Cases reported "Thyrotoxicosis"

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1/48. A germline mutation of the thyrotropin receptor gene associated with thyrotoxicosis and mitral valve prolapse in a Chinese family.

    Activating mutations of the TSH receptor (TSH-R) have been reported to result in toxic adenomas, multinodular goiters, sporadic neonatal hyperthyroidism, and familial autosomal dominant nonautoimmune hyperthyroidism. To date, all descriptions of such mutations, whether somatic or genomic, have been confined to the Caucasian population. We describe a Chinese family in whom a germline proline to serine substitution in position 639 resulted in familial thyrotoxicosis. This constitutively activating mutation has been previously described in a hyperfunctioning thyroid nodule. The three children in this family developed thyrotoxicosis during childhood; their father was diagnosed as thyrotoxic at the age of 38 yr. Two of the children and the father had mitral valve prolapse (MVP) associated with mitral regurgitation. There was a close temporal relationship between the onset of thyrotoxicosis and the diagnosis of mitral valvular disease in these patients. An increased prevalence of MVP has been reported in Graves' disease and chronic lymphocytic thyroiditis, but the pathophysiological mechanisms linking MVP and autoimmune thyroid disease are still not understood. This is the first report of an association between activating TSH-R mutations and MVP. We postulate that TSH-R activation may increase the clinical expression of MVP in genetically predisposed individuals.
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2/48. thyrotoxicosis due to the simultaneous occurrence of silent thyroiditis and Graves' disease.

    Silent thyroiditis (ST) and Graves' disease (GD) are two clinical entities belonging to the wide spectrum of autoimmune thyroid diseases (AITD). The two diseases are closely linked because sequential development of GD followed by ST, or the reverse course of events, ie, ST followed by GD, have been documented. However, the pathogenetic basis of the above association remains unknown. Some authors have suggested that the concomitant existence of ST and activation of GD can occur in thyrotoxic postpartum women with normal radioiodoine uptake. The simultaneous occurrence of the two diseases in different parts of the same thyroid gland has, however, to our knowledge, not been documented. We report the case of a 40-year-old thyrotoxic female with atypical presentation of GD. The titers of the antithyrotropin receptor antibodies were elevated and her initial 99mTc-pertechnetate thyroid scan showed the coexistence of ST and GD in different parts of the thyroid gland. Through serial thyroid scans, we document the recovery from ST in parts of the gland and demonstrate the progression to Graves' hyperthyroidism in the entire gland.
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3/48. Acute suppurative thyroiditis due to foreign body-induced retropharyngeal abscess presented as thyrotoxicosis.

    Acute suppurative thyroiditis is an uncommon condition. Most patients have preexisting oropharyngeal fistulae. Penetrating oropharyngeal injuries resulting from swallowed foreign bodies provide an acquired channel of infection spreading into the relatively resistant thyroid gland. The authors describe a patient with infective thyroiditis complicating retropharyngeal abscess caused by a chicken bone that perforated the upper esophagus. Transient thyrotoxicosis complicating acute suppurative thyroiditis is very rare. Pertechnetate and Ga-67 scans confirmed extensive inflammation of the thyroid gland and the release of hormones as the cause, as distinct from concurrent Graves' disease. awareness of this unusual complication is important to avoid inappropriate treatment for hyperthyroid disease.
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keywords = thyroiditis
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4/48. Transient diabetes insipidus and hypopituitarism after pituitary apoplexy: a rare association with pericardial effusion and painless thyroiditis.

    pituitary apoplexy in a 38-year-old male patient with acromegaly who presented with pericardial effusion, anterior pituitary dysfunction, and diabetes insipidus is described. With corticosteroid therapy, there was good initial recovery of pituitary function and regression of pericardial effusion. On withdrawal of corticosteroids, he developed painless thyroiditis, with transient thyrotoxicosis. Subsequently, the pituitary function tests remained normal for a year, but later he gradually developed hypogonadotropic hypogonadism, hypocortisolism, growth hormone deficiency, and progressive pituitary atrophy, resulting in empty sella syndrome.
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5/48. thyrotoxicosis in Down's and Turner's syndromes: the likelihood of Hashimoto's thyroiditis as the underlying aetiology.

    Biochemical thyrotoxicosis in young women is almost invariably due to Graves' disease. Its occurrence in females with Turner's and Down's syndromes, both of which are seldom associated with Graves' hyperthyroidism but are frequently allied to Hashimoto's thyroiditis, should alert physicians to the possibility of the latter. The discharge thyroiditis of Hashimoto's disease can be recurrent and protracted. A brisk response to antithyroid therapy would favour a thyroiditis and, in this circumstance, radio-iodine uptake should be reduced. The absence of TSH receptor antibodies in such cases, while not wholly refuting the notion of active Graves' disease, lends support to the existence of Hashimoto's thyroiditis.
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6/48. Transient thyrotoxicosis and hypothyroidism following administration of the GnRH agonist leuprolide acetate.

    A 45-year-old women with chronic idiopathic thrombocytopenic purpura was given monthly injections of the GnRH agonist leuprolide acetate for the treatment of uterine leiomyoma. Two weeks after the fifth injection, she showed mild symptoms of thyrotoxicosis. At that time, serum thyroxin (T4) and triiodothyronine (T3) levels were elevated whereas TSH level was suppressed. Anti-thyroglobulin (anti-Tg) and anti-thyroid peroxidase (anti-TPO) antibodies were positive, whereas TSH binding inhibitory immunoglobulin (TBII) was undetectable. Two months later, serum T4 and T3 levels spontaneously decreased below the normal ranges. Five months after the onset of the disease, they returned to normal without any treatment. Anti-TPO and anti-Tg antibodies gradually decreased during the clinical course. Thus, the present case was indicated to be an instance wherein silent thyroiditis developed after leuprolide acetate administration. This is the first report to demonstrate the association of thyroid disorder with leuprolide injection.
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7/48. Acute suppurative thyroiditis caused by an infected piriform sinus fistula with thyrotoxicosis.

    We report herein an unusual case of thyrotoxicosis caused by acute suppurative thyroiditis (AST) infected through a piriform sinus fistula (PSF). A 28-year-old man presented with pain over the thyroid gland and elevated serum thyroid hormone levels, a picture similar to subacute thyroiditis. A fine-needle aspiration biopsy from the left lobe showed neutrophil infiltration, and culture from the aspirate grew anaerobic peptostreptococcus. A neck computed tomography (CT) scan showed an abscess in the thyroid gland, and barium swallow revealed the presence of PSF. Appropriate antibiotic treatment ameliorated his symptoms of infection, followed by normalization of thyroid function. Three months later, he underwent fistulectomy and partial left lobectomy. The end of the PSF track was found in the left thyroid lobe. Thus infection of the thyroid gland through the infected PSF was likely the cause of supprative thyroiditis. The unusual clinical features of AST in this patient include the presence of severe thyrotoxicosis, relatively late onset (28-years-old) of infection despite the presence of congenital PSF, and the lack of acute inflammatory signs on the overlying skin of the thyroid gland. It is important to recognize this type of AST, since fistulectomy is required to prevent recurrent AST.
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keywords = thyroiditis
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8/48. Lopanoic acid rapidly controls type I amiodarone-induced thyrotoxicosis prior to thyroidectomy.

    amiodarone-induced thyrotoxicosis (AIT) may develop either in apparently normal thyroid glands (Type II AIT) or in the presence of sub-clinical thyroid abnormalities (either autonomous goiter or latent Graves' disease; Type I AIT). Mixed forms also occur. While Type I AIT is due to iodine-induced excess thyroid hormone synthesis, Type II AIT is a form of amiodarone (possibly iodine) -induced destructive thyroiditis. Type I AIT is usually treated by combined thionamide and potassium perchlorate therapy, but may be resistant to therapy. On the other hand, Type II AIT often responds favorably to glucocorticoids and may not require further therapy once euthyroidism has been restored. Not infrequently, however, AIT (especially Type I) is resistant to conventional treatment, and several weeks or months may elapse before euthyroidism is restored. thyroidectomy has been carried out in Type I AIT patients, but thyroid surgery in thyrotoxic patients, especially those with underlying cardiac problems, carries a high surgical risk. In this study we describe 3 patients with Type I AIT, who were successfully treated with a short course of iopanoic acid (IOP), an oral cholecystographic agent, which is rich in iodine and is a potent inhibitor of 5'-deiodinase, resulting in a marked decrease in the peripheral tissue conversion of T4 to T3, in preparation for thyroid surgery. Euthyroidism was rapidly restored in 7-12 days, allowing a subsequent safe and uneventful thyroidectomy in all cases. These patients were then treated with L-T4 for their hypothyroidism and amiodarone was safely re-instituted. We suggest that IOP is the drug of choice in the rapid restoration of euthyroidism prior to definitive thyroidectomy in patients with drug resistant Type I AIT.
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keywords = thyroiditis
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9/48. Anaplastic pseudothyroiditis.

    Anaplastic thyroid carcinoma (ATC) is one of the most aggressive solid tumours. It generally presents as a rapidly enlarging thyroid mass and produces local symptoms associated with mass effect. One of the very rare presentations of ATC is thyrotoxicosis. We report a patient with ATC whose course was complicated by severe thyrotoxicosis. His symptoms were controlled with beta-blockers. Two weeks into hospitalization, the patient became hypothyroid. Histopathology showed destruction of the normal thyroid follicles by the invasion of the tumour. As this form of thyrotoxicosis resembles various thyroiditides, we hereby refer this condition as "anaplastic pseudothyroiditis".
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keywords = thyroiditis
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10/48. Severe hypercalcaemia secondary to isolated adrenocorticotrophic hormone deficiency and subacute thyroiditis.

    Severe hypercalcaemia is usually due to either neoplastic disease or primary hyperparathyroidism. Rarer causes do exist, and exceptionally these may occur concomitantly. We describe the case of a 45-year-old man who presented in a debilitated state with severe hypercalcaemia (total serum calcium 3.56 mmol/L, albumin 35 g/L) and suppressed serum parathyroid hormone concentration. It was initially suspected that he had neoplastic disease, but routine thyroid function tests demonstrated evidence of thyrotoxicosis [thyroid-stimulating hormone <0.05 mU/L (0.15-3.5); free thyroxine 75 pmol/L (8-27); total tri-iodothyronine 7.0 nmol/L (1.0-2.6)], which was probably secondary to a silent or subacute thyroiditis. After extensive investigation, it was established that the patient also had isolated adrenocorticotrophic hormone deficiency, presumably secondary to lymphocytic hypophysitis. Glucocorticoid therapy resulted in a dramatic improvement in the patient's clinical state and 1 year later he remained euthyroid and normocalcaemic.
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ranking = 5
keywords = thyroiditis
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