Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The spontaneous course of 58 patients with compensated autonomous adenoma of the thyroid was followed. Scintigraphic appearance (compensated (CAA) or decompensated (DAA)) was documented and the serum levels of thyroxine (T4), triiodothyronine (T3) and thyroid-stimulating hormone after TSH-stimulating hormone were measured at the beginning of observation and 3.8 years (median) later. During follow-up period, 13 patients (22%) with CAA developed DAA. 9/13 patients (15%) had overt hyperthyroidism with elevated T4 and/or T3 levels, 4/13 patients (7%) had normal thyroid hormone levels. Life table analysis showed a risk for developing hyperthyroidism of 19% at five years. The size of all adenomata measured scintigraphically was increasing during follow-up, and there was no discrimination of CAA from DAA using this technique. Eight CAA patients received iodinated contrast medium but none develop DAA. In conclusion from these results as well as from the literature, there is no indication for surgery or radioiodine therapy of patients with a CAA, even if there are plans to administer iodinated contrast medium.
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PMID:[The spontaneous course of compensated autonomous thyroid gland adenomas]. 176 84

An invasive TSH-secreting adenoma inducing mild hyperthyroidism was diagnosed in a 16-year-old male. Initial surgical treatment led to a temporary clinical and biological improvement. Recurrence of the thyrotoxicosis was treated with the somatostatin analogue, SMS 201-995 (octreotide) with normalization of the serum thyroid hormone levels with a dose of 200 micrograms per day. With immunoelectron microscopy, the tumour cells appeared poorly granulated with small secretory granules located at the periphery of the cells; only part of those were immunoreactive with an anti-TSH beta monoclonal antibody. No specific TRH binding site was found in a tumour membrane preparation. By quantitative autoradiography, somatostatin specific binding sites were as numerous in the TSH-secreting tumour as in control GH-secreting tumours. Binding kinetics and guanosine triphosphate dependency of the binding were equivalent in the TSH and GH tumours tested. Although all of the tumour cells displayed the same ultrastructural features, some were non-immunoreactive, suggesting that they could secrete an altered form of TSH. The absence of TRH receptors in the tumour cells is in accordance with previous reports on this type of tumour. We confirm the efficiency of octreotide treatment in this case of neoplastic TSH inappropriate secretion. The therapeutic effect of octreotide goes along with the presence of a high density of guanine nucleotide-dependent somatostatin binding sites in the tumour cells.
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PMID:A human TSH-secreting adenoma: endocrine, biochemical and morphological studies. Evidence of somatostatin receptors by using quantitative autoradiography. Clinical and biological improvement by SMS 201-995 treatment. 185 93

Thyroidal concentrations of T4 and T3 and the T4/T3 ratio were analyzed in the nodular and paranodular tissues from two groups of patients with suppressed TSH secretion. The first group consisted of 17 patients with nontoxic nodular goitre (NG), 8 of whom received long-term levothyroxine therapy to suppress TSH, while remaining 9 were untreated. The second group consisted of 10 patients with autonomously functioning thyroid adenoma (AFTA), in whom TSH secretion was suppressed due to the adenoma-induced increase in thyroid hormone concentrations. In nodular tissues of NG patients, thyroidal T4 and the T4/T3 ratio were significantly higher in treated than in untreated patients (0.34 +/- 0.05 vs. 0.15 +/- 0.02 mol T4/mol of thyroglobulin (Tg) and 10.9 +/- 1.2 vs. 5.2 +/- 0.7 respectively). Analysis of paranodular tissues of NG patients also revealed a higher T4/T3 ratio in treated patients (16.0 +/- 2.1 vs. 6.9 +/- 0.9), although thyroidal T3 and T4 concentrations in treated and untreated patients were similar. In AFTA patients, both T3 and T4 concentrations were higher in the adenoma than in paranodular tissues (0.14 +/- 0.04 vs. 0.02 +/- 0.005 mol T3/mol Tg and 1.08 +/- 0.32 vs. 0.26 +/- 0.06 mol T4/mol Tg), whereas the T4/T3 ratio was significantly higher in paranodular tissues (23.2 +/- 5.9 vs. 9.3 +/- 1.8). These results indicate that suppression of TSH induced either exogenously or endogenously results in an increase in the thyroidal T4/T3 ratio that reflects an increase in T4 and/or a decrease in T3 concentrations. These findings also support the notion that TSH preferentially stimulates thyroidal T3 production.
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PMID:Exogenous and endogenous suppression of thyroid-stimulating hormone induces similar effects on thyroidal iodothyronines. 186 17

Serum beta 2-microglobulin concentrations were determined in 21 untreated hyperthyroid patients (12 with Graves' disease, and nine with toxic nodular adenoma) and in 20 healthy controls. All subjects had normal serum creatinine concentrations and urine analysis. Both total and free thyroid hormones were significantly higher in the hyperthyroid groups than in controls. Beta 2-microglobulin concentrations were significantly increased in both groups of hyperthyroid patients compared with controls. No difference was found in the thyroid hormone and beta 2-microglobulin concentrations between both sets of patients. The beta 2-microglobulin and thyroid hormone concentrations were not correlated. These data show that hyperthyroidism is another cause of increased beta 2-microglobulin production along with viral infections, immunologically mediated diseases, and malignant neoplasms. The increased serum beta 2-microglobulin concentration in thyroid hyperfunction is probably related to metabolic rate, even if autoimmunity might contribute to its overproduction.
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PMID:Increased serum beta 2-microglobulin concentrations in hyperthyroid states. 199 37

The rate of protein synthesis was measured in thyroid tissue obtained from three groups of patients undergoing thyroid surgery: group I (n = 18), hyperthyroid patients preoperatively treated with an antithyroid drug and T4; group II (n = 11), hyperthyroid patients preoperatively treated with a beta-adrenergic antagonist drug; and group III (n = 9), euthyroid patients operated on for multinodular goiter or adenoma. Quantitative morphology was studied in the resected thyroid tissue from the patients in groups I (n = 15) and II (n = 6) who had Graves' disease. While serum thyroid hormone levels became normal during preoperative treatment in group I, they remained elevated in the group II patients. The rate of protein synthesis was 2-fold higher in thyroid tissue from patients in group II than in those in groups I and III. A tendency toward an increased amount of epithelium and a reduced amount of colloid was found in thyroid tissue from patients in group II. There was a positive correlation between the rate of protein synthesis, and distribution of epithelium, and the epithelium to colloid ratio, respectively, in thyroid tissue. These results suggest that the thyroid gland of hyperthyroid patients remains hyperactive during treatment with beta-adrenergic antagonist drugs.
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PMID:Protein synthesis and quantitative morphology in thyroid tissue from hyperthyroid patients after preoperative treatment with antithyroid or beta-adrenergic antagonist drugs. 245 76

Parathyroid cysts are relatively uncommon lesions. Approximately 200 cases have been reported. Despite their location in the region of the thyroid gland, they have not previously been discussed in the otolaryngologic literature. They arise from remnants of the pharyngeal pouch or as a result of cystic degeneration of a parathyroid adenoma. A case of a parathyroid cyst occurring in a 13-year-old female is presented. This is the youngest case ever reported. Fine needle aspiration of an anterior neck mass yielded clear fluid, a finding highly suggestive of a parathyroid cyst. Radioimmunoassay of the fluid demonstrated a high level of parathormone and low level of thyroglobulin concentration, thereby confirming the diagnosis. In this case, which was diagnosed by FNA, the need for a trial of thyroid hormone suppression or hemithyroidectomy was obviated.
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PMID:Parathyroid cysts. 258 96

Pituitary function and structure were assessed in 69 endemic cretins from western China. In hypothyroid cretins (TSH greater than 10 mIU/l), CT imaging of the pituitary revealed adenoma in five of 20 (25%) and partially empty sella (PES) in a further eight of 20 (40%). The majority of tumours were microadenomas and showed a relation with higher levels of serum TSH but not with duration of hypothyroidism. Dynamic pituitary testing with TRH and GnRH in four patients with adenoma on CT gave a flat TSH response but significant rises in serum PRL, GH, LH and FSH concentrations. Hyperprolactinaemia (greater than 350 mIU/l) was present in hypothyroid cretins only (13 of 26; 50%) and serum PRL showed a curvilinear relation with serum TSH levels (r = 0.7, P less than 0.0001). Hypogonadism was seen in approximately half the cretins with high PRL levels. Our data suggest that severe protracted thyroid hormone deficiency may result in thyrotrophin adenomas of the pituitary gland. Disturbances of growth, puberty, and sexual function in endemic cretins are explained by the secondary effects of thyroid hormone deficiency on pituitary function.
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PMID:Effects of protracted hypothyroidism on pituitary function and structure in endemic cretinism. 277 53

A patient with a mixed pituitary tumor secreting TSH and GH was treated, starting 3 months after partial adenomectomy, with the somatostatin analog SMS 201-995 for 8 months. Somatostatin itself inhibited TSH, GH, and alpha-subunit release by the tumor both in vivo and in vitro. Long term treatment with twice daily sc injections of SMS 201-995 resulted in decreased TSH secretion and lower serum thyroid hormone levels. However, euthyroidism was achieved only when the patient was treated with three daily 200-micrograms injections of SMS 201-995. After 30 weeks of SMS 201-995 therapy, TSH secretion increased, while GH secretion remained suppressed. After withdrawal for 6 months, SMS 201-995 (100 micrograms, sc, twice daily) again completely inhibited TSH secretion. SMS 201-995 did not alter the volume of the residual adenomatous tissue. We conclude that SMS 201-995 may be a valuable therapeutic agent for the management of patients with a thyrotroph adenoma. However, desensitization may occur during long term treatment.
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PMID:Long term treatment with the somatostatin analog SMS 201-995 in a patient with a thyrotropin- and growth hormone-secreting pituitary adenoma. 289 19

Primary hypothyroidism is associated with hypertrophy and hyperplasia of thyrotropic cells. In addition, pituitary adenomas that produce thyroid-stimulating hormone occur in both hypothyroidism and hyperthyroidism. The relationship between thyrotropic hyperplasia and adenoma formation is, however, unsettled. We summarize the results of a histologic and immunocytologic study of the pituitary glands of 64 patients with long-standing primary hypothyroidism in an effort to characterize the changes in thyrotropic cells as related to the duration and severity of disease, to therapy, and to the development of thyrotropic adenomas. Diffuse and nodular thyrotropic cell hyperplasia was noted in 69% and 25% of glands, respectively. A crude correlation was observed between the degree of thyrotropic cell hyperplasia and the relative lack of thyroid hormone replacement therapy. In 12% of glands, tumorlet formation was observed, perhaps representing an intermediate stage between nodular hyperplasia and the development of microadenoma. Twelve adenomas were noted, five of which contained thyroid-stimulating hormone immuno-reactive cells. Although thyroid hormone deficiency seemed to selectively affect thyrotropic cells, lactotropic hyperplasia was observed in 20% of patients; the mechanism accounting for prolactin cell hyperplasia remains obscure.
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PMID:Pituitary gland in hypothyroidism. Histologic and immunocytologic study. 298 71

The symptoms called hyperthyroidosis are caused by a thyroid hormone intoxication, which may have various causes. More than 95% of the hyperthyroidosis are caused by an autoimmune thyropathy (Basedow's disease) or autonomy (autonomous adenoma, disseminated autonomy). Other causes are rare. The therapy has 2 aims: the normalisation of the supply of the thyroid hormone and the removal or influence of the cause. Thus apart from an exact functional diagnostics the etiopathogenetic coordination must be done which has an essential influence on the differential-therapeutic decision. Beside the general therapeutic measures the thyrostatic long-term therapy, the subtotal thyroid resection and the radioiodine therapy are at our disposal. Diagnosis, performance, advantages and disadvantages are demonstrated.
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PMID:[Therapy of hyperthyroidism]. 329 27


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