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PubMed1997

[Thyroid, ovarian and adrenal antibodies in female patients with autoimmune thyroiditis].

BACKGROUND: In patients with autoimmune thyroiditis confirmed by clinical and laboratory tests frequently complaints associated with ovarian disorders are encountered. In order to verify the polyclonal activation of the autoimmune response of patients with autoimmune thyroid disease the authors investigated the presence of autoantibodies against the thyroid and adrenals. METHODS AND RESULTS: 696 patients were selected (mean age 47.9 years) with autoimmune thyroiditis from a group of 1939 patients examined for the presence of antibodies against thyroid peroxidase (TPO). In these patients also the presence of antibodies against ovaries was assessed (in 183 women, i.e. 26.3%), the adrenals (zona glomerulosa in 136 women, i.e. 19.5%, zona fasciculata in 10 women, i.e. 1.4%, zona reticularis in 114 women, i.e. 16.4%) and the adrenal medulla in 46 women, i.e. 6.6%. The basic group was divided into two sub-groups depending on the presence of ovarian antibodies. In the group of 183 women with positive antibodies against the ovaries and TPO positivity against the zona glomerulosa was found in 93 women, i.e. 50.8%, the zona fasciculata in 7 women, i.e. 3.8%, the zona reticularis in 70 women, i.e. 38.3%, the adrenal medulla in 37% i.e. 20.2%. In the second group of 513 patients with positive TPO and negative antiovarian antibodies against the zona glomerulosa were found in 43 women, i.e. 8.4%, zona fasciculata in 3 women, i.e. 0.6%, zona reticularis in 44 women, i.e. 8.6% and against the adrenal medulla in 9 women, i.e. 1.8%. CONCLUSIONS: These results confirmed that in organ specific autoimmune thyroid disease also other autoantibodies against endocrine organs may be present, i.e. against the ovaries and adrenals. The relative frequency of a common finding of autoantibodies against organs which comprise steroid producing cells can be explained by the fact that for the ovaries and the adrenals a common antigen of steroid producing cells is typical.

Adrenal Glands↗

PubMed1989

Squamous metaplasia with Hashimoto's thyroiditis presenting as a thyroid nodule.

A 59-year-old Japanese female presented a well-limited and movable thyroid nodule. Histologically, the nodule consisted of clusters of squamous cells surrounded by dense connective tissue in Hashimoto's thyroiditis. The squamous cells were well arranged and showed no mitotic figures. We therefore interpreted this nodule as being squamous metaplasia with Hashimoto's thyroiditis rather than squamous carcinoma of the thyroid. There are no previous reports in the literature of nodular formation of squamous metaplasia in the thyroid.

Carcinoma, Squamous Cell↗

PubMed1984

[Changes of gastrin levels in autoimmune thyroid disorders. Part I: Thyroid functions and gastrin levels].

The relationship between thyroid disorders and gastric pathophysiology has been studied mainly from standpoints of gastric histology and gastric acid output capacity. Though anti-gastric antibody has been thought to play a part in this relationship, there have been no clear conclusions obtained about that. Since blood gastrin levels are easily measurable by radioimmunoassay today, the relationship between thyroid disorders and gastric pathophysiology has drawn attention again from a standpoint of gastrin levels. Seino et al. have reported about hypergastrinemia in hyperthyroidism, speculating that beta-adrenergic hyperresponsiveness of gastrin-producing cells could be the mechanism of hypergastrinemia. However, there are other reports which mentioned feedback mechanism between gastrin and gastric acid or interaction of gastrointestinal hormones as the main mechanism of hypergastrinemia. In this study, the problem of gastrin in Graves' disease and chronic thyroiditis were studied by measurement of fasting serum gastrin levels and gastric juice excretion in view of feedback mechanism between gastrin-producing cells and parietal cells which are the target cells of gastrin. Following results were obtained. Fasting serum gastrin levels in Graves' disease were 236.2 +/- 39.1 (mean +/- SE) pg/ml for 39 hyperthyroid patients and 126.3 +/- 23.9 pg/ml for 35 euthyroid patients. These levels were significantly higher than those of sex and age-matched control subjects with P less than 0.001 and P less than 0.05, respectively. Fasting serum gastrin levels in serial studies of 13 patients with Graves' disease were 222.3 +/- 56.7 pg/ml before treatment and 167.3 +/- 56.6 pg/ml at the time of euthyroid state after a mean observation period of 6.6 +/- 1.1 months. Fasting serum gastrin levels at the time of euthyroid state decreased significantly when compared with fasting serum gastrin levels before treatment (P less than 0.05). Fasting serum gastrin levels in chronic thyroiditis were 160.7 +/- 51.1 pg/ml for 24 hypothyroid patients and 96.4 +/- 24.7 pg/ml for 31 euthyroid patients. Each of these levels had no significant differences when compared with sex and age-matched control subjects. Fasting serum gastrin levels in serial studies of 10 patients with chronic thyroiditis were 81.1 +/- 18.0 pg/ml at the time of hypothyroid state and 91.5 +/- 15.2 pg/ml at the time of euthyroid state after a mean observation period of 7.1 +/- 2.1 months. Fasting serum gastrin levels before treatment had no significant differences when compared with fasting serum gastrin levels in euthyroid state.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

PubMed1985

Autoantibodies against thyroid hormones or iodothyronine. Implications in diagnosis, thyroid function, treatment, and pathogenesis.

The presence of antithyroid hormone autoantibodies in the sera of patients with thyroid and nonthyroid disorders is a well-known condition. When circulating thyroid hormones bind to the patients' immunoglobulins, serum levels of total and free thyroid hormones are often in discordance with clinical features. This problem occurs because the autoantibodies can interfere with radioimmunoassays. To avoid inappropriate treatment of such patients, it is clinically important to consider the presence of autoantibodies in patients with unexpectedly high or low total and free thyroid hormone values. We have reviewed the English and Japanese literature, both case reports and basic works, and summarize the incidence of antithyroid hormone autoantibodies, clinical features, effects on appropriate testing of the hypothalamic-pituitary-thyroid axis, diagnostic methods for confirming their presence of autoantibodies, treatment of patients with these disorders, and possible pathogenetic mechanisms.

Autoantibodies↗

PubMed1996

Histologic trends in thyroid cancer 1969-1993: a clinico-pathologic analysis of the relative proportion of anaplastic carcinoma of the thyroid.

BACKGROUND: It was observed that new presentations of anaplastic carcinoma of the thyroid had become infrequent in the last two decades. METHODS: All cases of thyroid cancer seen at our centre between 1969-1993 (n = 2921) were classified as papillary 49%, follicular 34%, medullary 7.5%, anaplastic 4.7%, and other 4.8%. The total number of thyroid cancers show a 3.5-fold rise. RESULTS: The differentiated thyroid cancers show a significant rising trend as against the relative proportion of anaplastic carcinoma, which shows a significant decline (P = 0.002). Clinicopathologic data on 124 patients of anaplastic carcinoma revealed 50% patients had either long-standing goitres, previous thyroid abnormalities, or associated differentiated thyroid carcinoma on histology. CONCLUSIONS: The decline in the relative proportion of anaplastic carcinoma may in part be explained by the clinicopathologic findings or it may be attributed to histological reclassification.

Adult↗

PubMed1996

Status and expression of the p16INK4 gene in human thyroid tumors and thyroid-tumor cell lines.

The p16INK4 tumor-suppressor gene (also known as CDKN2, CDK41 and MTS1) encodes a negative regulator of the cell cycle. This gene, located in 9p21, is mutated or homozygously deleted in a high percentage of tumor cell lines and specific types of primary tumors. We have examined the status of the p16INK4 gene in 31 thyroid tumors and 7 thyroid cell lines. No DNA abnormalities were found in primary tumors. Conversely, p16INK4 gene structural alterations, deletions and point mutations were found in 4 thyroid cell lines. The expression of the 2 different p16INK4 mRNAs, the p16alpha and p16beta transcripts, was determined by RNA-PCR experiments. All the primary thyroid tumors expressed the beta transcript, while the p16alpha was barely detectable. The thyroid cell lines always expressed the p16beta transcript, while the alpha transcript was absent or, whenever present, coded for a mutated form of the p16INK4 gene product. Taken together, our results suggest that loss of p16INK4 function is not directly involved in the process of thyroid-tumor development, but it probably gives cells in tissue culture a selective growth advantage.

Amino Acid Sequence↗

PubMed2000

Initial results from a prospective cohort study of 5583 cases of thyroid carcinoma treated in the united states during 1996. U.S. and German Thyroid Cancer Study Group. An American College of Surgeons Commission on Cancer Patient Care Evaluation study.

BACKGROUND: The American College of Surgeons Commission on Cancer (CoC) has conducted national Patient Care Evaluation (PCE) studies since 1976. METHODS: Over 1500 hospitals with CoC-approved cancer programs were invited to participate in this prospective cohort study of U.S. thyroid carcinoma cases treated in 1996. Follow-up will be conducted through the National Cancer Data Base. RESULTS: Of the 5584 cases of thyroid carcinoma, 81% were papillary, 10% follicular, 3.6% Hürthle cell, 0.5% familial medullary, 2.7% sporadic medullary, and 1.7% undifferentiated/anaplastic. Demographics and suspected risk factors were analyzed. Fine-needle aspiration of the thyroid gland (53%) or a neck lymph node (7%), thyroid nuclear scan (39%), and ultrasound (38%) constituted the most frequently utilized diagnostic modalities. The vast majority of patients with differentiated thyroid carcinoma presented with American Joint Committee on Cancer Stage I and II disease and relatively small tumors. For all histologies, near-total or total thyroidectomy constituted the dominant surgical treatment. No lymph nodes were examined in a substantial proportion of cases. Residual tumor after the surgical event could be documented in 11% of cases, hypocalcemia in 10% of cases, and recurrent laryngeal nerve injury in 1.3% of cases. Complications were most frequently associated with total thyroidectomy combined with lymph node dissection. Thirty-day mortality was 0.3%; when undifferentiated/anaplastic cancer cases were eliminated, it decreased to 0.2%. Adjuvant treatment, probably underreported in this study, consisted of hormonal suppression (50% overall) and radioiodine (50% overall). CONCLUSIONS: In addition to offering information concerning risk factors and symptoms, the current PCE study compliments the survival information from previous NCDB reports and offers a surveillance snapshot of current management of thyroid carcinoma in the U.S. Identified opportunities for improvement of care include 1) more frequent use of fine-needle aspiration cytology in making a diagnosis; 2) more frequent use of laryngoscopy in evaluating patients preoperatively, especially those with voice change; and 3) improved lymph node resection and analysis to improve staging and, in some situations, outcomes.

Adenocarcinoma, Follicular↗

PubMed1980

Ontogeny of the pituitary-thyroid system in fetal rats: observations on the fetal thyroid after maternal treatment with goitrogen.

The critical time of onset of the reciprocal relationship between the pituitary and the thyroid in fetal rats was assessed by the appearance of goiters in fetuses after maternal treatment with goitrogen, propylthiouracil (PTU), on various days of gestation. The assessment was based on changes in the weight and histology of the fetal thyroids. The day following overnight mating was regarded as day 1 of gestation. Pregnant rats were treated with 40 mg PTU each day for two days and autopsied on the third day. The various experimental periods were days 16--18, 17--19, 18--20, 19--21, and 20--22. PTU given to pregnant rats on days 16 and 17 did not cause any change in the fetal thyroids. PTU given on days 17 and 18 caused only a slight increase of fetal "thyroid weight/body weight" ratio. In all other experimental periods (days 18--20, 19--21, and 20--22), PTU induced conspicuous goiters in fetuses, which was reflected by an increased weight of thyroids, an increased height of follicular cells, and a decreased amount of colloid stored in follicles. The results suggest that in fetal rats, the reciprocal relationship between the pituitary and the thyroid is established on approximately days 19--20 of gestation.

Animals↗

PubMed1986

Differentiation and thyroid-stimulating hormone (TSH) sensitivity of the fetal rat thyroid in organ culture.

Thyroids from rat fetuses of different ages (from day 14 to day 19 of gestation) were transplanted to organ culture for 2 days, with or without added thyroid-stimulating hormone (TSH) in the medium. Thyroid tissue from 14-day fetuses that initially consisted of irregularly arranged cell cords did not form follicles when cultured in the presence or absence of TSH. Thyroids from 15- and 16-day fetuses initially consisted of epithelial cell masses. When cultured in the presence or absence of TSH they formed follicles, and a majority stored small amounts of colloid. In thyroid transplants from 17-day fetuses, the response to TSH appeared as a significant increase in the follicular diameter and cell height. Thereafter, in all transplants cultured in the presence of TSH, both the follicular diameter and the cell height were markedly greater than in the transplants cultured in the absence of added TSH. These results suggest that the initial formation of thyroid follicles is independent of TSH and that, once developed, follicles become able to respond to TSH.

Animals↗

PubMed1990

Thyroid tumors: cytomorphology of medullary, clinically anaplastic, and miscellaneous thyroid neoplasms.

Of 2,012 fine-needle aspirations (FNAs) of the thyroid performed between the years 1984 and 1988, detailed cytomorphologic analysis of 95 cases diagnosed as neoplastic on histology and/or cytology and those that received an equivocal cytodiagnosis are presented in this article. Discussed are medullary thyroid carcinomas (nine cases), clinically anaplastic thyroid tumors (CATT; eight cases), two cases of non-Hodgkin's lymphoma (NHL), and one primary leiomyosarcoma of the thyroid, for a total of 20 cases. Included in the category of CATT are all the thyroid tumors presenting clinically with an anaplastic growth pattern. The cytomorphology of these tumors varied, but the giant- and spindle-cell pattern was predominant. An accurate cytodiagnosis was possible, as per cytohistologic correlation, in seven cases, while in one case histological material was not available for study. Medullary carcinoma of the thyroid (MCT) showed a mixed spindle-cell and round-cell population in eight cases and an entirely spindle-cell population in one case. All cases of MCT were correctly diagnosed on cytology, and amyloid could be demonstrated in the cytologic smears in three cases. The cases of NHL and leiomyosarcoma could also be correctly interpreted on cytology.

Adult↗

PubMed2001

Effect of exogenous thyroid-stimulating hormone on thyroid papillary carcinoma cells in tissue culture.

BACKGROUND: To determine the prognostic value of thyroid suppression therapy in patients with thyroid carcinoma, we studied the effect of thyroid-stimulating hormone (TSH) on the morphology, proliferation rate, and the T3, T4 production rate of primary thyroid carcinoma cells in culture. METHODS: From August 1997 to February 1998 tissues were collected for immediate culture from 13 patients undergoing surgery for thyroid cancer. Cells were incubated for 48 h with TSH in different concentrations. T3 and T4 production was measured by radioimmunoassay; cell proliferation was measured in a radioactive counter. Morphology was determined by cytologic examination. RESULTS: Ten samples were eligible for analysis. Changes in TSH affected T3 and T4 levels. The proliferation rate was not influenced by TSH levels. CONCLUSIONS: Thyroid papillary carcinoma cells grown in culture maintain their T3 and T4 synthesis ability. This ability is TSH-dependent and correlates with TSH concentration. The morphology of the cells is also maintained. However, their proliferation is not TSH-dependent, placing the current postthyroidectomy treatment policy in question.

Carcinoma, Papillary↗

PubMed2001

Rapid and transient reduction in circulating thyroid hormones following systemic antigen priming: implications for functional collaboration between dendritic cells and thyroid.

The thyroid hormones T(3) (tri-iodothyronine) and T(4) (thyroxine) are disseminated throughout the body via the circulation and are maintained across a range of physiological concentrations under the control of thyroid-stimulating hormone (TSH). T(3) (and T(4) after conversion to T(3)) influences many biological activities, including gene expression and protein synthesis, though little is known about the nature of pituitary-thyroid immune interactions. In the present study we show that serum T(3) and T(4) levels are sharply but transiently reduced during the first 24 h of systemic antigen exposure and that this is followed by suppressed levels of free T(4), after which there is rapid recovery to normal levels. Splenic dendritic cells, depending upon the stage of maturation/activation, were found to be a rich source of TSH, and CD11c(+) cells with dendritic cell morphology were present in the thyroid 1-3 days after antigen exposure. Moreover, antigen priming of hypophysectomized mice that are unable to make pituitary-derived TSH resulted in significant increases in circulating T(4), implying that compensation in the drop in thyroid hormones can be regulated from extrapituitary sources. These findings thus identify a novel set of immune-endocrine interactions that transpire during the early phase of antigen exposure, and they suggest that under appropriate conditions the immune system directly participates in the process of maintaining physiological homeostasis by contributing to the regulatory control of thyroid hormone activity.

Animals↗

PubMed1985

Fine structural aspects of the black thyroid induced by minocycline, and the effects of a low iodine diet, propylthiouracil, thyroxine tablet and TSH, on the black discoloration of the rat thyroid.

Fine structural aspects of the effect of minocycline, an antibiotic of the tetracycline group, on the rat thyroid were studied. In all the rats administered minocycline (100 mg/kg/day) for 21 days, diffuse black discoloration of the thyroid gland occurred. However, when the rats were fed on a low iodine diet, given propylthiouracil (PTU) or thyroxine tablet with minocycline the black pigmentation of the thyroid gland did not take place. On the other hand, black discoloration of the thyroid was accelerated in the rats administered TSH and minocycline simultaneously. Ultrastructurally, numerous dense bodies containing highly electron-dense deposits were seen in the supranuclear region of the follicular epithelial cells of the black thyroid. These dense bodies, which showed positive acid phosphatase activity, are considered to be lysosomes containing minocycline or its derivatives. It is speculated that minocycline is taken up into follicular epithelial cells with iodine, and that the black discoloration of the thyroid gland is intimately related to iodine metabolism.

Animals↗

PubMed1997

Thyroid iodide transporter: local sequence homologies with thyroid autoantigens.

Here we show the existence of local amino acid (aa) sequence homologies between rat thyroid iodide transporter (Na+/l- symporter or NIS), whose gene was recently cloned, and known human thyroid autoantigens [thyroglobulin (Tg), thyroid peroxidase (TPO) and thyrotropin receptor (TSHR)] NIS sequences corresponding to the fourth (aa 264-282) and fifth extracellular loop (aa 386-414) are 15 to 40% identical and 30 to 60% similar to sequences corresponding to known or putative epitopes of Tg, TPO and TSHR. The sixth extracellular loop (aa 465-485) beared homology (44% identity, 52% similarity) only to a region of Tg which flanks one of its immunodominant domains. Sequences of thyroid autoantigens other than NIS shared homology, especially Tg and TPO. We conclude that in all likelihood NIS is an additional thyroid antigen, which shares common epitopes with the other thyroid autoantigens. Addendum: A study in abstract form appeared after submission of our paper finds experimental evidence for the antigenicity of two extracellular segments (aa 262-280 and 468-487) and of a portion of the intracellular C-terminus (aa 560-579).

Amino Acid Sequence↗

PubMed1994

Thyroid hormone autoantibodies in patients with Graves' disease: effect of anti-thyroid drug treatment.

We examined the effects of anti-thyroid drug treatment on serum autoantibodies against thyroid hormones (thyroid hormone autoantibodies, THAA), thyroglobulin (Tg) and thyroid peroxidase (TPO) in patients with Graves' disease by measuring each autoantibody level before and after treatment. Six patients among 40 untreated patients with Graves' disease had anti-thyroxine (T4) antibodies. One patient had both anti-T4 and anti-triiodothyronine (T3) antibodies. Thus the prevalence of THAA in untreated Graves' disease was 7 out of 40 (17.5%). Changes in T4-Ab levels after treatment varied. In five cases (cases 3-7) levels decreased 4-7 months after treatment. However, in the other two cases levels fluctuated 1, 3, 6 and 12 months after treatment. None of the previously THAA-negative patients became positive after treatment. Anti-Tg antibody (Tg-Ab) was positive in 34 out of 40 (85%) untreated cases and its level decreased in both THAA positive and negative patients after treatment. Anti-thyroid peroxidase antibody (TPO-Ab) was positive in 32 of the 40 (80%) untreated Graves' patients and its level significantly decreased after treatment. Our findings suggest that treatment with anti-thyroid drugs does not produce THAA in Graves' disease.

Adult↗

PubMed1990

Prediction of domain organisation and secondary structure of thyroid peroxidase, a human autoantigen involved in destructive thyroiditis.

Organ specific autoimmune diseases are relatively common immunological disorders in man which include thyroid autoimmune disease, insulin-dependent diabetes mellitus and myasthenia gravis. The target autoantigens in some of these diseases have recently been characterised. In thyroid autoimmune disease this includes the key enzyme, thyroid peroxidase (TPO), which is involved in the generation of thyroid hormone. Structural knowledge about autoantigens such as thyroid peroxidase will allow a greater understanding of the interaction between autoantigens and the aberrant immune response, and facilitate the development of strategies for antigen-specific therapeutic manipulation. We report here a prediction of the secondary structure of thyroid peroxidase, together with the results of circular dichroic spectroscopy of a homologous purified enzyme. A combination of 3 secondary structure prediction programs has been used, following multiple sequence alignment, and TPO has been found to consist mainly of alpha-helical conformation, with little beta-sheet present. This structure prediction, together with knowledge of the exon-intron boundaries allows a model for the domain organisation of the TPO molecule to be proposed.

Amino Acid Sequence↗

PubMed1989

Paradoxically subnormal serum T4 and T3 in dogs after prolonged excessive TSH stimulation of the thyroid caused by post-cAMP refractoriness of thyroid hormone secretion.

Several studies have demonstrated that excessive TSH stimulation of the thyroid for hours to days makes the thyroid gland less responsive to TSH. In this study we extended the period of excessive TSH stimulation of dog thyroids in vivo to 28 days. Serum T4 and T3 were considerably elevated initially but then gradually declined and became paradoxically subnormal after 3 weeks. This was not caused by production of TSH antibodies. At day 28 the thyroid lobes were perfused for measurements of T4 and T3 secretion. Both the basal secretion rate and the response to TSH were considerably lower after TSH pretreatment than in control dogs. This was not due to reduction of TSH receptors because the response to forskolin was similarly reduced. The cAMP response to TSH and forskolin was not blunted by TSH pretreatment. The total amount of thyroglobulin in the thyroid was not significantly altered by TSH pretreatment, but the T4, T3, and iodine content of thyroglobulin was reduced to 50% to 70% of control levels. Such a moderate reduction in hormone content could not explain the development of subnormal serum T4 and T3 during intensive TSH stimulation. Apparently one or more processes involved in thyroid hormone secretion after cAMP generation were made so refractory to TSH by the prolonged excessive stimulation, that a state of biochemical hypothyroidism developed.

Animals↗

PubMed1986

The nature of thyrotropin stimulation of thyroid function in Japanese quail: prolonged thyrotropin exposure is necessary to increase thyroidal 125I uptake.

Single injections of thyrotropin (TSH) increase serum T4 and thyroidal 32P uptake but not thyroidal 125I uptake regardless of dosage, exposure time or age. Chronic TSH exposure, with 3 or more days of injection, does increase thyroidal 125I uptake. Studies using iodine (I) supplementation indicated that the increased thyroidal radioiodine uptakes seen with chronic TSH administration were not due to an I deficiency in the thyroid resulting from high hormone release. Labeled and unlabeled experiments comparing the effects of single vs. multiple injections of TSH were used to describe the effects of TSH on hormone release, hormone production and thyroidal I uptake.

Animals↗