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 1,369 records · Page 76Linked to original sources
PubMed1979

Clinical evaluation of thyroid CT values in various thyroid conditions.

CT scans of the thyroid were performed with a Hitachi CT-W2 device. The CT value of the region of interest (ROI) was obtained from CT images of the thyroid. Mean and standard deviation was 112 +/- 10 in 44 normals. Out of 27 cases of hyperthyroidism, the CT value of 13 untreated cases of 58 +/- 4, and that of 13 cases under treatment was 73 +/- 7 in average. The CT value of the single cured case was 100. Twelve cases of chronic thyroiditis and 5 cases of hypothyroidism showed averages of 57 +/- 11 and 36 +/- 13, respectively. The results of the above-mentioned clinical study indicate the estimation of the CT value of the thyroid is useful for diagnosis of various thyroid conditions.

Humans↗
PubMed2003

Clear cells and thyroid transcription factor I reactivity in sclerosing mucoepidermoid carcinoma of the thyroid gland.

Clear cells have been described in mucoepidermoid carcinoma of the salivary glands, but to our knowledge these cells have not been recognized as a distinctive component of sclerosing mucoepidermoid carcinoma with eosinophilia of the thyroid gland. We report four examples in which sclerosing mucoepidermoid carcinoma of the thyroid gland contained a minor component (10% to 30%) of clear cells. The four tumors occurred in women with Hashimoto's thyroiditis whose ages ranged from 38 to 52 years. All four patients presented with thyroid nodules, but two also had enlarged cervical lymph nodes. Although two tumors metastasized to multiple cervical lymph nodes and one recurred in the soft tissues of the neck, all four patients are disease-free 6 months to 6 years after surgical treatment. The locally aggressive behavior of the first three tumors was probably related to their size, rather than to the presence of clear cells. Microscopically, these tumors showed the classical features of sclerosing mucoepidermoid carcinoma with eosinophilia, as well as nests of clear cells that appeared to be glycogen-rich squamous cells. Although the four tumors were thyroglobulin negative, two were immunoreactive to thyroid transcription factor 1 (TTF-1), supporting the idea that they originated from squamous metaplasia of follicular epithelium rather than from solid cell nests of the ultimobranchial body.

Adult↗
PubMed2002

[Thyroid scintigraphy: its place in preoperative diagnosis of thyroid nodules?].

AIM OF THE STUDY: To evaluate the real contribution of the thyroid radionuclid scanning in the preoperative evaluation of the thyroid nodules. MATERIAL AND METHOD: The authors prospectively studied 369 patients who underwent surgical intervention: 160 (43.4%) for isolated nodules and 209 (56.6%) for multinodular goiters. RESULTS: The scintigraphy of the thyroid was performed in 281 (76.2%) patients: 39 (13.8%) patients with nodules less than 1.5 cm in diameter and 242 (86.2%) patients with nodules more than 1.5 cm in diameter. In 234 patients (83.3%) the scintigraphic evaluation did not bring any utile information for the therapeutic decision. The scintigraphy proved its utility only in 47 patients, which represents 16.7% from the scintigraphic exams performed, or 12.7% from the patients that underwent a surgical procedure. CONCLUSIONS: In the presence of thyroid nodule or multinodular goiter, the scintigraphy is indicated only in decreased TSH level, suspicion of ectopic thyroid or retrosternal goiter.

Diagnosis, Differential↗
PubMed2000

Thyroid autoimmunity and its association with non-organ-specific antibodies and subclinical alterations of thyroid function in women with a history of pregnancy loss or preeclampsia.

Following the observation that non-organ-specific antibodies are related with pregnancy loss and preeclampsia, the role of organ-specific antibodies is currently being extensively investigated. The aim of this study was on the one hand to evaluate the incidence of antithyroid antibodies in a study group of 69 women with a history of early pregnancy loss (subgroup 1), foetal death (subgroup 2) or preeclampsia (subgroup 3) and in a control group, on the other hand to assess the possible association of these autoantibodies with non-organ-specific antibodies and subclinical alterations of thyroid function in the study group. Antithyroid antibodies were present in 26/69 (37.7%) women of the study group (37.9% in subgroup 1; 40.9% in subgroup 2; 33.3% in subgroup 3) and in 10/69 (14.5%) of controls, the difference being statistically significant. A significant difference in the distribution of antibodies to thyroglobulin and thyroid peroxidase was found in subgroup 2. In the study group, the incidence of antiphospholipid antibodies was not significantly different in women positive (26.9%) and negative (34.9%) for antithyroid antibodies. Also, the overall incidence of subclinical alterations of thyroid function in the study group was significantly different in women positive (53.8%) and negative (16.2%) for thyroid autoimmunity (P<0.02). The results of this study seem to confirm the association between thyroid autoimmunity and obstetric complications and suggest the usefulness of undertaking prospective studies in order to evaluate the reproductive outcome of women with a history of recurrent abortion, foetal death or preeclampsia and positivity for antithyroid antibodies.

Abortion, Habitual↗
PubMed1999

Thyroid-specific gene expression in the multi-step process of thyroid carcinogenesis.

Thyroid-specific transcription factors TTF-1 and Pax-8 play a decisive role in the determination and maintenance of cellular phenotype activating thyroglobulin (Tg), thyroperoxidase (TPO), thyrotropin receptor (TSH-R) and the sodium/iodide symporter (NIS) gene transcription. In the present work, we have studied the expression of TTF-1 and Pax-8 and their target genes in samples derived from thyroid neoplasms of follicular origin, as well as in medullary carcinoma (MTC), obtained from surgery or from fine needle aspiration (FNA) biopsies. The results show that TTF-1 and Pax-8 are expressed in well differentiated adenomas and that their expression decreases in less differentiated papillary and follicular carcinomas and is lost in undifferentiated anaplastic carcinomas. Parallel levels of Tg, TPO and TSH-R expression were found in the same neoplasm samples. Interestingly TSH-R and TTF-1 gene expression was found in MTC samples. Furthermore, the expression of the thyroid-specific genes and their transcription factors is lost in thyroid cells derived from follicular, papillary and anaplastic human carcinomas. In these cells, Tg, TPO and TSH-R promoter activities were absent. Cotransfection with expression vectors for TTF-1 and Pax-8 resulted in the stimulation of transcription to a different extent for each promoter. These results may be clinically relevant for the evaluation and prognosis of thyroid cancer since the loss of specific markers correlates with the degree of tumor differentiation.

Carcinoma, Medullary↗
PubMed2001

Serum thyroid-stimulating hormone measurement for assessment of thyroid function and disease.

Third generation thyroid stimulating hormone (TSH) assays have emerged as the single most useful test of thyroid function, and are used widely and appropriately as a screening test. TSH measurement alone may be misleading in complicated patients and those undergoing treatment for thyroid dysfunction. Before obtaining thyroid function tests, clinicians need to consider whether the patient might have pituitary or hypothalamic disease or severe nonthyroidal illness, and whether assessment of the pituitary-thyroid axis reflects steady-state conditions. Subclinical hyperthyroidism is associated with adverse effects on the skeleton and the heart, and is best assessed by measurement of serum TsH with a third-generation assay.

Humans↗
PubMed2006

A novel mutation (E333D) in the thyroid hormone beta receptor causing resistance to thyroid hormone syndrome.

Resistance to thyroid hormone (RTH) is an inherited syndrome characterized by elevated serum thyroid hormones (TH), failure to suppress pituitary thyroid stimulating hormone (TSH) secretion, and variable peripheral tissue responsiveness to TH. The disorder is associated with diverse mutations in the thyroid hormone beta receptor (TRbeta). Here, we report a novel natural RTH mutation (E333D) located in the large carboxy-terminal ligand binding domain of TRbeta. The mutation was identified in a 22-year-old French woman coming to medical attention because of an increasing overweight. Biochemical tests showed elevated free thyroxine (T4: 20.8 pg/ml (normal, 8.5-18)) and triiodothyronine (T3: 5.7 pg/ml (normal, 1.4-4)) in the serum, together with an inappropriately nonsuppressed TSH level of 4.7 mU/ml (normal, 0.4-4). Her father and her brother's serum tests also showed biochemical abnormalities consistent with RTH. Direct sequencing of the TRbeta gene revealed a heterozygous transition 1284A>C in exon 9 resulting in substitution of glutamic acid 333 by aspartic acid residue (E333D). Further functional analyses of the novel TRbeta mutant were conducted. We found that the E333D mutation neither significantly affected the affinity of the receptor for T3 nor modified heterodimer formation with retinoid X receptor (RXR) when bound to DNA. However, in transient transfection assays, the E333D TRbeta mutant exhibited impaired transcriptional regulation on two distinct positively regulated thyroid response elements (F2- and DR4-TREs) as well as on the negatively regulated human TSHalpha promoter. Moreover, a dominant inhibition of the wild-type TRbeta counterpart transactivation function was observed on both a positive (F2-TRE) and a negative (TSHalpha) promoter. These results strongly suggest that the E333D TRbeta mutation is responsible for the RTH phenotype in the proposita's family.

Adult↗
PubMed1994

Studies on the action of thyroid stimulation blocking antibody (TSBAb) on thyroid cell membrane.

The effect of thyroid stimulation blocking antibody (TSBAb) on stimulated cyclic AMP (cAMP) production induced by adenylate cyclase stimulators in porcine thyroid membrane (PTM) and porcine thyroid cells (PTC) has been studied. Ten TSBAbs with high TSH binding inhibitory immunoglobulin (TBII) activities significantly blocked TSH-stimulated cAMP production in PTC. The blocking effect of TSBAb on the cAMP increase induced by forskolin or GTP-gamma S stimulation in PTC was found in a few cases. However, there was no blocking action of TSBAb on the cAMP increase stimulated by forskolin, GTP gamma S, or NaF in isolated PTM. When TSBAb-globulin was absorbed with PTM or guinea pig epididymal fat membrane (GPFM), the TBII activity in TSBAb-globulin was significantly absorbed by these membranes. A decrease of TSBAb activity (blocking activity for TSH-stimulated cAMP production in PTC) by PTM absorption, but no decrease by GPFM absorption, was found in six cases. This suggests that the potent TSBAb-neutralizing component may be associated with a non-TSH receptor site in the thyroid membrane. The other four cases showed a decrease of TSBAb activity by absorption with both PTM and GPFM. This suggests that the TSBAb-neutralizing activity may be associated with the TSH receptor site of both PTM and GPFM. The results of the present study suggest that TSBAb may block TSH action either via the TSH receptor itself or via a non-TSH receptor component of the thyroid membrane and not at a postreceptor level.

Animals↗
PubMed2006

High prevalence of thyroid dysfunction and autoimmune thyroiditis in adolescents after elimination of iodine deficiency in the Eastern Black Sea Region of Turkey.

In the present study we evaluated the effects of iodine intake on the prevalence of thyroid dysfunction, autoimmunity, and goiter in two regions with different iodine status after two years of iodization in Turkey. In total 1733 adolescent subjects were enrolled into the study (993 from an iodine-sufficient area--the Eastern Black Sea Region (group 1) and 740 from an iodine-deficient area--Middle Anatolia (group 2)). We measured free thyroxine (FT(4)), thyrotropin (TSH), antithyroid peroxidase antibodies (Anti-TPO), antithyroglobulin antibodies (Anti-Tg), and urinary iodine (UI), and examined the thyroid gland by ultrasound. Median urinary iodine excretion was found to be significantly different in group 1 and group 2 (139 micro/l vs 61micro/l, p < 0.001). Hyperthyroidism was more frequent in group 1 (3.6% vs 0.7%; p < 0.001), but the hypothyroidism rate was similar between groups (1.8% vs 1.4 %; p>0.05). The percentage of anti-Tg positive subjects was found to be 17.6% in group 1 and 6.4% in group 2; that of anti-TPO positive subjects was 4.3% in group 1 and 1.5% in group 2. The prevalence of antithyroid antibody (anti-Tg and/or anti-TPO) positivity was significantly higher in group 1 than in group 2 (18.52% vs 6.62%; p < 0.001). Thyroid volumes of the hyperthyroid subjects in both groups were significantly higher than hypo- and euthyroid subjects. In conclusion, iodine supplementation in Turkey has resulted in the elimination of iodine deficiency in the Eastern Black Sea Region, and this has been accompanied by an increase in the prevalence of autoimmune thyroiditis and thyroid dysfunction.

Adolescent↗
PubMed2006

Effects of thyroid hormones on serum levels of adipokines as studied in patients with differentiated thyroid carcinoma during thyroxine withdrawal.

OBJECTIVE: Previous studies addressing the influence of thyroid hormones on serum levels of adipokines yielded conflicting results. We aimed to study the impact of short-term overt hypothyroidism on serum leptin, resistin, and adiponectin levels in an in vivo human model. DESIGN: Twenty-two women with differentiated thyroid carcinoma were studied the last day of their thyroxine-suppressive treatment, 4-7 days after withdrawal, and the day before whole-body scanning. Evaluations included serum thyroid hormone, leptin, resistin, and adiponectin concentrations, fasting glucose and insulin, lipid profiles, body temperature, body mass index, and total body fat mass. MAIN OUTCOMES: Thyroid function changed from subclinical or mild hyperthyroidism to normal free thyroxine and triiodothyronine levels, ending in overt hypothyroidism. Thyroxine withdrawal resulted in an increase in serum resistin (p = 0.007) and leptin (p = 0.006) concentrations, whereas adiponectin levels remain unchanged. A significant decrease in body temperature during thyroxine withdrawal was paralleled by a decrease in fasting glucose (p = 0.006) and insulin resistance (p = 0.033), which occurred despite an increase in estimated total body fat mass. CONCLUSION: Thyroid hormones are important regulators of energy balance and intermediate metabolism, influencing the serum concentrations of leptin and resistin.

Adiponectin↗
PubMed1997

The T3R alpha gene encoding a thyroid hormone receptor is essential for post-natal development and thyroid hormone production.

The diverse functions of thyroid hormones are thought to be mediated by two nuclear receptors, T3R alpha1 and T3R beta, encoded by the genes T3R alpha and T3R beta respectively. The T3R alpha gene also produces a non-ligand-binding protein T3R alpha2. The in vivo functions of these receptors are still unclear. We describe here the homozygous inactivation of the T3R alpha gene which abrogates the production of both T3R alpha1 and T3R alpha2 isoforms and that leads to death in mice within 5 weeks after birth. After 2 weeks of life, the homozygous mice become progressively hypothyroidic and exhibit a growth arrest. Small intestine and bones showed a strongly delayed maturation. In contrast to the negative regulatory function of the T3R beta gene on thyroid hormone production, our data show that the T3R alpha gene products are involved in up-regulation of thyroid hormone production at weaning time. Thus, thyroid hormone production might be balanced through a positive T3R alpha and a negative T3R beta pathway. The abnormal phenotypes observed on the homozygous mutant mice strongly suggest that the T3R alpha gene is essential for the transformation of a mother-dependent pup to an 'adult' mouse. These data define crucial in vivo functions for thyroid hormones through a T3R alpha pathway during post-natal development.

Acetylcholine↗
PubMed1989

C-cell hyperplasia of the thyroid in a patient with goitrous hypothyroidism and Hashimoto's thyroiditis.

A 63-year-old man with a goiter and primary hypothyroidism due to Hashimoto's thyroiditis was found to have hypercalcitonemia and, though hypothyroid, markedly elevated serum total and free T3 levels. The latter findings were attributable to circulating T3 autoantibodies and interference with radioimmunoassay. An infusion of calcium and pentagastrin resulted in abnormal increases in serum calcitonin levels. Because there was no evidence of a nonthyroidal cause for the hypercalcitonemia, the patient had a total thyroidectomy. Pathological examination of the thyroidectomy specimen revealed typical Hashimoto's thyroiditis and extensive C-cell hyperplasia symmetrically distributed throughout the upper and middle thirds of each lobe. The C cells stained strongly with immunoperoxidase stains for calcitonin, chromogranin, and CEA using absorbed polyclonal anti-CEA antibody. Less extensive staining for CEA was obtained using the monoclonal antibodies for CEA, 374/14, 250/183, and 431/31; only a few reactive cells were noted using 431/31. Postoperatively, serum calcitonin levels fell to normal and did not rise with a repeat calcium-pentagastrin infusion test. This patient appears to be the first instance of C-cell hyperplasia associated with Hashimoto's thyroiditis, while elsewhere an association with medullary thyroid carcinoma has been reported. These observations raise questions regarding a possible pathogenetic relationship between Hashimoto's thyroiditis and C-cell neoplasia.

Calcitonin↗
PubMed1991

Tl-201 thyroid imaging in differentiating benign from malignant thyroid nodules.

To evaluate the value of Tl-201 thyroid imaging in differentiating benign from malignant thyroid nodules, 58 patients with histologically proven thyroid masses were studied. The nature of the thyroid tumor was initially assessed by Tc-99m scans. Early and delayed Tl-201 thyroid imaging were performed in all patients, and thallium uptake and clearance in the cold nodules were assessed visually. Of the 20 patients with histologically proven malignant nodules, 19 showed increased Tl-201 activity in both the early and delayed images, indicating a sensitivity of 95%. On the other hand, 35 out of the 38 patients with benign nodules showed no increased thallium activity in the nodules on the delayed images, indicating a specificity of 92%. When early thallium images were analyzed separately, the sensitivity was 100% but the specificity was only 37%. By combining early and delayed Tl-201 images, differentiation between benign and malignant cold nodules is feasible. False-positive and false-negative cases will be discussed.

Adult↗
PubMed1997

Fetal thyroid function: diagnosis and management of fetal thyroid disorders.

The fetal hypothalamic-pituitary-thyroid axis develops independently of the maternal axis, but it is dependent on the maternal-placental system for adequate supply of iodide substrate. This iodide is supplied by direct transfer of maternal plasma iodide and by placental deiodination of T4. In addition, although placental transport of iodothyronines is limited, significant maternal-fetal transfer of T4 occurs, accounting for approximately 30% of the average 10 ug/dL serum-T4 concentration in fetal-cord blood at term. Current information suggests that this maternal contribution to the fetal-T4 levels is important for normal fetal maturation, particularly of the central nervous system. Combined maternal-fetal hypothyroxinemia can lead to irreversible fetal central nervous system damage. The timing of this fetal T4 dependency is not clear. It may be important in the first half of gestation, before the fetal thyroid gland is capable of T4 production, as well as the latter half of gestation when thyroid hormone effects on multiple organ systems are developing. Management of fetal thyroid dysfunction requires normalization of maternal serum T4 concentrations, avoidance or careful monitoring of potentially goitrogenic drug effects in the fetus, and in some instances, direct or indirect fetal therapy. In most cases fetal hypothyroidism is sporadic and undetected, and prognosis for normal growth and development is excellent if the mother is euthyroid and the hypothyroid state is detected and adequately treated at birth. Fetal treatment by intraamniotic thyroxine injection has been provided in cases of inadvertent maternal radioiodine treatment of Graves' disease between 10 and 20 weeks gestation and for fetal goiter detected by ultrasound. Effective treatment of fetal hyperthyroidism in pregnant women with high titers of thyroid stimulating autoantibody is possible by judicious administration of antithyroid drugs to the mother. Management of the hyperthyroid state in the neonate also is essential.

Female↗
PubMed1985

The assay for thyroid stimulating immunoglobulins using cultured human thyroid cells.

Recent reports have shown that thyroid-stimulating immunoglobulins (TSI) may be detected by measuring cyclic AMP increases in cultures of isolated thyroid cells in response to added patient immunoglobulins (Ig). We have compared the frequency that TSI may be detected in the Ig fraction of 114 sera from 112 patients with a variety of thyroid disorders, to the presence of thyrotrophin binding inhibitor Ig (TBII). Whereas the sera of 46 out of 48 (95.6%) patients with untreated thyrotoxic Graves' disease had detectable TSI, only 26 out of 48 (54.2%) had detectable TBII. We did not find any significant correlation between TSI and TBII for these patients but there was a significant correlation between TSI and both serum T3 (r = +0.55, P less than 0.01) and T4 (r = +0.50, P less than 0.01). Twelve patients were studied at the time of relapse of thyrotoxicosis due to Graves' disease. All sera contained detectable TSI whereas only one contained detectable TBII. Of the sera from 20 patients in remission after antithyroid drug therapy three were positive for TSI. One of these samples as well as two others had detectable TBII. The two samples with TBII in the absence of TSI came from patients who had developed hypothyroidism. TSI were detected in the serum of one out of nine patients with Hashimoto's thyroiditis but not in the sera of 20 other patients with a variety of non-autoimmune thyroid disorders including five patients with thyrotoxicosis not due to Graves' disease. However TSI was found in the sera of three out of five patients with exophthalmos and no history of hyperthyroidism.(ABSTRACT TRUNCATED AT 250 WORDS)

Cells, Cultured↗
PubMed1994

Acute suppurative thyroiditis in an asymptomatic woman: an atypical presentation simulating thyroid carcinoma.

Patients with acute suppurative thyroiditis usually have pain or tenderness in the anterior part of the neck associated with erythema and dysphagia. A 26-year-old Japanese woman with none of these symptoms presented with a left anterior cervical mass. Since physical examination and laboratory studies showed a firm and irregular tumour located in the left lobe of the thyroid without any inflammatory signs, we made a diagnosis of thyroid carcinoma. After surgery, histological examination of the thyroid specimen revealed various changes of severe inflammation, and a barium swallow demonstrated a left pyriform sinus fistula. We describe here a unique case of acute suppurative thyroiditis in an asymptomatic woman.

Acute Disease↗
PubMed2004

Stimulation of thyroid-stimulating hormone (TSH) receptor antibody production following painless thyroiditis.

OBJECTIVE: Development or recurrence of Graves' disease (GD) following painless thyroiditis (PT) has been documented. Therefore, we measured titres of TSH receptor antibodies (TSHR Ab) using a novel sensitive TSHR Ab assay in patients with PT to determine whether PT enhances TSHR Ab production, possibly triggering the development or recurrence of GD. DESIGN AND MEASUREMENTS: Ninety-two patients who developed PT were studied. Group G consisted of 40 patients with a history of GD (19 patients in remission, 21 who had stopped taking antithyroid drugs during pregnancy). Group P consisted of 52 patients with no history of GD. Serum thyroid hormone levels, thyroid autoantibodies including TSHR Ab, and 123I uptake at 24 h (RAIU) were measured in these patients at the time of PT onset. TSHR Abs were measured by radioreceptor assay using porcine TSH receptors (pTBII) or human TSH receptors (hTBII). RESULTS: There were no significant differences in serum thyroid hormone levels or pTBII values between groups G and P. Nor was there any significant difference between p- and h-TBII values in group P. There was also no significant difference in pTBII levels before, compared to at the time of PT onset in group G patients. However, hTBII values at the PT onset were significantly higher in the group G than in the group P (7.7 +/- 9.8%vs. 1.4 +/- 5.4%, P = 0.0014). The rate of hTBII positivity was also significantly higher in group G than in group P (12/40 vs. 3/52, P = 0.002). Furthermore, the RAIU in group G patients was significantly higher than that in group P patients (2.8 +/- 2.4%vs. 1.3 +/- 0.9%, P = 0.0002). GD recurrence was observed in seven patients in group G, whose hTBII levels were significantly higher than those of other patients in this group (17.0 +/- 11.8%vs. 5.7 +/- 8.2%, P = 0.02). Of these seven with relapses, five had hTBII values exceeding 15%. CONCLUSIONS: TBII elevation at the onset of PT in patients with a history of GD was detected by a sensitive hTBII assay. Destruction of the thyroid by PT may trigger GD recurrence in patients with a history of GD.

Adult↗
PubMed1987

Patterns of expression of cytoskeletal proteins in human thyroid gland and thyroid carcinomas.

By two-dimensional gel electrophoresis of proteins insoluble in detergents and high-salt buffer and immunofluorescence microscopy with a panel of polypeptide-specific antibodies to proteins of intermediate filaments (IF) and desmosomes, we have characterized the cytoskeletons of normal human thyroid gland, several kinds of benign lesion (goiter, Hashimoto's and Graves' diseases, adenomas), and the major thyroid carcinomas (follicular, papillary, medullary, and anaplastic). In all these tissues, desmoplakins and cytokeratins 7, 8, 18, and 19 were identified. While cytokeratins 8 and 18 occurred in all epithelial cells and cytokeratin 7 was also rather widespread, cytokeratin 19 occurred in amounts variable between the different types of tissues and in normal thyroid gland was restricted to certain clusters of follicular epithelial cells. Of all samples studied, in none did we detect cytokeratins commonly associated with stratified epithelia such as cytokeratins 4-6, 10, and 13-17, indicating that these are infrequent, if at all present, in such tissues. Coexpression of cytokeratins with vimentin appears to occur constitutively in follicular epithelial cells of normal thyroid gland and is also frequent in the diverse carcinomas, though to various degrees. Medullary carcinomas are exceptional, not only because they express neuroendocrine markers, but also because they coexpress combinations of cytokeratin IFs with neurofilaments and/or vimentin IFs in some cases, but not all. The results are discussed in relation to states of cell differentiation in normal and diseased thyroid gland and with respect to their value in tumor diagnosis.

Cytoskeletal Proteins↗