J Thyroid Carcinoma in Objective-C

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J Thyroid Carcinoma
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Metastatic functioning thyroid carcinoma is a rare cause of thyrotoxicosis (See Thyroid Cancer section)
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K Amiodarone-Induced Thyrotoxicosis
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Amiodarone is concentrated in thyroid, adipose tissue, heart, and skeletal muscle and is 38% iodine by weight; its elimination half-life can be as long as 100 days Among patients in the United States taking amiodarone, hyperthyroidism develops in about 3%; the incidence of hyperthyroidism is higher in Europe and in iodine-deficient geographic areas Hyperthyroidism can occur 4 months to 3 years after initiation of amiodarone and may develop many months after amiodarone has been discontinued Amiodarone-induced thyrotoxicosis can occur by various mechanisms Type I amiodarone-induced thyrotoxicosis is caused by active elaboration of excessive thyroid hormone and may occur by either of two mechanisms: (1) Free iodine may cause toxic multinodular goiter in iodine-deficient patients with preexisting autonomous thyroid nodules (jodbasedow phenomenon) This is infrequently encountered in iodinesufficient countries such as the United States Thyroid RAI uptake ranges from low to high (2) Excessive free iodine can trigger an immunologic attack on the thyroid; this may cause Graves disease, commonly with diffuse thyroid enlargement and antithyroid peroxidase antibodies (70%) Type II amiodarone-induced thyrotoxicosis is caused by destructive thyroiditis, which releases stored thyroid hormone from damaged cells; hyperthyroidism can last 1 3 months and may be followed by hypothyroidism
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Clinical Findings
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A Symptoms and Signs
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Thyrotoxicosis due to any cause produces many different manifestations of variable intensity among different individuals Patients may complain of nervousness, restlessness, heat intolerance, increased sweating, fatigue, weakness, muscle cramps, frequent bowel movements, or weight change (usually loss) There may be palpitations or angina pectoris Women frequently report menstrual irregularities Certain eye findings such as upper eyelid retraction (Dalrymple s sign), lid lag with downward gaze (von Graefe s sign), and a staring appearance (Kocher s sign) can occur with hyperthyroidism of any etiology Signs of thyrotoxicosis may include stare and lid lag, fine resting finger tremors, moist warm skin, hyperreflexia, fine hair, and onycholysis Chronic thyrotoxicosis may cause osteoporosis Clubbing and swelling of the fingers (acropachy) develop in a small number of patients Graves disease usually presents with additional findings of goiter (often with a bruit), but some patients have no palpable thyroid enlargement Cardiac manifestations of thyrotoxicosis commonly include a forceful heart beat, premature atrial contractions,
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presents abruptly with symmetric flaccid paralysis (and few thyrotoxic symptoms), often after intravenous dextrose, oral carbohydrate, or vigorous exercise Attacks last 7 72 hours
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B Laboratory Findings
Serum T3, T4, thyroid resin uptake, and FT4 are usually all increased Sometimes the T4 level may be normal but the serum T3 is elevated Serum T3 can be misleadingly elevated when blood is collected in tubes using a gel barrier, which causes certain immunoassays (eg, Immulite but not Axsym analyzers) to report serum total T3 levels that are falsely elevated in 24% of normal patients Serum T4 or T3 can be elevated in other nonthyroidal conditions Serum TSH is suppressed in hyperthyroidism, except in the very rare cases of pituitary inappropriate secretion of thyrotropin Serum TSH may be misleadingly low in other nonthyroidal conditions Hyperthyroidism can cause other laboratory abnormalities, including hypercalcemia, increased alkaline phosphatase, anemia, and decreased granulocytes Hypokalemia and hypophosphatemia occur in thyrotoxic periodic paralysis Problems of diagnosis occur in patients with acute psychiatric disorders; about 30% of these patients have hyperthyroxinemia without thyrotoxicosis The TSH is not usually suppressed, distinguishing psychiatric disorder from true hyperthyroidism T4 levels return to normal gradually In Graves disease, TSH-R Ab[stim] levels are usually high (65%) Antithyroglobulin or antithyroperoxidase antibodies are usually elevated but are nonspecific Serum ANA and antidouble-stranded DNA antibodies are also usually elevated without any evidence of lupus erythematosus or other collagen-vascular disease Since high levels of T4 and FT4 are normally seen in patients taking amiodarone, suppressed TSH (sensitive assay) must be present along with a greatly elevated T4 (> 20 mcg/dL) or T3 (> 200 ng/dL) in order to diagnose hyperthyroidism (Note: Hypothyroidism occurs in an additional 6% of patients receiving amiodarone after 2 39 weeks of therapy) In type I amiodarone-induced thyrotoxicosis, the presence of proptosis, TSH-R Ab[stim], or thyrotropin-binding inhibitory immunoglobulin (TBII) is diagnostic In type II amiodarone-induced thyrotoxicosis, serum levels of interleukin-6 (IL-6) are usually quite elevated Patients with subacute thyroiditis often have an increased erythrocyte sedimentation rate (ESR) Women with hyperthyroidism during pregnancy have an elevated FT4 while the TSH is suppressed However, apparent lack of full TSH suppression can be seen due to misidentification of hCG as TSH in certain assays Although the total T4 is elevated in most pregnant women, values over 20 mcg/ dL are encountered only in hyperthyroidism The T3 resin uptake, which is low in normal pregnancy because of high TBG concentration, is normal or high in thyrotoxic persons Pregnancy can have a beneficial effect on the thyrotoxicosis of Graves disease, with decreasing antibody titers and decreasing FT4 levels as the pregnancy advances
seen in other conditions as well A low RAI uptake is characteristic of subacute thyroiditis but can also be seen in other conditions In the United States, thyroid RAI uptake is usually negligible in patients with type I amiodarone-induced thyrotoxicosis; however, in Europe, up to 80% of such patients have detectable or normal RAI uptake In type II amiodaroneinduced thyrotoxicosis, thyroid RAI uptake is very low MRI of the orbits is the imaging method of choice to visualize Graves ophthalmopathy affecting the extraocular muscles CT scanning and ultrasonography can also be used Imaging is required only in severe cases or in euthyroid exophthalmos that must be distinguished from orbital tumors or other disorders
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