Miliary tuberculosis presenting with thyrotoxicosis.
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A male patient is described who presented with thyrotoxicosis, and a large painful neck mass. From the excised mass and stomach aspiration Mycobacterium tuberculosis was cultured and a diagnosis of miliary tuberculosis was made. The thyrotoxicosis was attributed to tuberculous thyroiditis. (+info)
Cholestatic jaundice caused by sequential carbimazole and propylthiouracil treatment for thyrotoxicosis.
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A 36-year-old Chinese man presented to the Queen Mary Hospital in August 1999 with a 2-week history of jaundice due to propylthiouracil treatment for thyrotoxicosis. He had previously received carbimazole but had developed an urticarial skin rash after 2 weeks of treatment. The patient developed liver failure and fulminant pneumonitis shortly after hospital admission. Despite receiving treatment with broad-spectrum antibiotics and intravenous immunoglobulin, he died 11 days after the onset of the respiratory symptoms. Postmortem examination using electron microscopy showed typical glycogen bodies within the cytoplasm of the hepatocytes, which corresponded to eosinophilic cytoplasmic inclusion bodies visible under light microscopy. Immunohistochemical studies of the inclusion bodies were positive for carcinoembryonic antigen and albumin, and negative for fibrinogen, complement protein C3, immunoglobulins G, M, and A, alpha-fetoprotein, and alpha-1-antitrypsin. This is the first report of a patient who received two sequential antithyroid drugs and developed predominate cholestasis with unique histological features. Extreme caution should be taken when a patient develops allergy to one type of antithyroid drug, because cross-reactivity may develop to the other type. (+info)
Identification of serum amyloid a protein as a potentially useful biomarker to monitor relapse of nasopharyngeal cancer by serum proteomic profiling.
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PURPOSE: Nasopharyngeal cancer (NPC) is a common cancer in Hong Kong, and relapse can occur frequently. Using protein chip profiling analysis, we aimed to identify serum biomarkers that were useful in the diagnosis of relapse in NPC. EXPERIMENTAL DESIGN: Profiling analysis was performed on 704 sera collected from 42 NPC patients, 39 lung cancer patients, 30 patients with the benign metabolic disorder thyrotoxicosis (TX), and 35 normal individuals (NM). Protein profile in each NPC patient during clinical follow up was correlated with the relapse status. RESULTS: Profiling analysis identified two biomarkers with molecular masses of 11.6 and 11.8 kDa, which were significantly elevated in 22 of 31 (71%) and 21 of 31 (68%) NPC patients, respectively, at the time of relapse (RP) as compared with 11 patients in complete remission (CR; RP versus CR, P = 0.009), 30 TX (RP versus TX, P < 0.001), or 35 NM (RP versus NM, P < 0.001). The markers were also elevated in 16 of 39 (41%) lung cancer patients at initial diagnosis. By tryptic digestion, followed by tandem mass spectrometry fragmentation, the markers were identified as two isoforms of serum amyloid A (SAA) protein. Monitoring the patients longitudinally for SAA level both by protein chip and immunoassay showed a dramatic SAA increase, which correlated with relapse and a drastic fall correlated with response to salvage chemotherapy. Serum SAA findings were compared with those of serum Epstein-Barr virus DNA in three relapsed patients showing a similar correlation with relapse and chemo-response. CONCLUSIONS: SAA could be a useful biomarker to monitor relapse of NPC. (+info)
Management of amiodarone-induced thyrotoxicosis.
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Amiodarone is used increasingly in a number of cardiac conditions. Amiodarone is heavily iodinated and can cause thyroid dysfunction. The diagnosis of amiodarone-induced thyrotoxicosis remains difficult and more common causes of thyrotoxicosis need to be considered and excluded. Amiodarone has a significant side effect profile, which includes thyroid dysfunction. Amiodarone is an effective drug and its withdrawal may have significant impact on a patient's already fragile cardiac status. There are three different types of amiodarone-induced thyrotoxicosis (AIT) (I, II and mixed). Identification of the different subtypes of AIT allows a rational and appropriate management strategy to be chosen. Type I occurs in patients with underlying thyroid disease, whilst type II is thought to result from a destructive thyroiditis. Differentiation is based on clinical grounds together with investigations, which can include thyroid function test, radioiodine uptake scanning, measurement of interleukin-6 levels and colour flow Doppler sonography. Amiodarone should be discontinued in both types of AIT if the indication for its use is not a life-threatening cardiac condition. The management of type I centres around antithyroid drugs to control thyrotoxicosis and later consideration of more definitive treatment. Type II AIT responds to steroid therapy, although antithyroid drugs may be useful if symptoms are severe. Therapeutic options for refractory cases of AIT include surgery, radioiodine and plasmapheresis. (+info)
Radioiodine ablation of the thyroid to prevent recurrence of amiodarone-induced thyrotoxicosis in patients with resistant tachyarrhythmias.
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Amiodarone-induced thyrotoxicosis (AIT) is a common complication of amiodarone therapy. Although permanent withdrawal of amiodarone is recommended due notably to the risk of worsening of tachyarrhythmias, some patients may require the reintroduction of amiodarone several months after normalizing their thyroid function. We, retrospectively, assessed the effects of (131)I therapy to prevent recurrence of AIT in euthyroid patients requiring reintroduction of amiodarone. SUBJECTS AND METHODS: Amiodarone was required in 10 cases of recurrent symptomatic paroxysmal atrial fibrillation (AF) and in 5 cases of ventricular tachycardia (VT) (M = 12, F = 3, mean age: 63 +/- 14). The underlying heart disease was dilated cardiomyopathy (n = 4), ischaemic heart disease (n = 4), hypertensive heart disease (n = 2), arrhythmogenic right ventricular dysplasia (n = 27) and valvulopathy (n = 1). Two patients had idiopathic paroxysmal AF. RESULTS: A mean (131)I dose of 579 +/- 183 MBq was administered 34 +/- 37 after the episode of AIT. Amiodarone was reintroduced in 14 of 15 patients after a mean interval of 103 +/- 261 d. Fourteen patients developed definite hypothyroidism necessitating l-thyroxine but we observed no late recurrence of AIT. After a mean follow-up of 22 +/- 16 months, tachyarrhythmias were controlled in 12 of 14 patients. CONCLUSION: (131)I therapy appears to be an effective and safe approach to prevent the recurrence of AIT in a patient requiring the reintroduction of amiodarone for tachyarrhythmias. (+info)
Abnormal stimulation of the thyrotrophin receptor during gestation.
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Pregnancy induces physiological alterations in thyroid function which may make difficult the interpretation of results of thyroid hormone measurement. A state of hyperstimulation of the thyroid gland is common in early pregnancy. In a few cases, thyroid hormone values will deviate from the normal range, which corresponds to the gestational transient thyrotoxicosis. This syndrome is closely associated with hyperemesis gravidarum. The relationship between the two syndromes, demonstrated by epidemiological studies, has been illustrated by an exceptional case of familial recurrent gestational thyrotoxicosis presenting as hyperemesis gravidarum due to hypersensitivity of the thyrotrophin receptor to hCG. However, the exact mechanisms of hyperemesis gravidarum have not yet been identified. Gestational transient thyrotoxicosis has to be distinguished from Graves' disease, because the latter is associated with potential maternal and fetal complications when thyrotoxicosis is not controlled, whereas the former has usually a favourable outcome. The existence of other cases of thyroid hypersensitivity or hCG endowed with abnormal thyrotrophic activity is suspected. They may be identified only by assessment of the thyroid function in cases of hyperemesis gravidarum. The identification of these cases would be helpful to understand the mechanisms of specificity of glycoprotein hormone receptors. (+info)
Thyrotoxic adenoma followed by atypical hyperthyroidism due to struma ovarii: clinical and genetic studies.
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OBJECTIVE: Atypical forms of hyperthyroidism represent a diagnostic challenge for clinicians. Struma ovarii is an ovarian teratoma and constitutes a rare cause of ectopic thyroidal hormonal production. We describe a case of struma ovarii that combined two different sources of hyperthyroidism in the same patient and report genetic studies in order to contribute a better understanding of the autonomy and tumorigenesis of the struma ovarii. CASE REPORT: A 73-year-old nulliparous woman presented a thyroid toxic adenoma that was successfully treated with 10 mCi radioiodine. Unexpectedly, a new onset of hyperthyroidism prompted us to look for a second etiology. A whole-body scan with (123)I detected a pelvic hyperfixation suggesting struma ovarii, and a thyroid differentiated left ovarian teratoma 3 cm in size was surgically removed. We screened for mutations of thyroid-stimulating hormone receptor and Gs-alpha protein genes, as these mutations are common in thyroid adenomas. We did not identify any mutations. Androgen receptor study demonstrated a monoclonal status. Comparative genomic hybridization did not reveal any chromosomal abnormality. However, loss of heterozygosity analysis showed several structural abnormalities, compared with the majority of benign ovarian teratomas, which show a normal karyotype. CONCLUSIONS: This is the first well-documented report of thyrotoxic struma ovarii revealed after treatment of a single thyroid toxic adenoma. We have shown in this case that struma ovarii originates from a single germ cell, and, albeit benign, this tumor presents several chromosomal abnormalities. Struma ovarii-induced hyperthyroidism is likely to be mediated by mechanisms different from those of the classical thyroid toxic adenoma. (+info)
Transient hyperthyroidism after withdrawal of antithyroid drugs in patients with Graves' disease.
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The development of silent thyroiditis in patients with a history of Graves' disease is common, especially in the postpartum period. We describe herein patients with Graves' disease who developed transient hyperthyroidism but not silent thyroiditis after withdrawal of antithyroid drug (ATD). If such patients are diagnosed as recurrence of Graves' disease, they may receive ATD or radioiodine therapy unnecessarily. We investigated the characteristics of these patients to prevent unnecessary therapy. We retrospectively studied 22 patients with Graves' disease who showed transient thyrotoxicosis after withdrawal of ATD. Two of 22 patients were male and the mean ages (+/- SD) were 33.7 +/- 12.6 yr. We observed these patients for 28.5 +/- 12.8 (mean +/- SD; range 12-53) months after transient thyrotoxicosis, and measured TSH, FT4, and TSH binding inhibitor immunoglobulin in sera. Radioiodine uptake was measured in 6 of them. The radioiodine uptake in the 4 patients was not suppressed (27.5%, 28.0%, 32.7%, 38.1%). These uptake levels indicate that their thyrotoxicosis was not caused by silent thyroiditis. Most of the 22 patients became euthyroid within 6 months. This study suggests a new therapeutic option as follows: in the case of young patients with mild thyrotoxicosis after withdrawal of ATD, physicians should follow them up for one month without medication unless they have unbearable symptoms or complications. (+info)