Thyrotoxicosis, treatment

Hyperthyroidism (thyrotoxicosis), defined as excessive thyroid activity, causes a state of thyroid hormone excess (thyrotoxicosis) characterized by an increased metabolic rate, increase in body temperature, sweating, tachycardia, tremor, nervousness, increased appetite and loss of weight. Common causes of hyperthyroidism are toxic multinodular goiter, toxic adenoma or diffuse toxic goitre ( Graves disease). Antithyroid diugs (methimazol, carbimazole, propylthiouracil) block thyroid hormone production and are hence suitable for the treatment of hyperthyroidism. 

Treatment of thyrotoxicosis due to hyperthyroidism is similar, regardless of the underlying cause. The goals of treating hyperthyroidism are to relieve symptoms, to reduce thyroid hormone production to normal levels and achieve biochemical euthyroidism, and to prevent long-term adverse sequelae. 

Erdogan ME, Gulec S, Tutar E, Baskal N, Erdogan G (2003) A stepwise approach to the treatment of amiodarone-induced thyrotoxicosis. Thyroid 13 205-209... 

Hyperthyroidism results from excess production of thyroid hormones due to various reasons. Treatment of the resulting thyrotoxicosis (Basedow s disease) consists of using... 

Autoimmune polyglandular syndrome-Chron c autoimmune thyroiditis may occur in association with other autoimmune disorders. Treat patients with concomitant adrenal insufficiency with replacement glucocorticoids prior to initiation of treatment. Failure to do so may precipitate an acute adrenal crisis when thyroid hormone therapy is initiated. Patients with diabetes mellitus may require upward adjustments of their antidiabetic therapeutic regimens. Nontoxic diffuse goiter or nodular thyroid disease Use caution when administering levothyroxine to patients with nontoxic diffuse goiter or nodular thyroid disease in order to prevent precipitation of thyrotoxicosis. If the serum TSH is already suppressed, do not administer levothyroxine. 

Three main modalities of therapy should be considered for patients with thyrotoxicosis, namely, medical therapy, surgical thyroidectomy, and radioiodine. The choice between these therapies should be dictated by the clinical nature of the disease, the patient s general health, her desire for pregnancy or need to care for young children, and overall patient preference. Treatment is initially monitored by free thyroxine (T4) values, as suppression of thyroid-stimulating hormone (TSH) may persist for months despite adequate management. 

Occasionally patients develop a dramatically acute and severe form of thyrotoxicosis which may be life-threatening, termed thyroid crisis or thyroid storm. In this condition the patient is at risk of cardiac complications, notably arrhythmia and ventricular failure, and it requires very urgent treatment. It is essential to use high doses of anti-thyroid drugs, and PTU is often preferred for this, particularly because of its fast absorption. Iodides or ipodate are often... 

Cooper DS. Treatment of thyrotoxicosis. In Braverman LE, Utiger RD, editors. Werner and Ingbar s the thyroid a fundamental and clinical text. 9th ed. Philadelphia (PA) Lippincott Williams Wilkins 2005. p. 665-94. 

In addition, the metabohsm of OCAs results in the release of large amounts of E into the circulation. As described for KI, I released from OCAs may have effects at the thyroid gland and if used alone to treat hyperthyroidism, OCAs carry the same potential to induce increased secretion of thyroid hormone and exacerbation of thyrotoxicosis. When an OCA is used in the treatment of hyperthyroidism, large doses of antithyroid agents are usually administered concomitantly. However, the combination of OCAs and antithyroid drugs may cause resistance to the antithyroid drugs with time, presumably because of the elevation in intrathyroidal 1 content. Thus, it is recommended that the use of OCAs be reserved for short-term treatment of patients with severe thyrotoxicosis and significant comorbidity (e.g., myocardial infarction, sepsis, stroke) for rapid control of plasma Tj concentrations. 

What is the primary reason for administering (3-adrenergic receptor blocking drugs as adjunct therapy in the treatment of thyrotoxicosis ... 

Unlabeled Uses Treatment of anxiety, chronic angina pectoris, hypertrophic cardiomyopathy, MI, pheochromocytoma, syndrome of mifral valve prolapse, thyrotoxicosis, tremors... 

Unlabeled Uses Acute alcohol withdrawal, arrhythmia (especially supraventricular and ventricular tachycardia), improved survival in diabetics with heart disease, mild to moderately severe CHF (adjunct) prevention of migraine, thyrotoxicosis, tremors treatment of hypertrophic cardiomyopathy, pheochromocytoma, and syndrome of mitral valve prolapse... 

I Contraindications Hypersensitivity to tablet components, such as tartrazine allergy to aspirin lactose intolerance Ml and thyrotoxicosis uncomplicated by hypothyroidism treatment of obesity... 

Unlabeled Uses To increase survival rate in diabetic patients with coronary artery disease (CAD) treatment orprevention of anxiety cardiacarrhythmias hypertrophiccar-diomyopathy mitral valve prolapse syndrome pheochromocytoma tremors thyrotoxicosis vascular headache... 

Unlabeled Uses Treatment of arrhythmias, hypertrophic cardiomyopathy. Ml, mitral valve prolapse syndrome, neuroleptic-induced akathisia, pheochromocytoma, tremors, thyrotoxicosis, vascular headaches... 

Unlabeled Uses Treatment adjunct for anxiety, mitral valve prolapse syndrome, thyrotoxicosis, behavioral disturbance in dementia... 

Unlabeled Uses Systemic-. Treatment of anxiefy, cardiac arrhyfhmias, chronic angina pecforis, hypertrophic cardiomyopathy, migraine, pheochromocytoma, thyrotoxicosis, tremors... 

The thioamides which include propyl thiouracil and methimazole are the major drugs for the treatment of thyrotoxicosis. In India carbimazole is most commonly used drug. They bind to thyroid peroxidase and... 

The thioamides methimazole and propylthiouracil are major drugs for treatment of thyrotoxicosis. In the United Kingdom, carbimazole, which is converted to methimazole in vivo, is widely used. Methimazole is about ten times more potent than propylthiouracil. 

Radioiodine therapy utilizing 1311 is the preferred treatment for most patients over 21 years of age. In patients without heart disease, the therapeutic dose may be given immediately in a range of 80-120 M3i/g of estimated thyroid weight corrected for uptake. In patients with underlying heart disease or severe thyrotoxicosis and in elderly patients, it is desirable to treat with antithyroid drugs (preferably methimazole) until the patient is euthyroid. The medication is then stopped for 5-7 days before... 

Different forms of radioiodine have been used at different times, including 123I, 12SI, and 131I. Radioactive iodine is used to scan the thyroid gland and in the treatment of thyrotoxicosis. See in the monograph on Radioactive iodine. 

In a series of thyrocardiac patients, of those dying primarily from thyrotoxicosis more than 21% did so within 3 weeks of 131I treatment (8), presumably reflecting too sudden a change in metabolic activity for patients with existing cardiac complications. 

MacFarlane IA, Shalet SM, Beardwell CG, Khara JS. Transient hypothyroidism after iodine-131 treatment for thyrotoxicosis. BMJ 1979 2(6187) 421. 

Rokke KE, Vogt JH. Combination of potassium perchlorate and propylthiouracil in the treatment of thyrotoxicosis. Acta Endocrinol (Copenh) 1968 57(4) 565-77. 

Johnson RS, Moore WG. Fatal aplastic anaemia after treatment of thyrotoxicosis with potassium perchlorate. BMJ 1961 5236 1369-71. 

Chan AO, Ng IO, Lam CM, Shek TW, Lai CL. Cholestatic jaundice caused by sequential carbimazole and propylthiouracil treatment for thyrotoxicosis. Hong Kong Med J 2003 9 377-80. 

Krolner B, Jorgensen JV, Nielsen SP. Spinal bone mineral content in myxoedema and thyrotoxicosis. Effects of thyroid hormone(s) and antithyroid treatment. Clin Endocrinol (Oxf) 1983 18(5) 439 16. 

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