Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027627 (metastases)
 103,950 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The levels of total organically bound 131I, per cent of labelled iodoproteins, total labelled iodinated amino acids and a percentage of individual iodinated amino acids (thin-layer chromatography) were measured in serum of 84 patients with thyroid cancer and of 16 patients with thyrotoxicosis at 48 h after the administration of therapeutic dose of 131I. In thyrotoxic patients treated with therapeutic doses of 131I (2 to 39.6mCi; 74 to 1500 MBq) the findings were similar to normal subjects. In patients with thyroid cancer a significant increase of iodotyrosines was found after thyroid radioiodide ablation (100 to 200 mCi; 3.7 to 7.4 GBq). No remarkable differences were found between two groups of patients with thyroid cancer, the first one being treated with thyroid eliminating dose in attempt to activate the metastases of functionally differentiated tumour, while the second one was treated with similar doses (i. e. 100 to 200 mCi) to suppressor destroy a functionally active tumour or its metastases. Even though the hormonogenesis in tumours was hardly distinguishable from the products of its radiation damage, it was suggested that the hormonogenesis in neoplastic tissue differs from that in normal thyroid only quantitatively, being less in patients with thyroid cancer than in these with thyrotoxicosis.
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PMID:Labelled amino acids in plasma of patients with thyrotoxicosis and thyroid cancer after radioiodine treatment. 31 82

We present a case with the unusual association of Graves' disease and functioning pulmonary metastases of follicular thyroid carcinoma. Unlike other reports of thyroid cancer and thyrotoxicosis, this patient's hyperthyroidism was related to a hyperfunctioning primary thyroid neoplasm and not merely to large amounts of functioning metastatic tumor. Thyroidectomy cured her hyperthyroidism. A lung biopsy confirmed the impression of metastatic thyroid cancer. Following therapeutic radioactive I131 pulmonary metastases completely disappeared.
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PMID:Graves' disease, follicular thyroid carcinoma and functioning pulmonary metastases. 58 60

A 57-year old woman with thyroid carcinoma manifesting overt thyrotoxicosis is presented. After the patient had been made euthyroid with propylthiouracil, right lobectomy and lymph node dissection were performed. Permanent paraffin sections revealed follicular adenocarcinoma with capsular and vascular invasion. Metastases to the right humerus, both femurs, the skull and pleural cavity became prominent with the recurrence of thyrotoxicosis and the patient died 2 years and 3 months after operation. The clinical evidence indicates that thyrotoxicosis in the present case is caused by the excessive secretion of thyroid hormone by both the original carcinoma and the secondary deposits. Twenty three similar cases reported in the English and Japanese literatures are summarized.
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PMID:Report on a case of functioning thyroid carcinoma provoking thyrotoxicosis with review of literature. 75 8

The cases of 3 patients with advanced metastatic choriocarcinoma and biochemical and clinical evidence of hyperthyroidism are reported. The thyroid-stimulating hormone (TSH) bioassay activity was increased in all 3 patients before chemotherapy. All patients had clinical signs and symptoms of overt thyrotoxicosis although goiter was present in only 1. Sinus tachycardia was present in all. The 1st symptom in all 3 cases was hemoptysis. An X-ray appearance of multiple pulmonary metastases was also present. There was biochemical evidence of improvement in thyrotoxicosis after chemotherapy. This improvement paralleled the fall in urinary human chorionic gonadotropin (HCG). As treatment, intermittent oral 5-day courses of methotrexate and iv actinomycin D were given at 3-week intervals. In 2 of the cases the ratio of bioassayable thyrotropic activity to HCG found in the serum was similar to the ratio in patients with hydatidiform moles. In the other case the ratio was much higher. It appears that the development of biochemical and clinical hyperthyroidism in patients with choriocarcinoma depends on the duration of the choriocarcinoma and the serum level of HCG. Findings suggest that there may be production of another TSH in addition to the thyrotropic activity of high HCG levels.
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PMID:Choriocarcinoma as a cause of thyrotoxicosis. 94 90

Twenty-one patients who underwent surgical treatment for thyrotoxicosis and who were found at operation to have thyroid cancer are presented. Sixteen had Graves' disease and 5 had toxic nodular goiter. The group with Graves' is compared with 110 euthyroid patients with thyroid cancer who underwent their initial surgery in the same time period and who were of the same age (+/- 1 yr) and sex as the patients with Graves' disease. None of the thyrotoxic patients died during follow-up of 2-24 yr or developed subsequent metastases. The 1 patient with a local lymph node metastasis has not shown evidence of recurrence. Hypoparathyroidism appeared as a complication in only 1 patient. The size of tumors in the patients with Graves' disease was significantly smaller than in the euthyroid group. The course of the disease in both the patients with Graves' disease and the thyrotoxic group as a whole was relatively benign. This series does not support the recent suggestions that thyroid cancer in patients with Graves' disease is more aggressive than in either patients with toxic nodular goiter or euthyroid subjects. Patients with Graves' disease and thyroid cancer should be treated identically to other patients with thyroid cancer. Therapy should consist of total thyroidectomy followed by a postoperative 131I scan. Residual tissue or metastases found on the scan should be ablated with 6 GBq 131I. The patient should receive a suppressive dose of T4.
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PMID:Does Graves' disease or thyrotoxicosis affect the prognosis of thyroid cancer. 151 81

A 59-year-old man with metastatic renal cell carcinoma developed symptomatic thyroid dysfunction following interleukin-2 (IL-2) and interferon-alpha (IFN-alpha) therapy. Thyroid evaluation prior to this therapy revealed evidence of subclinical Hashimoto's thyroiditis. Symptomatic thyrotoxicosis, including atrial fibrillation, developed after the initial two courses of intermittent intravenous bolus therapy with human recombinant IL-2 and IFN-alpha. At 4 weeks after initiation of immunotherapy, the thyroid antimicrosomal antibody (AMA) titer rose from 1:6,400 to 1:25,600; thyroid-stimulating immunoglobulin was negative. A technetium 99m-pertechnetate thyroid scan obtained while the patient was thyrotoxic showed diminished uptake in a symmetrically enlarged gland. The patient was temporarily treated with propranolol, digoxin, and quinidine. The atrial fibrillation quickly resolved, and thyrotoxicosis abated over the following 5 weeks, while the AMA titer rose further to 1:102,400. By 11 weeks after initiation of immunotherapy, hypothyroidism developed and persisted through two subsequent courses of cytokine therapy at Weeks 16 and 18. The tumor metastases partially responded to the immunotherapy. The patient has remained hypothyroid up to 27 weeks of follow-up. This case history suggests that IL-2 and IFN-alpha therapy may precipitate a fulminant autoimmune thyroiditis syndrome in a vulnerable patient with preexisting autoimmune thyroid disease.
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PMID:Transient thyrotoxicosis and persistent hypothyroidism due to acute autoimmune thyroiditis after interleukin-2 and interferon-alpha therapy for metastatic carcinoma: a case report. 155 92

From 1980 to 1989, 226 patients (199 females, 27 males, median age 41 [18-76] years) underwent surgery because of clinical hyperthyroidism. 152 patients had autoimmune thyrotoxicosis, and 74 functional autonomy. Histological examination of resected thyroid tissue revealed carcinoma in 6 cases (2.6%): 3 (2%) in autoimmune hyperthyroidism, and 3 (4%) in functional autonomy. Five tumours fulfilled the criteria for occult papillary thyroid carcinoma (highly differentiated, less than 1.5 cm diameter). One woman had both a multilocular papillary carcinoma and a medullary carcinoma without proven metastases. In none of the cases was a malignant tumour suspected preoperatively from sonography or scintigraphy studies. In the patients with occult carcinomas, extended bilateral subtotal resection was regarded as curative. In the patient with papillary and medullary carcinoma, remaining thyroid therapy was given. One patient with Basedow's (Graves') disease and a papillary carcinoma of diameter 1.3 cm received radioiodine at her own request. She and the four remaining patients received suppression therapy (150-200 micrograms L-thyroxine daily), with frequent follow-up. During follow-up for a mean period of 24 months (range 6-51 months) there were no metastases or tumour recurrences.
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PMID:[Frequency of thyroid gland carcinoma in hyperthyroidism]. 199 31

A case of metastatic adenocarcinoma of the thyroid is reported in which treatment by means of radioactive iodine has been successful. The patient was completely thyroidectomized for "malignant adenoma" in 1923, with neither thyrotoxicosis then nor hypothyroidism postoperatively; 15 years later there developed classic symptoms of hyperthyroidism and severe pain in the lower back. In October 1939 a pulsating tumor removed from the level of the 12th thoracic vertebra proved to be metastatic thyroid adenocarcinoma (histologically well differentiated, with small follicles and colloid). In the next two years hyperthyroidism increased and roentgenograms revealed new metastases in the lungs, upper part of the right femur, second rib on the left side, left ilium, and skull. Roentgenologic irradiation of the metastases proved ineffectual. In March 1943 a tracer dose of radioactive iodine revealed iodine retention by all the known lesions and no evidence of residual thyroid tissue in the neck. Therapeutic amounts of radioactive iodine were administered orally between May and October 1943. Definite and lasting clinical improvement followed. In April 1944 and March 1945 additional I* was administered with a resultant disappearance of pain, increase in weight, and progressive change in all clinical criteria in the direction of hypothyroidism. Roentgenographic evidence pointed to an arrest if not a regression of the disease. No untoward effects followed this therapy. Radioactive iodine seems to be an effective therapeutic agent in the control of this type of tumor.
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PMID:Radioactive iodine therapy: effect on functioning metastases of adenocarcinoma of the thyroid. 211 14

Well-differentiated follicular carcinoma causing thyrotoxicosis is a rare entity. The age and sex distribution is no different from that of other patients with follicular carcinoma, with 87% older than the age of 40 and a female:male ratio of 3:1. The clinical presentation is similar to that of Graves' patients except that evidence of metastatic disease is often present (soft tissue masses, bone pain). The metastases are in the usual locations (bone, lung, mediastinum) and are often bulky. Despite the poor efficiency of iodine uptake and thyroid hormone production, the large tumor mass is capable of producing excessive hormone. Laboratory data confirm the hyperthyroid state, but the occurrence of T3 elevations with normal T4 levels is common, and T3 toxicosis may be missed if only T4 levels are measured. The role of thyroid stimulating immunoglobulins is still evolving, but such stimulators may support the growth of metastatic thyroid carcinoma and promote the development of hyperthyroidism. The treatment of these patients varied. Most had thyroidectomy followed by 131I therapy. Dosimetry allows for the administration of the largest dose of 131I with acceptable side effects. A good response to radioiodine predicted a more favorable outcome. The survival of patients with metastatic thyroid carcinoma causing hyperthyroidism does not differ from euthyroid patients with metastatic follicular disease (10-year survival, 59%).
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PMID:Thyrotoxicosis caused by thyroid cancer. 226 8

Long-acting somatostatin analogues such as SMS 201-995 (Sandoz) are being evaluated in a wide range of clinical indications, including gut neuroendocrine tumours and acrogemaly. Long-term continuous SMS 201-995 treatment has achieved useful symptomatic improvement in diarrhoea in 4 patients with metastatic VIPomas who had relapsed following previous treatment. Clinical improvement has outlasted suppression of VIP secretion (suggesting an additional direct antisecretory action of SMS 201-995) and has occurred despite expansion of hepatic metastases. In 6 patients with tumours secreting gastrin and/or glucagon, secretion of these peptides was acutely inhibited by SMS 201-995. However, endocrine and clinical responses to chronic treatment have been less consistent. SMS 201-995 is active orally at doses of 4-8 mg and when given thrice-daily to 6 patients with active acromegaly, suppressed mean 24-h growth hormone levels by 51-88%. Despite significantly reduced plasma insulin concentrations, glucose tolerance did not deteriorate. SMS 201-995 was also effective in suppressing thyroid-stimulating hormone (TSH) and thyroid hormone secretion in a patient with mild thyrotoxicosis due to non-tumoural inappropriate TSH hypersecretion. In all cases SMS 201-995 treatment has been well tolerated and has few side-effects.
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PMID:Clinical evaluation of SMS 201-995. Long-term treatment in gut neuroendocrine tumours, efficacy of oral administration, and possible use in non-tumoural inappropriate TSH hypersecretion. 289 35


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