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Thyroid Peroxidase Expression in Diseased Human Thyroid Glands.

Histoenzymologic studies of the human thyroid have been restricted to attempts to differentiate benign from malignant tumors and, to our knowledge, there is no systematic study on the distribution and behavior of enzymes for several types of lesions of the thyroid gland. The aim of the present study was to investigate thyroid peroxidase (IPO) expression in diseased thyroids, as well as to study the role of this enzyme as a parameter to define the biological behavior of thyroid lesions. A total of 1 17 neoplastic and nonneoplastic lesions of the thyroid were evaluated. The expression of TPO was determined by the analysis of at least 200 cells/specimen. A rate of 80% of positive cells was considered a threshold for TPO positivity. TPO expression was detected in all nonneoplastic lesions of thyroid as well as in 78.8% of the adenomas. We also observed positivity for TPO in 20% of malignant lesions. Therefore, these findings do not allow separation of benign and malignant lesions of the thyroid based in the expression of TPO.

Journal Article↗

NADPH-dependent reductases in dog thyroid: comparison of a third enzyme "glyceraldehyde reductase" to dog thyroid aldehyde reductase.

The increased incidence of thyroiditis reported to occur in diabetes has also been observed in long-term galactose-fed dogs where it is reduced by the administration of aldose reductase inhibitors. Since this suggests that thyroidal changes are linked to the abnormal accumulation of sugar alcohols (polyols), present studies were conducted to confirm the presence of aldose and aldehyde reductases in dog thyroid through isolation and characterization. Aldose and aldehyde reductases were isolated from dog thyroid by a series of chromatographic steps which included gel filtration on Sephadex G-100, affinity chromatography on Matrex Gel Orange A and chromatofocusing on Mono P. A third, labile NADPH-reductase was partially purified by gel filtration on Sephadex G-100, affinity chromatography on Matrex Green A and hydroxylapatite chromatography on BIO-GEL HT. The kinetic properties of aldose and aldehyde reductases and their susceptibility to inhibition by aldose reductase inhibitors are similar to those of dog kidney aldose and aldehyde reductases. However, the levels of aldose reductase present in thyroid are extremely low compared to the levels of aldehyde reductase. A third NADPH-dependent reductase, tentatively identified as glyceraldehyde reductase, is also present in dog thyroid. This novel enzyme utilizes NADPH to reduce DL-glyceraldehyde and is clearly distinct from the other aldo-keto reductases in molecular weight, substrate specificity, inhibition by aldose reductase inhibitors and immunological properties. In summary aldose reductase, aldehyde reductase and a third novel glyceraldehyde reductase, all of which can utilize glyceraldehyde as substrate, have been identified and characterized in dog thyroid. Only aldose and aldehyde reductases, which can catalyze the production of polyols and were inhibited by aldose reductase inhibitors, appear to be linked to thyroiditis.

Aldehyde Reductase↗

Thyroid Hormone Stimulates Renin Gene Expression Through the Thyroid Hormone Response Element.

-We previously reported that thyroid hormone stimulates renin synthesis in vivo and in vitro. Here, we analyzed the 5'-flanking sequence of the human renin gene for promoter activity responsive to thyroid hormone using Calu-6 cells, which secrete renin endogenously and express thyroid hormone receptor-ss. The luciferase reporter gene was cloned together with 5'-flanking portions of the human renin gene of various lengths into the pGL3-Basic vector. Luciferase activity assays were performed using the Dual Luciferase Reporter Assay System. 3,3',5-Triiodo-L-thyronine stimulated the promoter activity of pGL3-Basic-1111/+12 and pGL3-Basic-1298/+12 by 2.3+/-0.1- and 1.7+/-0.1-fold, respectively. Shorter constructs (pGL3-Basic-144/+12, pGL3-Basic-226/+12, pGL3-Basic-452/+12, and pGL3-Basic-953/+12) were not stimulated by thyroid hormone. These results suggest that there is a possible thyroid hormone response element (5'-AGG TCA GGT CAc aat GTT CCT-3') between nucleotides -1111 and -953. In 3 constructs with site-directed mutations in this sequence, basal promoter activities were significantly increased, whereas promoter activation by thyroid hormone was abolished. Electrophoretic mobility shift assays showed that the -1111/-953 DNA fragment of the intact human renin gene was bound to nuclear proteins of Calu-6 cells; however, none of the 3 mutant probes were bound to any nuclear proteins. These results suggest that thyroid hormone stimulates the promoter activity of the human renin gene through thyroid hormone response element-dependent mechanisms in Calu-6 cells.

Journal Article↗

Influence of cigarette smoking on thyroid function, goiter formation and autoimmune thyroid disorders.

Both smoking and thyroid dysfunction are frequent in the general population. Many studies have shown that cigarette smoking interferes with thyroid function and with the evolution of thyroid pathology (e.g. goiter formation and thyroid cancer development). Some studies have also suggested a significant correlation of Graves' hyperthyroidism and Graves' ophthalmopathy with the severity of smoking. In addition, cigarette smoking may reduce the effectiveness of some therapeutic modalities, such as orbital radiotherapy or high-dose systemic glucocorticoid administration for severe thyroid eye disease. Tobacco smoking seems to induce similar changes in thyroid function in the adult and the fetus. This review article discusses the effect of cigarette smoking on thyroid function and morphology as well as on thyroid autoimmunity.

Journal Article↗

[Thyroid echogeneity as a useful tool for the differential diagnosis of hyperthyroidism in the course of Graves disease and Hashimoto thyroiditis].

Hashimoto's thyroiditis (HT) and Graves' disease (GD) constitute a spectrum of autoimmune thyroid diseases (AITD). They share an autoimmune pathogenesis, with a cellular and a humoral response to the thyroid gland. As a consequence, dysfunction of the gland itself may develop, characterized by hyperfunction in the case of GD and hypofunction in the case of HT, however at the onset of HT the hyperthyroidism might be observed as a result of a rapid destruction of thyrocytes. An abnormal thyroid echographic pattern characterized by a diffuse low echogeneity has been described in both AITD. This hypoechogeneity is due to three components: increase of intrathyroidal flow, functional changes in thyroid follicles with increased cellularity and decrease of the colloid content, resulting in the reduction of the cell/colloid interface, variable degree of lymphocytic infiltration. The first two components may be reversible during medical treatment and seem to be characteristic for GD, whereas lymphocytic infiltration may rather represent mostly HT. Here we present a 17-year-old girl with typical clinical signs of hyperthyroidism [firm goiter (II degrees), tachycardia, palpitations, nervousness, excessive sweating and tremor]. Laboratory tests were the following: fT3 - 6.59 pg/ml(increasing), fT4 - 1.99 ng/dl(increasing), TSH - 0.02 micro IU/ml(decreasing); anti-Tg-Ab - 840 IU/ml(increasing), anti-TPO-Ab - 190 IU/ml(increasing) (4 months later antithyroid antibodies were 2200 and 70, respectively). Ultrasound examination showed hypoechogeneity of the whole gland and enhanced vascular flow based on power Doppler analysis. Thyroid scan visualized the generally increased uptake of technetium. The girl was put on beta-blocker (propranolol) and later an antithyroid drug (thiamazole) was added. A course of disease was unstable, therefore the fine-needle aspiration biopsy was performed and showed the presence of single groups of normal thyrocytes and scanty colloid with no features of HT. Power Doppler analysis showed still enhanced blood flow within a gland inspite of euthyroid state. After a very unsteady period of the disease, the euthyroid state is maintained although the medical treatment was given up. The full recovery of normal blood flow and normal echogeneity of the thyroid was documented. The latter supports the diagnosis of GD. Follow-up of the thyroid echogeneity is of great diagnostic and prognostic value if the assay of TSHR-Ab is not available. On the other side, it has to be remembered that TSHR-Ab do not have to be positive in patients with GD and can be positive in patients with HT.

English Abstract↗

Prevalence of anti-thyroid peroxidase antibodies in serum in the elderly: comparison with other tests for anti-thyroid antibodies.

Autoimmune thyroid disease, especially chronic thyroiditis, is prevalent in elderly women and is probably the major cause of hypothyroidism in this population. The reported prevalence of chronic thyroiditis is variable, depending on the area of residence and the method(s) used to detect the presence of anti-thyroid antibodies. The recent finding that thyroid peroxidase (TPO) is the antigen for the thyroid anti-microsomal antibody (AbM) has resulted in the development of sensitive radioimmunoassays (RIA) to detect the presence of AbTPO. We have determined the prevalence of AbTPO (by RIA) in sera from 342 elderly subjects, 248 women and 94 men (mean age 80 years) residing in Reggio Emilia, Italy, and compared the results with other methods for detecting anti-thyroid antibodies, including anti-thyroglobulin (AbTg) and AbM measured by passive hemagglutination (PH) of tanned erythrocytes, and AbM measured by RIA. The prevalence of positive AbTPO was 2.3% in the men and 10.2% in the women, only slightly higher than the prevalence of AbM. However, in the antibody-positive sera, the mean value for AbTPO was approximately 20-fold greater than the upper limit of the normal range, whereas the mean value for AbM was only threefold greater. The prevalence of positive titers for AbM and AbTg measured by PH was far lower, 1.2% and 3.2%, respectively, and those sera weakly positive for AbM and AbTg by PH were strongly positive for AbTPO by RIA. AbTPO RIA may be more useful than AbM and AbTg hemagglutination and AbM RIA for detecting the presence of autoimmune thyroid disease.

Aged↗

Thyroid nodules in Graves disease and the risk of thyroid carcinoma.

BACKGROUND: The risk of thyroid carcinoma in patients with Graves disease has been particularly emphasized when nodules coexist with thyroid hyperplasia; a surgical approach has been suggested. OBJECTIVES: To detect thyroid nodules early in patients with Graves disease and to evaluate the risk of carcinoma. METHODS: The study group included 315 consecutive outpatients with Graves hyperthyroidism not previously treated with surgery or radioiodine therapy. Thyroid ultrasonography was performed at the time of enrollment and repeated annually in all patients; fine-needle aspiration (FNA) was carried out in those patients with nodules and repeated after 2 years or at shorter intervals. RESULTS: One hundred six of 315 patients with Graves disease had thyroid nodules 8 mm in diameter or larger detected by ultrasonography. In 49 patients, nodules were present at the time of the first examination; in 57 patients, nodules developed during follow-up. Fine-needle aspiration cytology results revealed features of carcinoma in only 1 patient; this was confirmed by histologic examination of excised thyroid tissue. The nodules with normal cytologic features at the time of the first examination did not show any clinical and/or cytologic evolution toward malignancy during follow-up. CONCLUSIONS: Ultrasonographic evidence of nodules was frequently found among our patients with Graves disease, but malignant FNA cytologic findings of the examined nodules were rare at the time of diagnosis and throughout the course of the disease. When FNA cytologic evaluation does not indicate malignancy, the presence of thyroid nodules in patients with Graves disease does not indicate an aggressive therapeutic approach.

Adult↗

Functional retinoid and thyroid hormone receptors in human thyroid-carcinoma cell lines and tissues.

Thyroid carcinomas no longer accessible to radio-iodide or TSH-suppressive T4 therapy, due to loss of thyroid-specific functions, might be sufficiently re-differentiated by retinoic acid (RA) to be treated by conventional methods again. To help evaluate the feasibility of RA re-differentiation therapy in thyroid carcinomas, we examined the functionality of RA receptors (RARs/RXRs), central RA signal mediators, in human thyroid-carcinoma cell lines as model systems. [3H]-RA binding assays with nuclear extracts from follicular thyroid-carcinoma cell lines FTC-133 and -238 revealed high-affinity binding sites for RA. Electrophoretic mobility shift and super-shift assays using a DR2 ("direct repeat" 2) RA response element demonstrated DNA-binding of RARalpha, RARgamma, RXRalpha and RXRbeta in nuclear extracts of FTC-133 and anaplastic HTh74 cells. Use of a DR5 RA response element revealed no difference in DNA binding. In supershift assays with a DR4 T3 response element, we found DNA-binding by TRalpha1, TRalpha2, and TRbeta. Northern-blot analysis showed low expression of RXRbeta mRNA in FTC-133 and of TRalpha1 mRNA in FTC-133 and FTC-238 cells. Using RT-PCR, we detected mRNA for RARalpha, RARbeta, RARgamma, RXRalpha, and RXRbeta in the 4 cell lines and in human thyroid-carcinoma samples. RARbeta mRNA was reduced in FTC-238 cells and RXRbeta mRNA was decreased in anaplastic C643 cells and 9 of 12 tumor samples. Differential RA regulation of RA-receptor-mRNA expression was observed in the various cell lines. Thus, RA and T3 nuclear receptors are present in thyroid-carcinoma cell lines or tissues, albeit with cell-line and tumor-dependent variations; in the cell lines, they were shown to be functional with respect to DNA and/or ligand binding.

Carcinoma↗

Evaluation of circulating thyroid-specific transcripts as markers of thyroid cancer relapse.

Circulating thyroid-specific transcripts have been suggested as potential molecular markers of residual or recurrent thyroid cancer. We assessed the accuracy of real-time RT-PCR-based detection of a panel of thyroid-specific markers, including TG, TPO, TSHR, NIS and PDS, in comparison with serum TG measurements in a series of 55 patients operated for differentiated thyroid cancer (DTC). Serum TG levels were higher in patients with residual thyroid tissue or metastatic cancer than in disease-free patients during thyroid hormone suppressive therapy (THST) and after stimulation with rhTSH (P < 0.05). Recombinant hTSH increased serum TG values in patients with tumor relapse (P < 0.05), but not in disease-free patients. This assay showed high specificity and good sensitivity in detecting tumor relapse (accuracy under THST = 81.4%; after rhTSH stimulation = 90.9%). TPO and TSHR mRNA, either under THST or after rhTSH, showed a significant correlation with disease status for molecular assays. Qualitative analysis of baseline and stimulated TG, NIS and PDS mRNA showed high sensitivity but low specificity in the prediction of thyroid cancer recurrence or metastases (accuracy under THST = 51%, 43% and 54%, respectively), whereas TPO and TSHR mRNA assays had higher specificity but low sensitivity, with accuracy under THST of 67% and 61%, respectively, that improved when these tests were combined. Our findings indicate that serum TG assay after TSH stimulation is the most accurate test for monitoring DTC. Combined measurements of TPO and TSHR mRNA levels during THST may represent a specific test for early detection of DTC relapse.

Adult↗

Expression of laminin in thyroid gland and thyroid tumors: an immunohistologic study.

Thirty-five thyroid tumors and four normal thyroids were immunohistochemically investigated for the presence of laminin, a major basement membrane component. The thyroid follicles in normal tissues and in nodular goiters were surrounded by a continuous rim of laminin positivity, as were also the papillae of papillary carcinomas. Follicular adenomas and well-differentiated follicular carcinomas also showed laminin positivity around most of the follicles. Anaplastic thyroid carcinoma lacking a distinct compartmentalization of tumor cells also lacked pericellular laminin. However, in contrast to all other thyroid tumors, an intense laminin positivity was found in scattered tumor cells of anaplastic carcinomas. Laminin positivity is thus a feature reflecting the differentiation level of thyroid tumors, but, unlike most other carcinomas, differentiated thyroid tumors have basal laminae surrounding the differentiated structural units.

Adenoma↗

Expression of galectin-1 in normal human thyroid gland and in differentiated and poorly differentiated thyroid tumors.

We previously reported that galectin-1 gene expression increases up to 100-fold in oncogene-transformed rat thyroid cells compared with their normal counterparts and that the relative mRNA levels correlate with the degree of malignancy. In the present study we investigated whether galectin-1 is differentially expressed in human thyroid neoplasms, which range from well-differentiated tumors to undifferentiated anaplastic carcinomas. We analyzed 74 human thyroid specimens of neoplastic, hyperproliferative and normal tissues and several tumor cell lines. Galectin-1 mRNA and protein levels were higher in 6 thyroid carcinoma-derived cell lines than in normal thyroid primary cultures and adenoma cells. Galectin-1 mRNA levels increased in 28/40 papillary carcinomas and in 6/7 anaplastic carcinomas compared with normal or hyperplastic thyroid. Conversely, galectin-1 expression was unaffected in follicular carcinomas and benign adenomas. Immunohistochemical analysis of normal thyroid and papillary carcinoma sections revealed a higher content of galectin-1 protein in neoplastic follicular cells than in normal cells.

Base Sequence↗

Thyroidal uptake and radiation dose after repetitive I-131-MIBG treatments: influence of potassium iodide for thyroid blocking.

BACKGROUND: In I-131-MIBG therapy, I-131-iodide can be released from the I-131-MIBG molecule. Hypothyroidism might result from the undesirable irradiation of the thyroid gland. To prevent this, stable iodide such as potassium iodide (KI) is given to oversaturate the thyroid before I-131-MIBG is administered. PROCEDURE: In the present study, the incidence of hypothyroidism (elevated TSH) was correlated with the thyroidal uptake of I-131 and dose (MIRD dosimetry) after 35 individual treatments in ten patients. Iodine-131-MIBG therapy was performed using a modified dosage of 1.9-11.1 GBq (50-300 mCi) IV. Premedication with KI was done as recommended with a dose of 100 mg KI orally from 2 days before until 4 weeks after I-131-MIBG. RESULTS: The absorbed thyroidal dose amounted to a very variable range of 0.2 (patient # 1) up to 30.0 (patient 3) Gy with 7.1 +/- 7.9 Gy per treatment and 24.1+/- 19.2 Gy per patient (mean+/- SD), despite the same and compliantly taken KI premedication protocol. Up to now, 4/10 or 40% of patients have developed hypothyroidism after a mean follow-up period of 11 months and a mean total administered dose of 18.7 GBq (505 mCi). A trend towards higher thyroidal doses was seen in the hypothyroid patients. CONCLUSIONS: This study observes a general high inter- and intra-individual variability in radio-iodide uptake in the thyroid after I-131-MIBG therapy despite KI premedication, as well as possible occurrence of hypothyroidism. A dose-response relationship needs confirmation on a larger cohort of patients to reach statistical value. An alternative thyroid cytoprotection strategy for possible long-term survivors may be considered.

3-Iodobenzylguanidine↗

Immunopathological studies on thyroid immunity. IX. Thyroid and renal amyloidosis in thyroglobulin immunized rabbits.

In serial studies of immunopathologic changes in an animal model of thyroiditis 52 rabbits were immunized with either bovine, porcine or human thyroglobulin (Tg) in Freund's complete adjuvant, while another 47 animals served as noninjected or adjuvant injected controls. The immunized animals were divided into two groups, one receiving an initial series of only three Tg injections while the other received, in addition, challenging injections over an 8-week period. The immunized animals were killed over a period of 6-34 months after the last Tg injection, and untreated controls were killed at comparable ages. In Tg immunized animals, lymphocytic thyroiditis was encountered in 25 per cent and thyroid amyloid in 17 per cent; glomerular amyloid was encountered in 44 per cent with diffuse lesions in 8 per cent, nodular lesions in 17 per cent and a mixture of the two in 19 per cent. That the thyroid and glomerular hyaline deposits contained amyloid was shown by various histochemical criteria, as well as by the presence of typical fibrils on electron microscopy. Immunohistochemical studies indicated that the amyloid was predominantly of the AA type. Rabbits receiving challenging Tg injections, in addition to the initial series, showed only thyroiditis and nodular glomerular lesions most of which were amyloid. Whilst the vast majority of rabbits with lymphocytic or amyloidotic responses showed both thyroid and renal lesions, a small percentage of animals showed only a lesion of one or the other of these two organs. It is of interest that the thyroid and renal amyloid lesions, described for the first time with induced thyroglobulin immunity, were not detected in other earlier short term investigations.

Amyloidosis↗

Autoantibody against thyroid iodide transporter in the sera from patients with Hashimoto's thyroiditis possesses iodide transport inhibitory activity.

Recently we have newly identified an autoantibody against thyroid iodide transporter (TIT) in the sera from patients with autoimmune thyroid disease. In order to study the function of these autoantibodies, we established CHO-KI cells stably expressing recombinant rat TIT (CHO-TIT cells), and the effect of IgGs from the patients with Hashimoto's thyroiditis on iodide uptake activity of CHO-TIT cells was investigated. We found that 4 out of 34 sera from patients with Hashimoto's thyroiditis strongly recognized TIT by Western blot analysis. These 4 IgGs, purified by protein A column chromatography, caused 14 to 62% inhibition of I- accumulation in CHO-TIT cells. Next, using synthetic peptides, we determined the recognition site of the autoantibody on the TIT molecule. The autoantibody reacted with the synthetic peptide corresponding to the 6th extracellular loop of the TIT molecule. These results suggest that autoantibody against TIT in the sera from patients with Hashimoto's thyroiditis binds to the 6th extracellular loop of TIT protein and inhibits I- transport into the thyrocytes. Anti-TIT autoantibody might participate in the pathogenesis of Hashimoto's thyroiditis and modulate thyroid function of patients with the disease.

Animals↗

Sensitization of T lymphocytes to thyroid antigen in autoimmune thyroid disease as demonstrated by the monocyte procoagulant activity test.

Monocyte procoagulant activity (PCA) production has been reported to have a close relation to cell-mediated immunity (CMI), and the collaboration of T lymphocytes is necessary to induce PCA. Antigen-specific sensitization of lymphocytes in patients with Graves' disease (GD) and Hashimoto's thyroiditis (HT) has been demonstrated by means of the production of cell-bound PCA by monocytes following antigen stimulation of whole peripheral blood mononuclear cells (PBM). These cells, obtained from both normal subjects and patients with autoimmune thyroid diseases, produced significant amounts of PCA with non-specific lectin, concanavalin A (Con A) stimulation; however, there was no significant difference between the two groups, suggesting that Con A stimulated T cells induced monocyte PCA nonspecifically. Peripheral mononuclear cells from patients with autoimmune thyroid diseases produced significantly greater amounts of PCA than PBM from normal subjects when stimulated with solubilized and IgG-free thyroid antigen. On the other hand, liver antigen did not induce significant amounts of PCA production in PBM from either normal subjects or patients. Significantly larger amounts of PCA were produced by PBM from patients following thyroid antigen stimulation than with liver antigen stimulation. Although monocytes were the major source of PCA, T cells were necessary to induce PCA in monocytes with thyroid antigen and Con A stimulation. Elimination of lymphocyte subsets in PBM from patients by negative selection (using monoclonal antibodies and complement) suggested that the collaboration of T lymphocytes, especially helper/inducer (T4+) T cells, was necessary to produce PCA with thyroid antigen stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

Thyroid dose from common head and neck CT examinations in children: is there an excess risk for thyroid cancer induction?

This study was conducted to estimate thyroid dose and the associated risk for thyroid cancer induction from common head and neck computed tomography (CT) examinations during childhood. The Monte Carlo N-particle transport code was employed to simulate the routine CT scanning of the brain, paranasal sinuses, inner ear and neck performed on sequential and/or spiral modes. The mean thyroid dose was calculated using mathematical phantoms representing a newborn infant and children of 1year, 5 years, 10 years and 15 years old. To verify Monte Carlo results, dose measurements were carried out on physical anthropomorphic phantoms using thermoluminescent dosemeters (TLDs). The scattered dose to thyroid from head CT examinations varied from 0.6 mGy to 8.7 mGy depending upon the scanned region, the pediatric patient's age and the acquisition mode used. Primary irradiation of the thyroid gland during CT of the neck resulted in an absorbed dose range of 15.2-52.0 mGy. The mean difference between Monte Carlo calculations and TLD measurements was 11.8%. Thyroid exposure to scattered radiation from head CT scanning is associated with a low but not negligible risk of cancer induction of 4-65 per million patients. Neck CT can result in an increased risk for development of thyroid malignancies up to 390 per million patients.

Adolescent↗

Activation of thyroid adenyl cyclase by antisera to thyroid plasma membrane preparations: effects of IgG and non-IgG antiserum components.

We have previously shown that IgG isolated from rabbit antibovine thyroid plasma membrane (anti-BTPM) antibodies exhibits properties similar to long acting thyroid stimulator (LATS) and HTS-lg in that it activates thyroid adenyl cyclase. In order to test whether another immunoglobulin class, eg, IgM, of anti-BTPM antiserum can also stimulate the bovine thyroid adenyl cyclase system, protein molecules of the antiserum were separated into different molecular sizes by gel filtration chromatography on Sephadex G-200. It was observed that the low molecular weight fraction, consisting predominantly of albumin, was inactive in stimulating adenyl cyclase of the thyroid gland. In contrast, both IgM-enriched and IgG-enriched fractions of the immune serum were fully active. Furthermore, the thyroid-stimulating activity of the IgM-enriched fraction can only be inhibited by anti-IgM and that of the IgG-enriched fraction by anti-IgG. Our data suggest that IgM, in addition to IgG, may also have LATS or LATS-like activities in terms of activating adenyl cyclase of the thyroid gland.

Adenylyl Cyclases↗

Thyroid infiltrating cells in juvenile autoimmune thyroiditis: a follow-up of 1 year.

The composition of the cellular infiltrate in thyroid glands of 12 patients with juvenile autoimmune thyroiditis (JAIT) was followed for a period of 1 year. The diagnosis of JAIT was based on a firm goiter and on cytologic criteria of lymphocytic thyroiditis. Samples from the thyroid gland were obtained by fine-needle aspiration biopsy three times at 6-month intervals. Lymphocytes with a few lymphoid blasts and plasma cells dominated the cellular infiltrate. The relative number of the different cell types remained unchanged during the follow-up time of 1 year. Analysis of the lymphocytes revealed that about 60% of the infiltrating lymphoid cells were T cells and about 30% expressed B-cell markers. The T helper/suppressor ratio was significantly higher in the thyroid (2.2) than in the corresponding blood sample (1.2). Practically no changes were seen in the proportions of lymphocyte subclasses either in the gland or in the blood of the patients during the follow-up. At the time of diagnosis more than half of lymphocytes in the thyroid were HLA class II positive as were most of the glandular epithelial cells. The proportion of cells expressing class II was similar in samples taken at diagnosis and 6 and 12 months later, indicating a continuous state of immunoactivation in the thyroid gland.

Adolescent↗