Cases reported "Hyperthyroidism"

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1/9. 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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2/9. bromocriptine and Triac therapy for hyperthyroidism due to pituitary resistance to thyroid hormone.

    Although a number of patients with generalized resistance to thyroid hormone have been treated with bromocriptine (Brc), only one previously reported patient with nontumoral TSH-mediated hyperthyroidism, presumably due to pituitary resistance to thyroid hormone (PRTH), has been successfully treated with bromocriptine (Brc). In addition, several studies suggested that the T3 analog 3,5,3'-triiodothyroacetic acid (Triac) may control hyperthyroidism in patients with PRTH. In the current study a patient with PRTH diagnosed at age 15 yr underwent separate therapeutic trials with Brc and Triac, during which time physical parameters, thyroid function tests, systolic time intervals (STI), and oxygen consumption (VO2) were measured. On Brc therapy (12.5 mg/day), heart rate decreased (108 to 72/min), TSH decreased (5.7 to 1.2 mU/L), T3 decreased (9.9 to 1.7 nmol/L), free T4 decreased (205 to 21 pmol/L), STI lengthened (left ventricular ejection time, 0.389 to 0.405 s), and VO2 did not change (164 to 162 mL/min). We found no significant clinical improvement with a maximal dose of Triac (2.1 mg/day), only minimal reduction in goiter size; mild decreases in T3 (9.9 to 6.7 nmol/L), free T4 (205 to 113 pmol/L), and TSH (5.7 to 5.4 mU/L); no change in STI (left ventricular ejection time, 0.389 to 0.401 sec); and an increase in O2 consumption (VO2, 164 to 209 mL/min). Thus, the results favor Brc as effective therapy for this patient with PRTH.
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3/9. Thyrotropin-secreting pituitary tumor and Hashimoto's disease: a novel association.

    A 69-year-old man was referred for elevated thyroid hormone levels. He had no symptoms apart from mild hyperhidrosis and heat intolerance with occasional headaches. Past medical history included a right hemithyroidectomy for a multinodular goiter and Hashimoto's disease. At presentation the patient had a firm, slightly enlarged left thyroid lobe. There were no visual abnormalities, and the rest of the physical findings were unremarkable. Laboratory findings included elevated values of free T4, free T3, total T3, thyrotropin-secreting hormone (TSH), antithyroglobulin, and antimicrosomal antibodies. Normal values were found for cortisol, prolactin, testosterone, follicle-stimulating hormone, luteinizing hormone, alpha-subunit, and thyroid-stimulating immunoglobulin. Thyroid 123I scan showed an increased 5-hour uptake of 23% and a 24-hour uptake of 53% with a diffuse uniform enlargement of the left side. TSH level did not increase after a thyrotropin-releasing hormone stimulation test. serum sex hormone binding globulin was elevated. magnetic resonance imaging of the pituitary revealed a pituitary macroadenoma with suprasellar extension to the optic chiasm. Histologic examination of the adenoma after transsphenoidal hypophysectomy showed cells that stained positive for TSH. TSH-secreting pituitary adenomas account for 1% of functioning pituitary tumors and are an exceedingly rare cause of hyperthyroidism. To our knowledge, this is the first report of pituitary tumor inducing hyperthyroidism in the setting of Hashimoto's disease. There is a possibility that TSH elevation related to Hashimoto's disease might have contributed to the development of a TSH-secreting pituitary adenoma.
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4/9. TSH-induced hyperthyroidism caused by a pituitary tumor.

    BACKGROUND: A 45-year-old man presented with frontal headache and visual disturbances to our clinic. For the previous 5 years, he had been receiving treatment for long-lasting mild hyperthyroidism with antithyroid therapy, but therapy had not been carefully followed. During the last 2 years he had also complained of erectile dysfunction and loss of libido. On physical examination, he had a small goiter, normal skin, no Graves' ophthalmopathy, normal BMI, and reduced testis volume and pubic hair. INVESTIGATIONS: serum levels of free T3 and T4, serum prolactin, testosterone, serum gonadotropins, insulin-like growth factor 1, adrenocorticotropic hormone, and cortisol were measured. MRI scan, TSH-releasing hormone test, and T3 suppression test were carried out. Levels of pituitary glycoprotein hormone alpha-subunit and sex-hormone-binding protein were also measured. diagnosis: hyperthyroidism caused by a mixed pituitary adenoma that secretes prolactin and TSH. MANAGEMENT: Trans-sphenoidal resection of the pituitary tumor. After surgery, T3 suppression test failed to completely suppress TSH secretion, which suggested a persistence of residual adenomatous cells. hyperthyroidism and hypogonadism recurred after 5 years, therefore, treatment with lanreotide was initiated, and resulted in complete resolution of signs and symptoms of the disease.
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5/9. The thyroid gland and the dental practitioner.

    The thyroid gland has an important function in almost every aspect of human physiology. As well, its location in the neck allows for easy evaluation by the dentist. Part I of this paper reviews the normal functions of the thyroid gland as well as systemic effects caused by abnormal function. This is supplemented by easily-acquired methods of physical examination of the thyroid gland suitable for the dental practitioner. Part II is a case report highlighting the potential adverse effects of dental treatment of a patient who had poorly controlled thyroid function following total thyroidectomy.
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6/9. Apathetic thyrotoxicosis due to hemorrhage into a hyperfunctioning thyroid nodule after excessive anticoagulation.

    Hyperfunctioning thyroid nodule was diagnosed in a 72-year-old woman. When the nodule reached a diameter of 3.5 cm, overt thyrotoxicosis of the apathetic type was precipitated by hemorrhage into the nodule during a period of excessive anticoagulation. All abnormal physical signs and symptoms as well as laboratory findings returned to normal within a month, without any specific treatment. It was possible to follow this process by repeated B-mode sonographic examinations and thyroid scans.
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7/9. Peripheral resistance to thyroid hormone in a family: heterogeneity of clinical presentation.

    We describe a family with thyroid hormone resistance. Juvenile graves disease was diagnosed in the propositus, an 8-month-old boy. He was initially given propylthiouracil, and at 22 months of age underwent subtotal thyroidectomy. A diagnosis of hyperthyroidism was made in a younger sister at 3 months of age. Because of the unusual occurrence of juvenile graves disease in two siblings, we evaluated the parents. The mother was euthyroid on physical examination and by thyroid hormone measurements. The father, although clinically euthyroid, had markedly elevated thyroid hormone values. In the three affected members, serum thyrotropin concentrations and results of thyrotropin-releasing hormone infusion tests were inappropriate for the elevated serum thyroid hormone levels. The father was given increasing doses of triiodothyronine. Complete suppression of TRH-induced TSH release did not occur until a daily dose of 300 micrograms triiodothyronine was administered. Furthermore, this large dose of T3 did not produce clinical evidence of hyperthyroidism or result in changes in his systolic ejection time intervals. This family therefore had the unusual feature of clinical heterogeneity. The two children had mainly pituitary resistance to thyroid hormone and were hyperthyroid; the euthyroid father, on the other hand, had generalized tissue resistance to thyroid hormone.
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8/9. growth hormone-prolactin-thyrotropin-secreting pituitary adenoma in atypical McCune-Albright syndrome with functionally normal Gs alpha protein.

    The McCune-Albright syndrome (MAS) comprises a triad of physical signs: localized bone lesions termed polyostotic fibrous dysplasia, cafe-au-lait pigmentation of the skin, and autonomous hyperfunction of multiple endocrine systems, including overproduction of GH and T4. A somatic activating point mutation in the gene for the alpha-subunit of the G-protein (Gs alpha) in the affected tissue has been claimed to be the underlying defect. A 29-yr-old patient with MAS, showing polyostotic fibrous dysplasia associated with acromegalic features, underwent endocrinological studies, including oral glucose tolerance test and pituitary stimulation test, and magnetic resonance imaging, revealing elevated plasma concentrations of GH, PRL, and secondary hyperthyroidism due to pituitary macroadenoma infiltrating the sphenoid cavity and extending to the suprasellar space. Subsequently, reduction of tumor mass by a transsphenoidal and a subsequent subfrontal operation led to only marginal amelioration of the excessive hormone production. Postsurgery octreotide and bromocriptine therapy induced near-normalization of hormone concentrations. immunohistochemistry of tumor tissue confirmed the plurihormonal character, but dna sequence analysis did not detect any of the two known activating mutations in the Gs alpha gene. Furthermore, biochemical tests revealed normal Gs alpha function, ruling out other mutations that lead to constitutive Gs alpha activation. Our study documents that MAS is a heterogeneous disease. Some, but clearly not all, patients have oncogenic mutations of the gene coding for Gs alpha. Any gene acting down-stream of Gs can theoretically be predicted to result in the same phenotype. In addition, hyperthyroidism of MAS may be secondary to a TSH-producing pituitary macroadenoma.
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9/9. hyperthyroidism due to lymphoma involving the thyroid gland in a patient with acquired immunodeficiency syndrome: case report and review of the literature.

    A 31-year old woman with acquired immunodeficiency syndrome (AIDS) and a history of lymphoma presented with a 2-week history of severe hyperthyroid symptoms and new-onset neck swelling. On physical examination, she was found to be clinically hyperthyroid, with a markedly enlarged, diffuse, tender goiter. Thyroid function testing confirmed hyperthyroidism. The patient had a rapidly deteriorating clinical course and died within days of her presentation. At autopsy, near-complete replacement of the thyroid gland with anaplastic large cell lymphoma was found, without coexisting infectious or autoimmune processes in the gland. This is the first case report of a patient with AIDS developing symptomatic thyroid involvement by lymphoma, and one of only a few case reports of hyperthyroidism associated with lymphoma in general.
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