Cases reported "Hyperthyroidism"

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1/198. TSH-secreting pituitary macroadenoma: rapid tumor shrinkage and recovery from hyperthyroidism with octreotide.

    A 44-year-old man with atrial fibrillation caused by hyperthyroidism is described. The underlying disease was a TSH-secreting macroadenoma of the pituitary. Treatment with the somatostatin analog octreotide eliminated hyperthyroidism and atrial fibrillation within 4 days and the tumor size diminished substantially within 3 weeks.
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2/198. Thyroid autonomy (Plummer's disease) with contralateral malignancy--mere coincidence?

    A patient with an autonomously functioning nodule in the left lobe and a papillary carcinoma in the right lobe of the thyroid gland is described. Some evidence suggests the association to be more than coincidental.
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3/198. hyperpigmentation caused by hyperthyroidism: differences from the pigmentation of Addison's disease.

    Two cases of hyperthyroidism with hyperpigmentation are presented. In both cases, hyperpigmentation was seen on the lower extremities, most strikingly on the shins, backs of the feet and the nail bed. histology of the pigmented skin showed basal melanosis and heavy deposition of haemosiderin around dermal capillaries and sweat glands. Treatment with mercazol in both cases resulted in no significant waning of pigmentation. Distribution of hyperpigmentation, haemosiderin deposition and poor response to the treatment may be characteristic features of the pigmentation caused by hyperthyroidism, and may represent differences from the pigmentation seen in Addison's disease.
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4/198. struma ovarii and hyperthyroidism.

    struma ovarii is a teratoma of the ovaries that contains a large amount of thyroid tissue. Like the cervical thyroid gland, this ectopic thyroid tissue can become autonomous. We present a case of hyperthyroidism caused by thyroid tissue in a large ovarian cystic teratoma and provide detailed endocrinological, radiological, and pathological preoperative and postoperative data. This is also the first documented case of struma ovarii in association with a secreting pituitary tumor. In addition, we provide a retrospective pathological analysis of 1390 surgically removed ovarian tumors at 2 major academic centers.
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5/198. Long-term treatment with bromocriptine of a plurihormonal pituitary adenoma secreting thyrotropin, growth hormone and prolactin.

    A 48-year-old female presented with acromegaly, amenorrhea and hyperthyroidism associated with high serum free T4 levels and measurable TSH concentrations. The administration of GHRH induced significant increases in GH, PRL and TSH. Conversely, intravenous infusion of dopamine or oral administration of bromocriptine effectively inhibited GH, PRL and TSH secretion. serum alpha-subunit levels were neither affected by GHRH, dopamine nor bromocriptine. Transsphenoidal surgery was performed and immunostaining of the tissue showed that the adenoma cells were positive for GH, PRL or TSH. The patient was treated with bromocriptine at a daily oral dose of 10 mg after surgery. serum TSH were initially suppressed but returned within reference intervals with persistent normalized free T4 levels. serum PRL became undetectable and GH levels were stable around 6 ng/ml except the periods of poor drug compliance, when serum TSH, GH and PRL levels rose considerably. The patient was followed-up for 10 years without any change in the residual adenoma tissues as detected by magnetic resonance imaging. These findings suggest that long-term bromocriptine therapy is effective in treating the hypersecretory state of a plurihormonal adenoma secreting TSH, GH and PRL.
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6/198. Rational therapy for thyroid storm.

    An approach to the management of patients with thyroid storm is described. The treatment regimen, which is directed against the abnormalities as they are presently understood, incorporates: (a) propranolol to inhibit the catecholamine-mediated peripheral effects of the circulating thyronines; (b) propylthiouracil to inhibit thyroid hormone synthesis and to inhibit peripheral conversion of thyroxine to triiodothyronine (T3), the predominant source of T3 production; (c) iodine to block the glandular release of thyroid hormones; (d) dexamethasone along with general supportive therapy. The regimen has been used for a 13 year old schoolgirl with thyroid storm, and the induced rapid fall in serum T3 levels is illustrated. It has also been used in patients with florid thyrotoxicosis undergoing emergency surgery and has resulted in marked clinical improvement associated with rapid decreases in serum T3 levels. It is a simple and efficient regimen, rendering cumbersome forms of therapy such as plasmapheresis and peritoneal dialysis unnecessary.
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7/198. Gestational thyrotoxicosis with acute wernicke encephalopathy: a case report.

    A 35-year-old hyperthyroid woman who developed nausea, vomiting, tachycardia, nystagmus and mental disturbance, was referred to our hospital with a suspected diagnosis of thyroid storm. However, the thyroid gland was only slightly palpable, bruits were not audible, and exophthalmos was not present. serum levels of thyroid hormone were increased, but TSH receptor antibodies were negative. Echography and color flow doppler ultrasonography revealed a slightly enlarged thyroid gland and a slightly increased blood flow, both of which were much less milder than those expected for severe hyperthyroid Graves' disease. Under the diagnosis of hyperthyroidism due to gestational thyrotoxicosis associated with wernicke encephalopathy, vitamin B1 was administered on the first day of admission. Her consciousness became nearly normal on the second day except for slight amnesia. Her right abducent nerve palsy rapidly improved, but horizontal and vertical nystagmus, diminished deep tendon reflexes and gait ataxia improved only gradually. MRI findings of the brain were compatible with acute wernicke encephalopathy. We concluded that history taking and physical findings are important to make a differential diagnosis of gestational thyrotoxicosis with acute wernicke encephalopathy from Graves' thyroid storm, and that wernicke encephalopathy should be treated as soon as possible to improve the prognosis.
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8/198. Coexistent insulin dependent diabetes mellitus and hyperthyroidism in a patient with Down's syndrome.

    The prevalence of thyroid disease is increased in Down's syndrome. Compared with adults, thyroid dysfunction in children with Down's syndrome is less frequently reported. insulin dependent diabetes mellitus is also uncommon in Down's syndrome children. Coexistent insulin dependent diabetes mellitus and hyperthyroidism in Down's syndrome was only reported once previously in literature. We report an 8-year-old girl with Down's syndrome that had polyuria, polydipsia, abdominal pain and urinary incontinence one and half a month prior to admission. physical examination revealed typical face of Mongolism and tachycardia. Thyroid glands were not palpable. Laboratory data revealed diabetic ketoacidosis with plasma glucose: 860 mg/dl. She had thyroid hyperfunction with TSH: < 0.1 microU/ml, T3: 219.7 ng/dl, T4: 15 micrograms/dl. Thyroid autoimmune antibodies were also increased. There was markedly increased radiotracer uptake in the bilateral thyroid glands in Tc-99 thyroid scan. We suggest that Down's syndrome children with insulin dependent diabetes mellitus should be evaluated carefully for thyroid function and autoimmune disease.
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9/198. Treatment of a thyrotropinoma with octreotide-LAR in a patient with multiple endocrine neoplasia-1.

    OBJECTIVE: To note that a thyrotropin (TSH)-secreting macroadenoma may be part of the multiple endocrine neoplasia-1 (MEN-1) syndrome and to report the use of octreotide-LAR (OCT-LAR) to treat a TSH-secreting macroadenoma in a patient with MEN-1 with previous surgery for hyperparathyroidism and gastrinoma. methods: We present a patient with a TSH-secreting pituitary macroadenoma and report the results of her endocrine, genetic, radiologic, and nuclear medicine testing and her response to treatment with octreotide (OCT), octreotide-LAR, and estrogen. RESULTS: This patient's TSH-induced hyperthyroidism responded to octreotide for 5 months and octreotide-LAR for more than 11 months. Her hypercalcemia normalized while she was taking estrogen. Her genetic testing is reported to show a genetic defect that is typical of patients with MEN-1. CONCLUSION: This report describes: (1) The use of octreotide-LAR to treat both a TSH-secreting pituitary tumor and a gastrinoma over 12 months; (2) the importance of including these tumors into the MEN-1 syndrome with its attendant implications; and (3) a genetic defect, typical of patients with MEN-1, associated with this tumor.
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10/198. Generalized resistance to thyroid hormone associated with possible selective cardiac nonresistance.

    OBJECTIVE: To review the condition of generalized resistance to thyroid hormone and to report a case of generalized thyroid hormone resistance associated with atrial fibrillation. methods: A case report is presented of a 52-year-old man with atrial fibrillation who was referred by a cardiologist for thyroid ablation because of "hyperthyroidism," when his free thyroxine was found to be 4.35 ng/dL (normal, 0.55 to 2.46) and his free triiodothyronine was 6.5 pg/mL (normal, 1.4 to 4.4). RESULTS: This clinically euthyroid man with no signs or symptoms of hyperthyroidism except for the possibly related atrial fibrillation had a thyrotropin level of 3.45 mIU/L (normal, 0.46 to 4.7) in conjunction with the aforementioned increased levels of thyroid hormones. Further evaluation revealed normal 6-hour (11.7%) and 24-hour (27.6%) (123)I uptakes. magnetic resonance imaging of the pituitary revealed a normal-sized gland with no masses. CONCLUSION: This is a rare case of generalized resistance to thyroid hormone in a patient with only atrial fibrillation. Whether the heart was selectively nonresistant to thyroid hormone as the cause of his atrial fibrillation or whether his atrial fibrillation was due to his mitral valve prolapse documented on echocardiography could not be determined with certainty. His ventricular rate of 83 per minute and laboratory evaluation suggest that thyroid hormone was not the cause of the atrial fibrillation.
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keywords = pituitary, gland
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