Development hyperthyroidism

A 62-year-old man took amiodarone for 2 years and developed hyperthyroidism carbimazole 40 mg/day, prednisolone, lithium, and colestyramine were ineffective and he died with hepatic encephalopathy and multiorgan failure. 

D Amiodarone may decrease warfarin metabolism within a week of coadministration, or the effects of the interaction may be delayed for several weeks. Patients who develop hyperthyroidism secondary to amiodarone may have an additional increased anticoagulant effect, because the turnover of clotting factors is more rapid. If amiodarone is discontinued, effects of the decreased warfarin metabolism may last 1 to 3 months. 

The fetal thyroid-pituitary axis functions independently from the mother s axis in most cases. However, if the mother has preexisting Graves disease (see Chapter 52), her autoantibodies can cross the placenta and stimulate the fetal thyroid gland. Thus the fetus can develop hyperthyroidism. Measurement of thyrotropin-binding inhibitory immmioglobu-lins (TBII) is useful for assessing risk of fetal or neonatal Graves disease. 

Both alpha- and beta-adrenoceptors are blocked by labetalol Glucagon can be useful in reversing cardiac depression caused by a beta blocker They mask the signs of developing hyperthyroidism Treatment of glaucoma commonly involves the topical use of propranolol... 

Chesney and his coworkers at Johns Hopkins Hospital demonstrated, in 1928, that goiter could be produced in rabbits by the feeding of cabbage, which was later found to contain goitrogenic agents. It was also found that the metabolic rate of the animals was lowered. The disorder was corrected by feeding Lugol s solution of iodine, but many animals developed hyperthyroidism and died, a demonstration of the effects of overzealous therapy. 

The difference in presentation of hyperthyroidism was even more striking when comparing the ages at which patients developed hyperthyroidism in the two areas (fig 2). The age specific incidence of hyperthyroidism in the age groups 20 - 40 years was... 

Interferon-a causes hypothyroidism in up to 39% of patients being treated for hepatitis C infection. Patients may develop a transient thyroiditis with hyperthyroidism prior to becoming hypothyroid. The hypothyroidism may be transient as well. Asians and patients with preexisting anti-TPOAbs are more likely to develop interferon-induced hypothyroidism. The mechanism of interferon-induced hypothyroidism is not known. If LT4 replacement is initiated, it should be stopped after 6 months to re-evaluate the need for replacement therapy. 

LT4 doses sufficient to suppress tumor growth may result in a suppressed TSH and mild hyperthyroidism. These patients must be monitored closely for complications of the mild hyperthyroid state, such as bone mineral loss and development of atrial fibrillation. 

Common adverse reactions seen with phentermine use include heart palpitations, tachycardia, elevated blood pressure, stimulation, restlessness, dizziness, insomnia, euphoria, dysphoria, tremor, headache, dry mouth, constipation, and diarrhea. Phentermine should be avoided in patients with unstable cardiac status, hypertension, hyperthyroidism, agitated states, or glaucoma. In combination with fenfluramine or dexfenfluramine, pulmonary hypertension and valvular heart disease have been reported. The risk of developing either serious adverse effect cannot be ruled out with use of phentermine alone. Since phentermine is related to the amphetamines, the... 

Thyroid Disease. Hypothyroidism (myxedema) [169] and hyperthyroidism [170] alter small bowel motility. Although today these diseases are usually recognized before such symptoms develop, thyroid function must be examined in unexplained intestinal pseudoobstruction. 

Nicholson JL, Altman J (1972) The effects of early hypo- and hyperthyroidism on the development of the rat cerebellar cortex. II. Synaptogenesis in the molecular layer. Brain... 

The thyroid hormone thyroxine is necessary for the development and function of cells throughout the body. It increases protein synthesis and oxygen consumption in almost all types of body tissue. Excess thyroxine causes hyperthyroidism, with increased heart rate, blood pressure, overactivity, muscular weakness, and loss of weight. 

Short-term thyroid suppression (C). Iodine in high dosage (> 6000 pg/d) exerts a transient "thyrostatic effect in hyperthyroid, but usually not in euthyroid, individuals. Since release is also blocked, the effect develops more rapidly than does that of thioamides. 

Cytokines Interferon- and interleukin-2 - Therapy with interferon- has been associated with the development of antithyroid microsomal antibodies in 20% of patients and some have transient hypothyroidism, hyperthyroidism, or both. Patients who have antithyroid antibodies before treatment are at higher risk of thyroid dysfunction during treatment. Interleukin-2 has been associated with transient painless thyroiditis in 20% of patients. 

Thyrotoxicosis -adrenergic blockers may mask clinical signs (eg, tachycardia) of developing or continuing hyperthyroidism. Abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm. 

Special risk patients Administer with caution to patients with diabetes mellitus, hyperthyroidism, prostatic hypertrophy (ephedrine) or history of seizures elderly psychoneurotic individuals, patients with long-standing bronchial asthma and emphysema who have developed degenerative heart disease (epinephrine). 

Endocrine disorders Peginterferon alfa-2a causes or aggravates hypothyroidism and hyperthyroidism. Hyperglycemia, hypoglycemia, and diabetes mellitus have developed in patients treated with peginterferon alfa-2a. 

Juvenile or adult patients with primary hypothyroidism (as indicated by low serum free T4 and high serum TSH concentrations) are usually treated with thyroxine with the aim of relieving symptoms and reducing the serum TSH concentration into the normal reference range. If the primary hypothyroidism is the result of iodine deficiency, then gradually increasing dietary iodine supplementation may also be instituted in addition to the thyroxine replacement therapy. Iodine supplementation alone may lead to the development of acute hyperthyroidism. 

In older patients toxic multinodular goiter typically presents as longstanding asymptomatic multinodular goiters. Functional autonomy of the nodules develops over time by an unknown mechanism and causes the disease to move from the nontoxic to the toxic phase. The onset of hyperthyroidism is gradual, and the symptoms are usually milder than those of Graves disease. 

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