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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary hypothyroidism accompanies more than 50% of clinically significant pituitary thyrotroph adenomas. Hypothyroidism may also produce pituitary enlargement secondary to thyrotroph hyperplasia and present with a sellar mass and hyperprolactinemia. Three hypothyroid patients who presented with presumed prolactin-producing adenomas are reported. Although laboratory and radiologic abnormalities of pituitary enlargement may resolve after corrective thyroid therapy, our patients showed no such response and underwent operation. Histologic examination revealed no adenomas, but thyrotroph and lactotroph hyperplasia were present. Thyrotroph hyperplasia probably results from lack of negative feedback of thyroid hormone upon the anterior pituitary. Whether this is due to hypothalamic release of thyrotropin-releasing hormone (TRH) or another mechanism is unclear. Lactotroph hyperplasia may result from excess TRH, which stimulates lactotrophs with resultant hyperprolactinemia, or from reduced hypothalamic dopamine, thereby facilitating prolactin secretion. This study suggest that (a) hyperprolactinemia in hypothyroidism is not necessarily due to the "stalk section effect" secondary to pituitary enlargement, and (b) patients with primary hypothyroidism and sellar mass should initially be managed medically so that potentially reversible pituitary hyperplasia is not mistaken for adenoma.
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PMID:Combined thyrotroph and lactotroph cell hyperplasia simulating prolactin-secreting pituitary adenoma in long-standing primary hypothyroidism. 334 69

In a prospective multicentric study, 924 untreated hyperthyroid patients were investigated, coming consecutively within one year into 17 thyroid centers of 6 European countries. With the aid of clinical information, evaluation of thyroid scan and centrally assayed thyroid hormones, thyroid antibodies, TSH-binding inhibiting immunoglobulins (TBII), and urinary iodine, different types of hyperthyroidism could be shown. Two types of hyperthyroidism could be defined directly: autonomous adenoma in cases of hot nodules in thyroid scan and Graves' disease, defined as hyperthyroidism with eye symptoms, and/or measurable TBII levels. The remainder, called "non-classifiable", included TBII negative Graves' patients, comprising of Hashitoxicosis, toxic nodular goiter, and other multifocal autonomies. 9.2% of the patients had an autonomous adenoma, 59.6% Graves' disease, and 31.2% unclassified hyperthyroidism. The main and significant difference between these types were mean age, goiter size, nodularity, and severity of the disease, being especially expressed in Graves' disease. Graves' patients had significantly increased T3/T4 ratios. Using as additional criteria diffuse regular uptake and/or increased T3/T4 ratios for immunogenic types of hyperthyroidism at least half of the 31.2% unclassified hyperthyroidism are probably Graves' disease. Forming two groups of iodine-deficient areas (IDA) and iodine-sufficient areas (ISA) according to the urinary iodine, it was possible to elucidate some characteristics independently of local factors. Autonomous adenoma was more frequent in IDA (10.1%) than in ISA (3.2%). Differences in iodine supply are reflected in the three types of hyperthyroidism by a significant higher prevalence of goiter, thyroid nodularity, lower thyroid hormone concentrations, and a higher rate of T3 toxicosis in IDA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The different types of hyperthyroidism in Europe. Results of a prospective survey of 924 patients. 337 59

Twenty-one papillary thyroid carcinomas (PTCs), grouped into predominantly papillary (14 cases), predominantly follicular (5 cases), and extremely follicular, i.e., follicular variant (2 cases) types, were studied in comparison with three cases each of follicular lesions including follicular carcinoma, follicular adenoma, adenomatous goiter and Graves' disease. Histochemical, immunoperoxidase, and electron microscopic analyses demonstrated no remarkable differences between the predominantly papillary and predominantly follicular PTCs, but the presence of common characteristics distinct from those of the follicular lesions. These two types of PTCs showed less glycogen, more mucoid material, more epidermal keratin, less thyroid hormone with relative predominance of T3 over T4, and more interdigitating reticulum cells (IDCs) than most of the follicular lesions. Ultrastructurally, the tumor cells of these PTCs had markedly irregular nuclei, a vesicular chromatin pattern, and small basally located lysosomes, in contrast with the cells in the follicular lesions which had smooth round nuclei, more heterochromatin, and apical or dispersed lysosomes of various sizes. The follicular variant PTCs showed some mixed features, such as glycogen in the follicular portion and mucoid material in metastatic papillary foci, positive keratin and IDCs but greater amounts of thyroid hormone, and a rather intermediate type of ultrastructure with only mildly irregular but vesicular nuclei and large apical as well as small basal lysosomes. These findings cytologically support the WHO definition of papillary carcinoma that includes tumors with variable mixtures of papillary and follicular patterns. However, separate consideration may be necessary with regard to the follicular variant.
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PMID:Papillary carcinoma of the thyroid. A histochemical, immunohistochemical and ultrastructural study with special reference to the follicular variant. 343 81

We examined basal and bTSH-stimulated human thyroglobulin (hTg) secretion by autologous normal and abnormal (benign and malignant) human thyroid cell monolayers. Basal and bTSH-stimulated hTg secretion was highly variable and ranged from 50-700 ng/ml/10(5) cells over a 6 day period. All normal and benign 'non-functioning' adenoma cells demonstrated a dose and time related stimulation of hTg secretion in response to bTSH. Comparison of hTG secretion by autologous normal and abnormal cells showed that in six of eight pairs, the normal thyroid cells had a greater output of hTg than the benign adenoma cells in contrast to our previous studies using non-autologous cells. Malignant thyroid cell hTg production was less predictable than that obtained with normal and benign thyroid cells varying from absent to normal responses to bTSH. Characterization studies of the secreted hTg showed no difference between normal, benign and malignant thyroid cell hTg with reference to molecular weight. However, hTg secreted in vitro was non-iodinated and had a marked reduction (up to 200-fold) in immunoreactivity assessed by both polyclonal and monoclonal antibodies to hTg when compared to hTg standard prepared from intact thyroid tissue (which had 4.58 micrograms iodine/mg). This reduction in hTg immunoreactivity was greatest for hTg secreted by malignant thyroid cells. These data demonstrate the wide variability in the hTg secretory capacity of human thyroid cell monolayers and indicate, when compared to autologous normal cells, that abnormal human thyroid epithelial cells may be relatively deficient in their ability to secrete hTg in vitro. There were also qualitative differences in the immunoreactivity, and iodine content, of in-vitro secreted hTg. These observations suggest that there may be much greater heterogeneity in hTg secreted in vitro than previously realized, perhaps secondary to differences in iodine content and/or degree of glycosylation. Human thyroglobulin (hTg) is the major secretory protein of the thyroid cell (Van Herle et al., 1979). Intracellular hTg is the site of thyroid hormone iodination yet its extrathyroidal role, if any, remains unclear. While hTg is usually present in the peripheral circulation of normal individuals, in species of differing molecular weight (Feldt-Rasmussen et al., 1978), there have been few studies of in-vitro production of hTg by isolated human thyroid cells. Our interest in hTg is in its role as an antigen in thyroid autoimmune disease (De Bernardo et al., 1983; 1986).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Variability in production and immunoreactivity of in-vitro secreted human thyroglobulin. 345 72

A thirty-seven-year-old housewife whose chief complaints were recurrence of galactorrhea and amenorrhea three years after having a selective adenomectomy. Hormonal examination done as a result of the continuation of the endocrinism revealed a hyperprolactinemia and high level of TRH due to hypothyroidism. Serum prolactin responded to neither TSH stimulation nor L-Dopa suppression tests. In addition, serum TSH did not react to TRH test. Contrast enhancement CT showed an intrasellar enhancing mass the size of which was less than 1 cm in diameter. A unilateral septal transsphenoidal operation was performed; and a soft white-yellowish mass 7 X 5 X 5 mm in size was found in the left inferolateral aspect of the pituitary gland. Histological studies of frozen sections of this revealed it to be a pituitary adenoma, with the border between tumor and normal tissue being quite distinct. Immunocytochemical diagnosis further confirmed it to be both PRL and TSH producing adenoma. Electron microscopy showed more than three different hormone-producing cells. The PRL cells contained large, and the TSH cells had small hormone granules; but some tumor cells contained secretory granules of both sizes suggesting production of both PRL and TSH in the cytoplasm. It is necessary in the management of patients like this, during the post-operative period, to adequately institute a thyroid hormone replacement therapy so as to prevent recurrence.
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PMID:[A recurrent case of TSH-PRL secreting microadenoma following hypothyroidism]. 382 56

The coupling of iodotyrosine (coupling reaction) is one of the least studied in the formation of thyroid hormone, particularly in human thyroid diseases. This paper describes a method of measuring iodotyrosine coupling catalyzed by human thyroid peroxidase (TPO) in vitro. There were two important requirements to demonstrate the coupling reaction: 1) thyroglobulin with a low thyroid hormone content, and 2) partially purified TPO. Thyroglobulin with low thyroid hormone content was obtained from Grave's and follicular adenoma tissues after propylthiouracil (PTU) therapy and L-T4 therapy, respectively. TPO was prepared from Graves' thyroid by solubilizing the 100,000 X g pellet of thyroid homogenate with sodium deoxycholate and trypsin, followed by Sephacryl S-300 gel filtration. Before the coupling reaction, thyroglobulin was iodinated with chloramine-T and potassium iodide, followed by dialysis. The coupling reaction was carried out by incubating newly iodinated thyroglobulin with TPO, diiodotyrosine, a coupling stimulator, and a H2O2-generating system (glucose and glucose oxidase) for 20 min at 37 C. After thyroglobulin was digested with Pronase, the thyroid hormone content of the thyroid digest was measured by RIA. Coupling activity was measured by the amount of newly formed T3 (nanograms of T3 per mg thyroglobulin). The time course of coupling reaction showed a progressive increase in coupling activity up to 30 min, and the reaction was temperature and pH dependent, with a pH optimum of 7.0. Coupling activity in the presence of H2O2 and TPO was 43 +/- 5.0 ng T3/mg thyroglobulin (mean +/- SD of triplicate samples), and addition of diiodotyrosine to the H2O2-TPO system caused a nearly 3-fold increase in coupling activity. This method has potential utilization for measurement of peroxidase coupling activity, since there was a linear relationship between the measured coupling activity and the amount of added TPO when the TPO concentration was over 3 micrograms/300 microliter. Methimazole (MMI) and PTU had similar potencies in inhibiting the TPO-catalyzed coupling reaction, whereas MMI was distinctly more potent than PTU as an inhibitor of TPO-mediated iodination in vitro. The different potencies of MMI in the two reactions suggest that different inhibitory mechanisms may be involved in iodination and coupling. The reducing agent, sodium metabisulfite, was also found to be a more potent inhibitor of the TPO-mediated coupling reaction than of the TPO-mediated iodination reaction. The method of iodotyrosine coupling described here may be useful to investigate the coupling step of thyroid hormone formation in human thyroid diseases.
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PMID:Coupling of iodotyrosine catalyzed by human thyroid peroxidase in vitro. 383 97

In the case of thyrostatic therapy of autonomous adenoma with iodinization blocker type drugs (here carbimazol), there is a relative increase of uptake of 99mTc-pertechnetate by the suppressed thyroid tissue before TSH becomes detectable by TRH testing (400 micrograms). As soon as endogenous TSH stimulation occurs (due to the decrease of thyroid hormone induced by the thyrostatic therapy), relatively more uptake of 99mTc-pertechnetate by the non-autonomous tissue is observed. 56 patients suspected of having autonomous thyroid adenoma were investigated. The activities in the regions of interest measured over autonomous and non-autonomous thyroid tissue before and after thyrostatic therapy were expressed in form of a double-ratio. 22 of the 56 patients were found to have an autonomous adenoma (double-ratio greater than or equal to 1.74). In 19 patients an adenoma was excluded with certainty (double-ratio less than or equal to 1.22). The remaining cases fell in-between and were difficult to classify. However, the gradual transition between the two groups so classified was harmonious. The different reactions of autonomous and non-autonomous thyroid tissue to thyrostatic therapy appear to be helpful in the differentiation between the two types of tissue.
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PMID:[Reaction of autonomous and non-autonomous thyroid tissue to iodination blockers]. 618 27

Subcutaneous inoculation of the prolactin secreting MtTW15 adenoma in male Wistar Furth rats for 4 weeks produced a significant increase in serum prolactin and a corresponding decrease in peripheral beta-adrenergic responsiveness. Both the isoproterenol induced drink and heart rate responses used to assess the beta-adrenergic responsiveness were significantly reduced in the hyperprolactinemic rat. Serum T3 and T4 levels were measured as was cardiac beta-adrenergic receptor number to ascertain if an alteration of thyroid hormone and a resultant decrease in beta-adrenergic receptor number was responsible for the attenuated beta-adrenergic responsiveness. Serum T4 was significantly reduced in the hyperprolactinemic group (1.9 +/- 0.3 microgram%) as compared to the control group (6.4 +/- 0.l5 microgram%). However there was no significant difference in serum T3 or in cardiac beta-adrenergic receptor number between the two groups. Removal of the MtTW15 adenoma resulted in a normalization of serum prolactin, T4, and in the responsiveness of the peripheral beta-adrenergic system within 4-6 weeks. These results indicate that the attenuated beta-adrenergic responsiveness associated with hyperprolactinemia is reversible and not dependent on a reduction in beta-adrenergic receptor number.
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PMID:Effects of elevated prolactin and its normalization on thyroid hormone, cardiac beta-adrenoreceptor number and beta-adrenergic responsiveness. 632 74

Human thyroid blood flow rate (TBF) was measured during operations by electromagnetic flowmetry in 75 euthyroid patients with normal thyroid tissue, nodular goiter, or solitary adenoma, and in 22 hyperthyroid patients with diffuse or nodular goiter. Blood flow rate was measured in one to four of the thyroid arteries. No difference in blood flow rate was seen between the left and right lobes. The slight difference found between the inferior and superior arteries was not significant. In each subject, total TBF was calculated as 4 times the mean of the recorded blood flow in the single arteries. The total TBF was 31 (9-109) ml/min (inner 95 percentile range) in euthyroid patients, similar in all 3 groups. This is less than in most earlier reports. The relative TBF was 1.2 (0.4-3.8) ml/min/g thyroid tissue in normal thyroid tissue and 0.6 (0.1-3.7) ml/min/g in nontoxic nodular goiter (p less than 0.01). Patients with hyperthyroidism had a higher total TBF 54 (15-197) ml/Min (p less than 0.001), despite preoperative treatment giving euthyroidism, Similar TBF rates were found in 3 hyperthyroid patients given propranolol preoperatively. Electromagnetic flowmetry is applicable to study thyroid blood flow rate. Human TBF shows considerable interindividual variations, which must be kept in mind when studying directly the rate of thyroid hormone secretion from arteriovenous gradients.
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PMID:Thyroid blood flow rate in man. Electromagnetic flowmetry during operation in euthyroid normal gland, nontoxic goiter, and hyperthyroidism. 645 60

A 35-year-old woman with an otherwise normal heart had been suffering from recurrent paroxysmal supraventricular tachycardia during the past 3 years. Serum thyroid function tests were repeatedly normal. When a thyroid nodule became evident, a toxic adenoma was diagnosed. Serum total hormone values were normal, but a few hours after the last recurrence of paroxysmal supraventricular tachycardia, total T3, free T3 and free T4 became clearly elevated. At that time hemorrhagic necrosis of the adenoma, though localized only at the periphery of the tumor, heavily impaired nodule overactivity, as judged by the disappearance of paroxysmal supraventricular tachycardia, by normal free thyroid hormone levels and by the return of a normal TSH response to TRH.
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PMID:Long-standing recurrent paroxysmal supraventricular tachycardia disappearing after cystic degeneration of an episodically hypersecreting toxic adenoma of the thyroid. 646 14


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