Cases reported "Thyrotoxicosis"

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1/37. Thyroid disease in pregnancy.

    This review article provides a broad overview of thyroid disease and pregnancy.
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2/37. Recognizing thyrotoxicosis.

    Clinical manifestations of thyrotoxicosis range from silent to florid and can mimic those of other conditions occurring in pregnancy and old age. The diagnosis may be particularly vexing in elderly patients with apparent dementia. Once clinical suspicion has been aroused, the workup to confirm the diagnosis and establish the cause is easily accomplished.
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3/37. A novel thyrotropin receptor mutation in an infant with severe thyrotoxicosis.

    An infant girl was born at 37 weeks gestation and found to be clinically thyrotoxic at 9 months of age. Thyroid autoantibodies were negative, and thyroid function failed to normalize with medical treatment. The patient underwent a total thyroidectomy. dna obtained from her thyroid gland and leukocytes was analyzed for thyrotropin receptor (TSHR) mutations using single strand conformation polymorphism and direct sequencing. A mobility shift of polymerase chain reaction (PCR)-amplified dna was detected on single strand conformation polymorphism gel. Direct sequencing identified a novel point mutation in the fifth transmembrane domain of the TSH receptor at codon 597 (GTC to CTC), resulting in the amino acid substitution of leucine for valine. The mutation was heterozygous and germline, and was not identified in dna from either of her parents. Expression of the V597L mutant is transiently transfected COS 7 cells displayed increased constitutive cyclic adenosine monophosphate (cAMP) production compared with the wild-type receptor. The mutant is expressed at very low levels on the surface of cos cells, and its response to TSH is marginal.
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keywords = gestation
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4/37. Recurrent fetal thyrotoxicosis in a woman with Graves' disease: case report.

    The thyroid stimulating immunoglobulins are generally believed to be the cause of hyperthyroidism in Graves' disease. Placental transfer of these antibodies from a mother with autoimmune thyroid disease can result in fetal thyroid disorders. We report the case of a 31-year-old woman who had a history of Graves' disease. She received thyroxine therapy for post thyroidectomy hypothyroidism. Two years after the thyroidectomy, she became pregnant. Unfortunately, intrauterine fetal death occurred in midgestation. One year later, she became pregnant again. In the 26th week of gestation, fetal thyrotoxicosis was diagnosed using clinical pictures, including fetal tachycardia and cardiomegaly, and a hormonal evaluation of a periumbilical blood sampling (T4: 18 micrograms/dl, T3: 65.3 ng/dl, TSH: < 0.03 microU/ml) was performed. Antimicrosomal antibodies were not detectable in either the maternal or fetal blood. In this case, high levels of TBII were detected during pregnancy and crossed the placenta to result in a thyrotoxic fetus in the second pregnancy. We recommend that both the regular monitoring of the thyrotropin receptor antibodies of pregnant women with a history of autoimmune thyroid disease, and routine measurements of the fetal heart rate and intrauterine growth during gestation be mandatory for the early detection of fetal thyroid disorders. cordocentesis for measuring fetal thyroid function is helpful in reaching a definite diagnosis and for guiding therapy.
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keywords = pregnancy, gestation
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5/37. Congenital chylothorax in neonatal thyrotoxicosis.

    We report a patient with congenital chylothorax who also had neonatal thyrotoxicosis secondary to maternal Graves' disease. Fetal tachycardia with hydrops was detected at 28 weeks' gestational age. The fetus responded to antithyroid medication in utero but had persistent bilateral pleural effusion. At birth, he had respiratory distress due to massive pleural effusion. Cytologic studies of pleural fluid were consistent with chylothorax. To the best of our knowledge, the association of congenital chylothorax with fetal (neonatal) thyrotoxicosis, has not been reported previously.
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6/37. 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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keywords = gestation
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7/37. Successful treatment of graves disease in pregnancy with Lugol's iodine.

    We report a case of Grave's disease in pregnancy complicated by intolerance of standard antithyroid drug therapy. We describe the success of prolonged use of organic iodine as a primary treatment prior to surgical intervention.
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8/37. thyrotoxicosis in a male patient associated with excess human chorionic gonadotropin production by germ cell tumor.

    We report a case of a man with thyrotoxicosis due to excess production of human chorionic gonadotropin (hCG) by metastatic choriocarcinoma, followed by alterations of his thyroid function tests by nonthyroidal illness. All reported cases of thyrotoxicosis due to high hCG levels in male patients are reviewed. patients with this syndrome usually have widespread choriocarcinoma and relatively few symptoms of thyrotoxicosis. Typically, if the patient survives the metastatic germ cell tumor, the thyrotoxicosis resolves as the hCG levels decrease after chemotherapy directed at the choriocarcinoma. Only rarely are specific antithyroid medications required. The hCG molecule directly stimulates the thyroid gland, and these patients appear to have in the serum a predominance of acidic variants of hCG with greater intrinsic thyroid-stimulating activity than the hCG secreted during a normal pregnancy. In general, these patients have a poor prognosis due to the usually widespread nature of the germ cell tumor at the time of diagnosis.
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9/37. Superior sagittal sinus thrombosis induced by thyrotoxicosis. Case report.

    There is a wide variety of disorders associated with thrombosis of the superior sagittal sinus (SSS), including infectious disease. noninfectious conditions such as vasculitis and hypercoagulable states, and complications arising from pregnancy or use of oral contraceptive medications. Despite these well-defined associations, approximately 25% of the cases remain idiopathic. In this article the authors describe a patient who was found to have SSS thrombosis while experiencing a thyrotoxic phase of graves disease. The patient presented with intracerebral hemorrhage, subarachnoid hemorrhage, seizure, coma, a raised fibrinogen concentration, low protein c activity, and atrial fibrillations. Thrombolysis was successfully performed despite the coexistence of thrombosis and intracranial hemorrhage. patients with thyrotoxicosis and a diffuse goiter may be predisposed to the development of SSS thrombosis, as a result of hypercoagulation and stasis of local venous blood flow. In the present case, a patient in whom thrombosis coexisted with intracranial hemorrhage was successfully treated using thrombolytic therapy.
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10/37. Resistance to thyroid hormone does not abrogate the transient thyrotoxicosis associated with gestation: report of a case.

    We report the occurrence of transient thyrotoxicosis during pregnancy in a subject with resistance to thyroid hormone. Before pregnancy, the subject was euthyroid, with normal serum TSH and elevated levels of free T(3) and free T(4) caused by a mutation in the TRbeta gene (R243Q). Beginning at the fourth week of gestation serum levels of free T(3) and T(4) increased in parallel with an increase in hCG. At 6-7 wk gestation she manifested hypermetabolic features, with mild nausea and vomiting. Peak levels of serum hCG and thyroid hormone concentrations were attained at 12 wk gestation, when serum TSH was fully suppressed. In the following weeks of gestation, thyroid hormone levels declined, with amelioration of the symptoms. A baby boy also affected with resistance to thyroid hormone harboring the same TRbeta gene mutation was born by normal vaginal delivery.
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ranking = 1.4816587493542
keywords = pregnancy, gestation
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