adolescent↗
PubMed1998

Fibroblast growth factor-2 free from extracellular matrix is increased in papillary thyroid carcinomas and Graves' thyroids.

Fibroblast growth factor (FGF)-2 is stored in the extracellular matrix (ECM). We hypothesized that FGF-2 is mobilized from the ECM and binds to receptors on the surface of FGF-2 responsive cells during thyroid enlargement. To test this hypothesis, we estimated levels of FGF-2 free from ECM in thyroids by comparing the efficiency of two methods for FGF-2 extraction (low salt and high salt). Because the high salt concentration (more than 1.5 M NaCl) is necessary to release FGF-2 from the normal ECM, FGF-2 extracted by low salt is indicative of ECM-free FGF-2. Human papillary thyroid carcinomas, normal part thyroid, and Graves' thyroid tissues were homogenized separately in an extraction buffer containing either 0 M NaCl (low salt) or 2.0 M NaCl (high salt), and the concentration of FGF-2 in the extracts was measured by enzyme-linked immunosorbent assay (ELISA). The yields of low and high salt extracts of immunoreactive (ir)FGF-2 from papillary carcinomas (low salt: 40.0 +/- 7.5, high salt: 233 +/- 53 ng/g tissue, mean +/- SE) were significantly higher than those of normal thyroid tissues extracted by the corresponding salt concentration (low salt: 14.6 +/- 1.8, high salt: 123 +/- 12 ng/g tissue). On the other hand, the extractable irFGF-2 from Graves' thyroid tissues (low salt: 25.2 +/- 2.5, high salt: 135 +/- 24 ng/g tissue) were not significantly different from that of normal thyroid tissues. However, the ratio of the extractable irFGF from carcinomas and Graves' thyroids by low salt to that by high salt (0 M/2 M ratio = 0.206 +/- 0.051, 0.209 +/- 0.025) were significantly higher than that of normal thyroids (0.120 +/- 0.014) (p < 0.05). These results suggest that intratissue ECM-free FGF-2 is increased in papillary thyroid carcinomas and Graves' thyroid tissues, and therefore a greater amount of FGF-2 may be available for stimulation of FGF-2 responsive cells.

Blotting, Western↗