Hyperthyroidism therapy

Three common treatment modalities are used in the management of hyperthyroidism surgery, antithyroid medications, and radioactive iodine (RAI) (Table 73-5). The overall therapeutic objectives are to eliminate the excess thyroid hormone and minimize the symptoms and long-term consequences of hyperthyroidism. Therapy must be individuahzed based on the type and severity of hyperthyroidism, patient age and gender, existence of nonthyroidal con-... 

Initial daily doses of 10-40 and 100-600 mg are recommended in clinical practice for MMI and PTU, respectively [1, 2]. Several studies have shown that treatment of hyperthyroidism with single daily doses of 10-40 mg of MMI is effective in the induction of euthyroidism in 80-90% of patients within 6 weeks [2]. The aim of the further antithyroid therapy is to maintain euthyroidism with the lowest necessary diug dose. Intrathyroidal diug accumulation is one cause for the efficiency of a single daily dose regimen. Moreover, a once daily dose yields better patients compliance. Single daily doses of PTU have been shown to be less effective in achieving euthyroidism than administration of three divided doses a day. If a once daily... 

During initial therapy, the most common adverse reactions seen are signs of overdose and hyperthyroidism (see Table 51-1). Adverse reactions other than symptoms of hyperthyroidism are rare. 

Before a patient starts therapy with an antithyroid drug, die nurse obtains a history of the symptoms of hyperthyroidism. It is important to include vital signs, weight, and a notation regarding the outward symptoms of die hyperthyroidism (see Table 51-1) in the physical assessment. If die patient is prescribed an iodine solution, it is essential that die nurse take a careful allergy history, particularly to iodine or seafood (which contains iodine). 

The common causes of thyrotoxicosis are shown in Table 41-6.29,30 Thyrotoxicosis can be related to the presence or absence of excess hormone production (hyperthyroidism). Graves disease is the most common cause of hyperthyroidism. Thyrotoxicosis in the elderly is more likely due to toxic thyroid nodules or multinodular goiter than to Graves disease. Excessive intake of thyroid hormone may be due to overtreatment with prescribed therapy. Surreptitious use of thyroid hormones also may occur, especially in health professionals or as a self-remedy for obesity. Thyroid hormones can be obtained easily without a prescription from health food stores or Internet sources. 

Some neonates born to mothers with Graves disease will be hyperthyroid at delivery. Antithyroid drug therapy (propylthiouracil 5-10 mg/kg per day or methimazole 0.5-1 mg/kg per day) may be required for up to 12 weeks. One drop per day of SSKI may be used in the first few days to rapidly reduce thyroid hormone synthesis and release. 

The growth and spread of thyroid carcinoma is stimulated hy TSH. An important component of thyroid carcinoma management is the use ofLT4 to suppress TSH secretion. Early in therapy, patients receive the lowest LT4 dose sufficient to fully suppress TSH to undetectable levels. Controlled trials show that suppressive LT4 therapy reduces tumor growth and improves survival. These patients are purposefully overtreated with LT4 and rendered subclinically hyperthyroid. Postmenopausal women should receive aggressive osteoporosis therapy to prevent LT4-induced bone loss. Other thyrotoxic complications, such as atrial fibrillation, should be monitored and managed appropriately. 

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. 

Blockers are usually used as adjunctive therapy with antithyroid drugs, RAI, or iodides when treating Graves disease or toxic nodules in preparation for surgery or in thyroid storm. /3-Blockers are primary therapy only for thyroiditis and iodine-induced hyperthyroidism. 

The goal of therapy is to destroy overactive thyroid cells, and a single dose of 4,000 to 8,000 rad results in a euthyroid state in 60% of patients at 6 months or less. A second dose of RAI should be given 6 months after the first RAI treatment if the patient remains hyperthyroid. 

After therapy (thionamides, RAI, or surgery) for hyperthyroidism has been initiated, patients should be evaluated on a monthly basis until they reach a euthyroid condition. 

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. 

Hyperthyroidism Long-term therapy may lead to disease remission. Also used to ameliorate hyperthyroidism in preparation for subtotal thyroidectomy or radioactive iodine therapy. 

Synthetic levothyroxine sodium is used most commonly and is the drug of choice. Oral doses are incompletely absorbed. In plasma levothyroxine is for more than 99% bound to proteins, mainly to TBG. Maximal effects are reached in 3 weeks and the activity persists for 1-3 weeks after withdrawal of chronic therapy. It has a half-life of 7 days which permits once-daily administration. Its adverse effects mainly consist of signs and symptoms of hyperthyroidism. 

The 3-blockers significantly reduce the peripheral manifestations of hyperthyroidism, particularly elevated heart rate, increased cardiac output, and muscle tremors. Although the 3-blockers can improve the clinical status of the hyperthyroid patient, the patient remains biochemically hyperthyroid. The 3-blockers should not be used as the sole form of therapy in hyperthyroidism. They are most logically employed in the management of hyperthyroid crisis, in the preoperative preparation for thyroidectomy, and during the initial period of administration of specific antithyroid drugs (see Chapter 65). 

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. 

Contraindications Advanced arteriosclerosis, agitated states, cardiovascular disease, concurrent use or within 14 days of discontinuation of MAOI therapy, glaucoma, history of drug abuse, hypertension (moderate-to-severe), hyperthyroidism, hypersensitivity to phentermine or sympathomimetic amines... 

Radioactive iodine is indicated in hyperthyroidism due to Graves disease or toxic nodular goitre and also used as palliative therapy after thyroidectomy for papillary carcinoma of thyroid. 

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