Hypothyroidism is a syndrome resulting from deficiency of thyroid hormones and is manifested largely by a reversible slowing down of all body functions (Table 38–4). In infants and children, there is striking retardation of growth and development that results in dwarfism and irreversible mental retardation.
The etiology and pathogenesis of hypothyroidism are outlined in Table 38–5. Hypothyroidism can occur with or without thyroid enlargement (goiter). The laboratory diagnosis of hypothyroidism in the adult is easily made by the combination of low free thyroxine and elevated serum TSH levels (Table 38–2).
TABLE 38–5Etiology and pathogenesis of hypothyroidism. ||Download (.pdf) TABLE 38–5 Etiology and pathogenesis of hypothyroidism.
|Cause ||Pathogenesis ||Goiter ||Degree of Hypothyroidism |
|Hashimoto’s thyroiditis ||Autoimmune destruction of thyroid ||Present early, absent later ||Mild to severe |
|Drug-induced1 ||Blocked hormone formation2 ||Present ||Mild to moderate |
|Dyshormonogenesis ||Impaired synthesis of T4 due to enzyme deficiency ||Present ||Mild to severe |
|Radiation, 131I, X-ray, thyroidectomy ||Destruction or removal of gland ||Absent ||Severe |
|Congenital (cretinism) ||Athyreosis or ectopic thyroid, iodine deficiency; TSH receptor-blocking antibodies ||Absent or present ||Severe |
|Secondary (TSH deficit) ||Pituitary or hypothalamic disease ||Absent ||Mild |
The most common cause of hypothyroidism in the United States at this time is probably Hashimoto’s thyroiditis, an immunologic disorder in genetically predisposed individuals. In this condition, there is evidence of humoral immunity in the presence of antithyroid antibodies and lymphocyte sensitization to thyroid antigens. Genetic mutations as discussed previously and certain medications also can cause hypothyroidism (Table 38–5).
MANAGEMENT OF HYPOTHYROIDISM
Except for hypothyroidism caused by drugs, which can be treated in some cases by simply removing the depressant agent, the general strategy of replacement therapy is appropriate. The most satisfactory preparation is levothyroxine, administered as either a branded or generic preparation. Multiple trials have documented that combination levothyroxine plus liothyronine is not superior to levothyroxine alone although some patients remain unwell on thyroxine alone. Genetic variations in deiodinases or hormone transporters may account for some of this lack of efficacy.
There is some variability in the absorption of thyroxine; dosage will also vary depending on age and weight. Infants and children require more T4 per kilogram of body weight than adults. The average dosage for an infant 1–6 months of age is 10–15 mcg/kg per day, whereas the average dosage for an adult is about 1.7 mcg/kg per day (0.8 mcg/lb per day) or 125 mcg/d. Older adults (>65 years of age) may require less thyroxine (1.6 mcg/kg per day or 0.7 mcg/lb per day) for replacement as body mass declines. In patients requiring suppression therapy post-thyroidectomy for thyroid cancer, the average daily dosage of T4 is 2.2 mcg/kg or 1 mcg/lb. Higher thyroxine requirements have also been reported in patients with celiac disease and Helicobacter pylori gastritis; thyroxine doses may be lower following treatment.
Since interactions with certain foods (eg, bran, soy, coffee) and drugs (Table 38–3) can impair its absorption, thyroxine should be administered on an empty stomach (eg, 60 minutes before meals, 4 hours after meals, or at bedtime) to maintain TSH within an optimal range of 0.5–2.5 mIU/L. Its long half-life of 7 days permits once-daily dosing. Children should be monitored for normal growth and development. Serum TSH and free thyroxine should always be measured before a change in dosage to avoid transient serum alterations. It takes 6–8 weeks after starting a given dose of thyroxine to reach steady-state levels in the bloodstream. Thus, dosage changes should be made slowly.
In younger patients or those with very mild disease, full replacement therapy may be started immediately. In older patients (>50 years) without cardiac disease, levothyroxine can be started at a dosage of 50 mcg/d. In long-standing hypothyroidism and in older patients with underlying cardiac disease, it is imperative to start with reduced dosages of levothyroxine, 12.5–25 mcg/d for 2 weeks, before increasing by 12.5–25 mcg/d every 2 weeks until euthyroidism or drug toxicity is observed. In cardiac patients, the heart is very sensitive to the level of circulating thyroxine, and if angina pectoris or cardiac arrhythmia develops, it is essential to stop or reduce the thyroxine dosage immediately.
Thyroxine toxicity is directly related to the hormone level. In children, restlessness, insomnia, and accelerated bone maturation and growth may be signs of thyroxine toxicity. In adults, increased nervousness, heat intolerance, episodes of palpitation and tachycardia, or unexplained weight loss may be the presenting symptoms. If these symptoms are present, it is important to monitor serum TSH and FT4 levels (Table 38–2), which will determine whether the symptoms are due to excess thyroxine blood levels. Chronic overtreatment with T4, particularly in elderly patients, can increase the risk of atrial fibrillation and accelerated osteoporosis.
Special Problems in Management of Hypothyroidism
A. Myxedema and Coronary Artery Disease
Since myxedema frequently occurs in older persons, it is often associated with underlying coronary artery disease. In this situation, the low levels of circulating thyroid hormone actually protect the heart against increasing demands that could result in angina pectoris, atrial fibrillation, or myocardial infarction. Correction of myxedema must be done cautiously to avoid provoking these cardiac events. If coronary artery surgery is indicated, it should be done first, prior to correction of the myxedema by thyroxine administration.
Myxedema coma is an end state of untreated hypothyroidism. It is associated with progressive weakness, stupor, hypothermia, hypoventilation, hypoglycemia, hyponatremia, water intoxication, shock, and death.
Myxedema coma is a medical emergency. The patient should be treated in the intensive care unit, since tracheal intubation and mechanical ventilation may be required. Associated illnesses such as infection or heart failure must be treated by appropriate therapy. It is important to give all preparations intravenously, because patients with myxedema coma absorb drugs poorly from other routes. Intravenous fluids should be administered with caution to avoid excessive water intake. These patients have large pools of empty T3 and T4 binding sites that must be filled before there is adequate free thyroxine to affect tissue metabolism. Accordingly, the treatment of choice in myxedema coma is to give a loading dose of levothyroxine intravenously—usually 300–400 mcg initially, followed by 50–100 mcg daily. Intravenous T3 5–20 mcg initially, followed by 2.5–10 mcg every 8 hours also can be added but may be more cardiotoxic and more difficult to monitor. Lower T4 and T3 doses should be considered for smaller or older patients, or those with concomitant cardiac disease or arrhythmias. Intravenous hydrocortisone is indicated if the patient has associated adrenal or pituitary insufficiency but is probably not necessary in most patients with primary myxedema. Opioids and sedatives must be used with extreme caution.
C. Hypothyroidism and Pregnancy
Hypothyroid women frequently have anovulatory cycles and are therefore relatively infertile until restoration of the euthyroid state. This has led to the widespread use of thyroid hormone for infertility, although there is no evidence for its usefulness in infertile euthyroid patients. In a pregnant hypothyroid patient receiving thyroxine, it is extremely important that the daily dose of thyroxine be adequate because early development of the fetal brain depends on maternal thyroxine. In many hypothyroid patients, an increase in the thyroxine dose (about 25–30%) is required to normalize the serum TSH level during pregnancy. It is reasonable to counsel women to take one extra dose of their current thyroxine tablet twice a week separated by several days as soon as they are pregnant. Thyroxine should also be administered apart from prenatal vitamins and calcium by at least 4 hours. Because of the elevated maternal TBG levels and, therefore, elevated total T4 levels, adequate maternal thyroxine dosages warrant maintenance of TSH between 0.1 and 3.0 mIU/L (eg, first trimester, 0.1–2.5 mIU/L; second trimester, 0.2–3.0 mIU/L; third trimester, 0.3–3.0 mIU/L) and the total T4 at or above the upper range of normal.
D. Subclinical Hypothyroidism
Subclinical hypothyroidism, defined as an elevated TSH level and normal thyroid hormone levels, occurs in 4–10% of the general population and increases to 20% in women older than age 50. Levothyroxine should be individualized based on the risks and benefits of treatment. The consensus of expert thyroid organizations concluded that thyroid hormone therapy should be considered for patients with TSH levels greater than 10 mIU/L while close TSH monitoring is appropriate for those with lower TSH elevations.
E. Drug-Induced Hypothyroidism
Drug-induced hypothyroidism (Table 38–3) can be satisfactorily managed with levothyroxine therapy if the offending agent cannot be stopped. In the case of amiodarone-induced hypothyroidism, levothyroxine therapy may be necessary even after discontinuance because of amiodarone’s very long half-life.
Hyperthyroidism (thyrotoxicosis) is the clinical syndrome that results when tissues are exposed to high levels of thyroid hormone (Table 38–4).
The most common form of hyperthyroidism is Graves’ disease, or diffuse toxic goiter. The presenting signs and symptoms of Graves’ disease are set forth in Table 38–4.
Graves’ disease is considered to be an autoimmune disorder in which a defect in suppressor T lymphocytes stimulates B lymphocytes to synthesize antibodies (TSH-R Ab [stim]) to thyroidal antigens. The TSH-R Ab [stim] is directed against the TSH receptor in the thyroid cell membrane and stimulates growth and biosynthetic activity of the thyroid cell. Genetics, the postpartum state, cigarette smoking, and physical and emotional stress increase TSH-R Ab [stim] development. A genetic predisposition is shown by a high frequency of HLA-B8 and HLA-DR3 in Caucasians, HLA-Bw46 and HLA-B5 in Chinese, and HLA-B17 in African Americans. Spontaneous remission occurs but some patients require years of antithyroid therapy.
In most patients with hyperthyroidism, T3, T4, FT4, and FT3 are elevated and TSH is suppressed (Table 38–2). Radioiodine uptake is usually markedly elevated as well. Antithyroglobulin, thyroid peroxidase, and TSH-R Ab [stim] antibodies are usually present.
Management of Graves’ Disease
The three primary methods for controlling hyperthyroidism are antithyroid drug therapy, destruction of the gland with radioactive iodine, and surgical thyroidectomy. None of these methods alters the underlying pathogenesis of the disease.
A. Antithyroid Drug Therapy
Drug therapy is most useful in young patients with small glands and mild disease. Methimazole (preferred) or propylthiouracil is administered until the disease undergoes spontaneous remission. This is the only therapy that leaves an intact thyroid gland, but it does require a long period of treatment and observation (12–18 months), and there is a 50–60% incidence of relapse.
Methimazole is preferable to propylthiouracil (except in pregnancy and thyroid storm) because it has a lower risk of serious liver injury and can be administered once daily, which may improve adherence. Antithyroid drug therapy is usually begun with divided doses, shifting to maintenance therapy with single daily doses when the patient becomes clinically euthyroid. However, mild to moderately severe thyrotoxicosis can often be controlled with methimazole given in a single morning dose of 20–40 mg initially for 4–8 weeks to normalize hormone levels. Maintenance therapy requires 5–15 mg once daily. Alternatively, therapy is started with propylthiouracil, 100–150 mg every 6 or 8 hours until the patient is euthyroid, followed by gradual reduction of the dose to the maintenance level of 50–150 mg once daily. In addition to inhibiting iodine organification, propylthiouracil also inhibits the conversion of T4 to T3, so it brings the level of activated thyroid hormone down more quickly than does methimazole. The best clinical guide to remission is reduction in the size of the goiter. Laboratory tests most useful in monitoring the course of therapy are serum FT3, FT4, and TSH levels.
Reactions to antithyroid drugs have been described above. A minor rash can often be controlled by antihistamine therapy. Because the more severe reaction of agranulocytosis is often heralded by sore throat or high fever, patients receiving antithyroid drugs must be instructed to discontinue the drug and seek immediate medical attention if these symptoms develop. White cell and differential counts and a throat culture are indicated in such cases, followed by appropriate antibiotic therapy. Treatment should also be stopped if significant elevations in transaminases (two to three times the upper limit of normal) occur.
A near-total thyroidectomy is the treatment of choice for patients with very large glands or multinodular goiters. Patients are treated with antithyroid drugs until euthyroid (about 6 weeks). In addition, for 10–14 days prior to surgery, they receive saturated solution of potassium iodide, 5 drops twice daily, to diminish vascularity of the gland and simplify surgery. About 80–90% of patients will require thyroid supplementation following near-total thyroidectomy.
Radioiodine therapy (RAI) utilizing 131I 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 μCi/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 stopped for 2 to 3 days before RAI is administered so as not to interfere with RAI retention but can be restarted 3–5 days later, and then gradually tapered over 4–6 weeks as thyroid function normalizes. Iodides should be avoided to ensure maximal 131I uptake. Six to 12 weeks following the administration of RAI, the gland will shrink in size and the patient will usually become euthyroid or hypothyroid. A second dose may be required if there is minimal response 3 months post-RAI. Hypothyroidism occurs in about 80% of patients following RAI. Serum FT4 and TSH levels should be monitored regularly. When hypothyroidism develops, prompt replacement with oral levothyroxine, 50–150 mcg daily, should be instituted.
D. Adjuncts to Antithyroid Therapy
During the acute phase of thyrotoxicosis, β-adrenoceptor–blocking agents without intrinsic sympathomimetic activity are appropriate in symptomatic patients aged 60 years or more, in those with heart rates greater than 90 beats/min, and in those with cardiovascular disease. Propranolol, 20–40 mg orally every 6 hours, or metoprolol, 25–50 mg orally every 6–8 hours, will control tachycardia, hypertension, and atrial fibrillation. Beta-adrenoceptor–blocking agents are gradually withdrawn as serum thyroxine levels return to normal. Diltiazem, 90–120 mg three or four times daily, can be used to control tachycardia in patients in whom β blockers are contraindicated, eg, those with asthma. Dihydropyridine calcium channel blockers may not be as effective as diltiazem or verapamil. Adequate nutrition and vitamin supplements are essential. Barbiturates accelerate T4 breakdown (by hepatic enzyme induction) and may be helpful both as sedatives and to lower T4 levels. Bile acid sequestrants (eg, cholestyramine) can also rapidly lower T4 levels by increasing the fecal excretion of T4.
TOXIC UNINODULAR GOITER & TOXIC MULTINODULAR GOITER
These forms of hyperthyroidism occur often in older women with nodular goiters. Free thyroxine is moderately elevated or occasionally normal, but FT3 or T3 is strikingly elevated. Single toxic adenomas can be managed with either surgical excision of the adenoma or with radioiodine therapy. Toxic multinodular goiter is usually associated with a large goiter and is best treated by preparation with methimazole (preferable) or propylthiouracil followed by subtotal thyroidectomy.
During the acute phase of a viral infection of the thyroid gland, there is destruction of thyroid parenchyma with transient release of stored thyroid hormones. A similar state may occur in patients with Hashimoto’s thyroiditis. These episodes of transient thyrotoxicosis have been termed spontaneously resolving hyperthyroidism. Supportive therapy is usually all that is necessary, such as β-adrenoceptor–blocking agents without intrinsic sympathomimetic activity (eg, propranolol) for tachycardia and aspirin or nonsteroidal anti-inflammatory drugs to control local pain and fever. Corticosteroids may be necessary in severe cases to control the inflammation.
Thyroid storm, or thyrotoxic crisis, is sudden acute exacerbation of all of the symptoms of thyrotoxicosis, presenting as a life-threatening syndrome. Vigorous management is mandatory. Propranolol, 60–80 mg orally every 4 hours, or intravenous propranolol, 1–2 mg slowly every 5–10 minutes to a total of 10 mg, or esmolol, 50–100 mg/kg per min, is helpful to control the severe cardiovascular manifestations. If β blockers are contraindicated by the presence of severe heart failure or asthma, hypertension and tachycardia may be controlled with diltiazem, 90–120 mg orally three or four times daily or 5–10 mg/h by intravenous infusion (asthmatic patients only). Release of thyroid hormones from the gland is retarded by the administration of saturated solution of potassium iodide, 5 drops orally every 6 hours starting 1 hour after giving thioamides. Hormone synthesis is blocked by the administration of propylthiouracil, 500–1000 mg as a loading dose, followed by 250 mg orally every 4 hours. If the patient is unable to take propylthiouracil by mouth, a rectal formulation* can be prepared and administered in a dosage of 400 mg every 6 hours as a retention enema. Methimazole may also be prepared for rectal administration in a dose of 60–80 mg daily. Hydrocortisone, 50 mg intravenously every 6 hours, will protect the patient against shock and will block the conversion of T4 to T3, rapidly reducing the level of thyroactive material in the blood.
Supportive therapy is essential to control fever, heart failure, and any underlying disease process that may have precipitated the acute storm. In rare situations, where the above methods are not adequate to control the problem, oral bile acid sequestrants (eg, cholestyramine), plasmapheresis, or peritoneal dialysis has been used to lower the levels of circulating thyroxine.
Although severe ophthalmopathy is rare, it is difficult to treat. A 15–20% risk of aggravating severe eye disease may occur following RAI, especially in those who smoke. Management requires effective treatment of the thyroid disease, usually by total surgical excision or 131I ablation of the gland plus oral prednisone therapy (see below). In addition, local therapy may be necessary, eg, elevation of the head to diminish periorbital edema and artificial tears to relieve corneal drying due to exophthalmos. Smoking cessation should be advised to prevent progression of the ophthalmopathy. For the severe, acute inflammatory reaction, prednisone, 60–100 mg orally daily for about a week and then 60–100 mg every other day, tapering the dose over 6–12 weeks, may be effective. If steroid therapy fails or is contraindicated, irradiation of the posterior orbit, using well-collimated high-energy X-ray therapy, will frequently result in marked improvement of the acute process. Threatened loss of vision is an indication for surgical decompression of the orbit. Eyelid or eye muscle surgery may be necessary to correct residual problems after the acute process has subsided.
Dermopathy or pretibial myxedema will often respond to topical corticosteroids applied to the involved area and covered with an occlusive dressing.
Thyrotoxicosis During Pregnancy
Ideally, women in the childbearing period with severe disease should have definitive therapy with 131I or subtotal thyroidectomy prior to pregnancy in order to avoid an acute exacerbation of the disease during pregnancy or following delivery. If thyrotoxicosis does develop during pregnancy, RAI is contraindicated because it crosses the placenta and may injure the fetal thyroid. Propylthiouracil (fewer teratogenic risks than methimazole) can be given in the first trimester, and then methimazole can be given for the remainder of the pregnancy in order to avoid potential liver damage. The dosage of propylthiouracil must be kept to the minimum necessary for control of the disease (ie, <300 mg/d), because it may affect the function of the fetal thyroid gland. Alternatively, a subtotal thyroidectomy can be safely performed during the mid trimester. It is essential to give the patient a thyroid supplement during the balance of the pregnancy.
Graves’ disease may occur in the newborn infant, due either to passage of maternal TSH-R Ab [stim] through the placenta, stimulating the thyroid gland of the neonate, or to genetic transmission of the trait to the fetus. Laboratory studies reveal an elevated free T4, a markedly elevated T3, and a low TSH—in contrast to the normal infant, in whom TSH is elevated at birth. TSH-R Ab [stim] is usually found in the serum of both the child and the mother.
If caused by maternal TSH-R Ab [stim], the disease is usually self-limited and subsides over a period of 4–12 weeks, coinciding with the fall in the infant’s TSH-R Ab [stim] level. However, treatment is necessary because of the severe metabolic stress the infant experiences. Therapy includes propylthiouracil at a dosage of 5–10 mg/kg daily in divided doses at 8-hour intervals; Lugol’s solution (8 mg of iodide per drop), 1 drop every 8 hours; and propranolol, 2 mg/kg daily in divided doses. Careful supportive therapy is essential. If the infant is very ill, oral prednisone, 2 mg/kg daily in divided doses, will help block conversion of T4 to T3. These medications are gradually reduced as the clinical picture improves and can be discontinued by 6–12 weeks.
Subclinical hyperthyroidism is defined as a suppressed TSH level (below the normal range) in conjunction with normal thyroid hormone levels. Cardiac toxicity (eg, atrial fibrillation), especially in older persons and those with underlying cardiac disease, is of greatest concern. The consensus of thyroid experts concluded that hyperthyroidism treatment is appropriate in those with TSH less than 0.1 mIU/L, while close monitoring of the TSH level is appropriate for those with less TSH suppression.
In addition to those patients who develop hypothyroidism caused by amiodarone, approximately 3% of patients receiving this drug will develop hyperthyroidism instead. Two types of amiodarone-induced thyrotoxicosis have been reported: iodine-induced (type I), which often occurs in persons with underlying thyroid disease (eg, multinodular goiter, Graves’ disease); and an inflammatory thyroiditis (type II) that occurs in patients without thyroid disease due to leakage of thyroid hormone into the circulation. Treatment of type I requires therapy with thioamides, while type II responds best to glucocorticoids. Since it is not always possible to differentiate between the two types, thioamides and glucocorticoids are often administered together. If possible, amiodarone should be discontinued; however, rapid improvement does not occur due to its long half-life.
Nontoxic goiter is a syndrome of thyroid enlargement without excessive thyroid hormone production. Enlargement of the thyroid gland is often due to TSH stimulation from inadequate thyroid hormone synthesis. The most common cause of nontoxic goiter worldwide is iodide deficiency, but in the United States, it is Hashimoto’s thyroiditis. Other causes include germ-line or acquired mutations in genes involved in hormone synthesis, dietary goitrogens, and neoplasms (see below).
Goiter due to iodide deficiency is best managed by prophylactic administration of iodide. The optimal daily iodide intake is 150–200 mcg. Iodized salt and iodate used as preservatives in flour and bread are excellent sources of iodine in the diet. In areas where it is difficult to introduce iodized salt or iodate preservatives, a solution of iodized poppy-seed oil has been administered intramuscularly to provide a long-term source of inorganic iodine.
Goiter due to ingestion of goitrogens in the diet is managed by elimination of the goitrogen or by adding sufficient thyroxine to shut off TSH stimulation. Similarly, in Hashimoto’s thyroiditis and dyshormonogenesis, adequate thyroxine therapy—150–200 mcg/d orally—will suppress pituitary TSH and result in slow regression of the goiter as well as correction of hypothyroidism.
Neoplasms of the thyroid gland may be benign (adenomas) or malignant. The primary diagnostic test is a fine needle aspiration biopsy and cytologic examination. Benign lesions may be monitored for growth or symptoms of local obstruction, which would mandate surgical excision. Levothyroxine therapy is not recommended for the suppression of benign nodules, especially in iodine sufficient areas. Management of thyroid carcinoma requires a total thyroidectomy, postoperative radioiodine therapy in selected instances, and lifetime replacement with levothyroxine. The evaluation for recurrence of some thyroid malignancies often involves withdrawal of thyroxine replacement for 4–6 weeks—accompanied by the development of hypothyroidism. Tumor recurrence is likely if there is a rise in serum thyroglobulin (ie, a tumor marker) or a positive 131I scan when TSH is elevated. Alternatively, administration of recombinant human TSH (Thyrogen) can produce comparable TSH elevations without discontinuing thyroxine and avoiding hypothyroidism. Recombinant human TSH is administered intramuscularly once daily for 2 days. A rise in serum thyroglobulin or a positive 131I scan will indicate a recurrence of the thyroid cancer.
SUMMARY Drugs Used in the Management of Thyroid Disease
|Subclass, Drug ||Mechanism of Action and Effects ||Indications ||Pharmacokinetics, Toxicities, Interactions |
|Thyroid Preparations |
• Levothyroxine (T4)
• Liothyronine (T3)
|Activation of nuclear receptors results in gene expression with RNA formation and protein synthesis ||Hypothyroidism ||See Table 38–1 • maximum effect seen after 6–8 weeks of therapy • Toxicity: See Table 38–4 for symptoms of thyroid excess |
|Antithyroid Agents |
• Propylthiouracil (PTU)
|Inhibit thyroid peroxidase reactions • block iodine organification • inhibit peripheral deiodination of T4 and T3 (primarily PTU) ||Hyperthyroidism ||Oral • duration of action: 24 h (methimazole), 6–8 h (PTU) • delayed onset of action • Toxicity: Nausea, gastrointestinal distress, rash, agranulocytosis, hepatitis (PTU black box), hypothyroidism |
• Lugol’s solution
• Potassium iodide
|Inhibit organification and hormone release • reduce the size and vascularity of the gland ||Preparation for surgical thyroidectomy ||Oral • acute onset within 2–7 days • Toxicity: Rare (see text) |
|BETA BLOCKERS |
|• Propranolol, other β blockers lacking partial agonist activity ||Inhibition of β adrenoreceptors • inhibit T4 to T3 conversion (only propranolol) ||Hyperthyroidism, especially thyroid storm • adjunct to control tachycardia, hypertension, and atrial fibrillation ||Onset within hours • duration of 4–6 h (oral propranolol) • Toxicity: Asthma, AV blockade, hypotension, bradycardia |
|RADIOACTIVE IODINE 131I (RAI) |
| ||Radiation destruction of thyroid parenchyma ||Hyperthyroidism • patients should be euthyroid or on β blockers before RAI • avoid in pregnancy and in nursing mothers ||Oral • half-life 5 days • onset in 6–12 weeks • maximum effect in 3–6 months • Toxicity: Sore throat, sialitis, hypothyroidism |
|GENERIC NAME ||AVAILABLE AS |
|THYROID AGENTS |
|Levothyroxine (T4) ||Generic, Levoxyl, Levo-T, Levothroid, Levolet*, Novothyrox, Synthroid, Tirosint (capsule), Unithroid |
|Liothyronine (T3) ||Generic, Cytomel, Triostat (IV) |
|Liotrix (a 4:1 ratio of T4: T3) ||Thyrolar |
|Thyroid desiccated (USP) ||Generic, Armour, Nature-Throid, Westhroid |
|ANTITHYROID AGENTS |
|Radioactive iodine (131I) sodium ||Iodotope, Sodium Iodide I 131 Therapeutic |
|Methimazole ||Generic, Tapazole |
|Potassium iodide || |
| Oral solution (SSKI) ||ThyroShield |
| Oral solution (Lugol’s solution) ||Lugol’s solution |
| Oral potassium iodide tablets ||IOSAT, Thyro-Block, Thyro-Safe |
|Propylthiouracil [PTU] ||Generic |
|DIAGNOSTIC AGENT |
|Thyrotropin; recombinant human TSH ||Thyrogen |