Brody's Human Pharmacology: With STUDENT CONSULT

Chapter 42 Thyroid and Antithyroid Drugs


Thyroid hormones

Antithyroid drugs



Therapeutic Overview

Thyroid gland hormones, L-tetraiodothyronine (T4, also known as thyroxine) or L-triiodothyronine (T3), are potent effectors of energy metabolism. Specifically a direct correlation exists between the levels of these hormones and whole body O2 consumption, heart rate and force of contraction, glucose and fatty acid use by muscle, lipolysis by adipose tissue, hepatic glycogenolysis, and gluconeogenesis. Further, these hormones are essential for neonatal growth and development. Levels of thyroid hormones are tightly regulated to properly maintain function. When circulating levels are excessive,hyperthyroidism ensues, and when levels are deficient, hypothyroidism is manifest.

Acquired hypothyroidism is commonly associated with loss of thyroid, usually involving advanced-stage thyroiditis, in which autoantibodies destroy the thyroid gland. Childhood hypothyroidism usually has a genetic origin and is complicated by its effects on growth and maturation, particularly in the brain. Other causes of hypothyroidism include familial goiter and surgical removal of the thyroid. Irrespective of the cause, hypothyroidism is treated by thyroid hormone replacement with either T4 or T3.

The most common causes of hyperthyroidism are Graves’ disease (a thyroid autoimmune disease) and toxic nodular goiter. In Graves’ disease, autoantibodies directed at thyroid-stimulating hormone (TSH) receptors in the thyroid membrane stimulate the unregulated overproduction of thyroid hormone. Although not presently possible, optimal therapy would be to specifically block the formation or effects of these antibodies. Current treatment strategies are directed at interfering with the effects of excess thyroid hormone levels through the use of β adrenergic receptor antagonists or cortisol, inhibiting the synthesis of thyroid hormones with antithyroid drugs, or ablation therapy through the use of radioactive iodine or surgery. Treatments for hypothyroidism and hyperthyroidism are summarized in the Therapeutic Overview Box.



Cyclic adenosine monophosphate


Iodothyronine deiodinase type 1


Iodothyronine deiodinase type 2


Iodothyronine deiodinase type 3






Reduced nicotinamide adenine dinucleotide phosphate




Reverse T3


L isomer of triiodothyronine


L isomer of thyroxine, tetraiodothyronine


Transthyretin, thyroxine-binding prealbumin


Thyroxine-binding globulin




Thyroid hormone receptor


Thyrotropin-releasing hormone


Thyroid-stimulating hormone, thyrotropin

Therapeutic Overview


Replacement therapy with synthetic thyroxine (T4)


Thioureylene drugs

β Adrenergic receptor antagonists


Radioactive iodine


Mechanisms of Action

Thyroid Hormones

Thyroid Hormone Biosynthesis

The iodinated compounds in thyroid follicular cells (thyrocytes) are derived by enzymatic condensation of the iodinated tyrosyl residues in thyroglobulin (Fig. 42-1). Among these are the two major thyroid hormones, L-isomers of T4 and T3. All of the T4 that is made is derived from the thyroid. In contrast, only a small fraction of the most biologically active form, T3, is produced and released from the thyroid. Most T3 is produced by peripheral tissues by removing an iodide from the outer ring of T4 through the action of 5’-deiodinase.


FIGURE 42–1 Structures of tyrosine and its iodinated derivatives.

The synthesis and release of T3 and T4 are shown in Figure 42-2. Thyrocytes concentrate iodide from the circulation via a symporter present on their basolateral surface that admits Na+ down its electrochemical gradient. This sodium/iodide symporter, which is also present in salivary glands, breast, and stomach, can transport other anions, such as pertechnetate and perchlorate, which can competitively inhibit iodide transport. Once iodide enters the thyrocyte, it is transported to the follicular lumen by an anion transporter in the apical membrane termed pendrin. As iodide reaches the follicular lumen, it is oxidized by a mechanism involving thyroperoxidase, H2O2, and two reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidases. Activated iodide forms covalent links with specific tyrosyl residues on thyroglobulin (Tg), which is present in the follicular lumen, producing the thyroid hormone precursors monoiodotyrosine (MIT) and diiodotyrosine (DIT). This process is referred to as organification of iodide. MIT or DIT can donate their iodinated phenolic rings to acceptor iodotyrosyl residues on DIT in the Tg backbone and form an ether linkage with the acceptor phenolic ring to form T4 and T3 covalently bound to Tg. This process is called coupling. Iodinated Tg is transported to and stored associated with the apical membrane. When thyroid hormone is required, iodinated Tg is transported into follicular cells by endocytosis, where it undergoes proteolysis, releasing T4 and T3 into the circulation. MIT and DIT are deiodinated and reused.


FIGURE 42–2 Intrathyroidal synthesis and processing of thyroid hormones. (1) Iodide is taken up at the basolateral cell membrane and transported to the apical membrane. (2) Polypeptide chains of Tg are synthesized in the rough endoplasmic reticulum, and posttranslational modifications take place in the Golgi. (3) Newly formed Tg is transported to the cell surface in small apical vesicles (AV). (4) Within the follicular lumen, iodide is activated and iodinates tyrosyl residues on Tg, producing fully iodinated Tg containing MIT, DIT, T4, and a small amount of T3 (organification and coupling), which is stored as colloid in the follicular lumen. (5) Upon TSH stimulation, villi at the apical membrane engulf the colloid and endocytose the iodinated Tg as either colloid droplets (CD) or small vesicles (MPV). (6)Lysosomal proteolysis of the droplets or vesicles hydrolyzes Tg to release its iodinated amino acids and carbohydrates. (7) T4 and T3 are released into the circulation. (8) DIT and MIT are deiodinated, and the iodide and tyrosine are recycled.

If the circulating level of iodide is elevated persistently, it may cause the thyroid to overproduce thyroid hormone. Thyrocytes use several mechanisms to maintain iodide homeostasis to prevent hormone overproduction from occurring. Initially, high levels of iodide cause thyrocytes to shut down organification and coupling, an inhibitory response referred to as the Wolff-Chaikoff effect. With continued iodide elevations, this inhibitory effect diminishes. However, the activity of the sodium/iodide symporter decreases in response to elevated iodide levels, preventing overproduction of thyroid hormone. In some patients with thyroiditis or in the fetus, the thyroid does not escape from the Wolff-Chaikoff effect, and persistently high iodine levels can cause hypothyroidism, leading to goiter formation.

Hormone synthesis in thyrocytes is regulated by TSH released from the pituitary. If the circulating level of thyroid hormone is abnormally elevated, pituitary sensitivity to thyrotropin-releasing hormone (TRH) is reduced, causing decreased production of TSH. Pituitary portal blood also carries counter-regulatory compounds that inhibit TSH release (i.e., dopamine and somatostatin) (see Chapter 38).

If levels of circulating thyroid hormone are abnormally decreased, pituitary sensitivity to TRH is increased, which stimulates TSH secretion and ultimately increases the release thyroid hormone.

Thyroid Hormone Receptors

Thyroid hormones exert their major effects by binding to thyroid hormone receptors (TRs), members of the nuclear receptor superfamily (see Chapter 1). Two genes encode TRs, and each can be transcribed into alternatively spliced products. The relative proportions of each isoform expressed are developmentally dependent and tissue specific. TRs can homodimerize but are generally present as heterodimers, most commonly with the receptor for 9-cis-retinoic acid but also with other nuclear hormone receptors. TRs associate with DNA as part of a complex of transcription factors, even in the absence of thyroid hormone. When T3 binds to its receptor, the interactions of the receptor with transcription corepressors and coactivators change, and local chromatin structure is modified by changes in histone acetylation. Binding of T3 increases transcription of some genes and decreases the transcription of others. Thyroid hormones also regulate the processing of ribonucleic acid transcripts and the stability of specific messenger ribonucleic acids, and have other non-nuclear actions. Another potential regulatory process is the expression of the TR splice variant (TRα2), which interacts with thyroid hormone response elements but is not activated by T3. Consequently, expression of TRα2 can reduce sensitivity to thyroid hormone.

Antihyperthyroid Drugs

As shown in Table 42-1, antithyroid drugs can inhibit the synthesis, release, and metabolism of thyroid hormone and alter its peripheral effects.

TABLE 42–1 Antithyroid Drugs


Mechanism of Action


Inhibition of iodide transport


Inhibition of organification and coupling

Iodide, lithium

Inhibition of deiodination of T4 to T3


Inhibition of hormone release

β Adrenergic receptor blockers

Antagonize hypersensitivity for circulating catecholamines


Treat potential adrenal crisis

Iopanoate (radiographic contrast agent)

Causes rapid decrease in serum T4 and T3

Drugs that Inhibit Thyroid Hormone Production

As depicted in Figure 42-2, thyroid hormone synthesis involves several processes including uptake, organification, and coupling of iodide, each of which can be inhibited. Perchlorate decreases thyroid hormone production by competing with iodide for the sodium/iodide symporter. Although perchlorate can be used briefly as a clinical antithyroid agent, cases of aplastic anemia have limited its usefulness. A single dose of perchlorate is used occasionally as a diagnostic agent after administration of a tracer dose of radioactive iodine to determine whether a defect exists in a patient’s ability to organify iodide.

Administration of pharmacological doses of iodide also transiently inhibits iodide uptake, synthesis, and release of thyroid hormone and reduces vascularity of the thyroid gland, which can reduce surgical complications.

The thioureylene drugs propylthiouracil (PTU) and methimazole interact with thyroperoxidase and NADPH oxidases to inhibit organification of iodide and its coupling to Tg. PTU also inhibits deiodination of T4 to T3, contributing to its antithyroid activity.

Lithium, an element used for the treatment of bipolar (manic-depressive) disorder (see Chapter 30), suppresses the release of thyroid hormone, and when used chronically can lead to hypothyroidism and TSH-induced nontoxic goiters.

Drugs that Affect the Action of Thyroid Hormones

Some symptoms of hyperthyroidism, such as tachycardia, mimic overactivity of the sympathetic nervous system. This phenomenon is related to thyroid hormone-induced increased density of β adrenergic receptors, expression of G-protein subunits, cyclic adenosine monophosphate (cAMP) levels, and expression of proteins that are both T3-responsive and cAMP-responsive, such as uncoupling protein 1, which is involved in thermogenesis. In addition, activation of β adrenergic receptors apparently facilitates the conversion of T4 to T3. Consequently, β adrenergic receptor-blocking drugs can be used to reduce the clinical symptoms of hyperthyroidism such as tremor and tachycardia and are used as adjunct therapy.

Glucocorticoids are often included in acute therapy of severe hyperthyroidism. Although there is no convincing evidence that patients with hyperthyroidism have clinical adrenal deficiency, hyperthyroidism increases Δ-4 steroid reductase activity, which enhances the rate of cortisol degradation. In addition, the glucocorticoids inhibit deiodinases, decreasing catabolism of T4 to T3. In severe hyperthyroidism, glucocorticoids may have an antipyretic effect.

Several iodine-rich oral agents developed for radiological visualization of the gallbladder (cholecystography) are potent inhibitors of all three deiodinases. Iopanoic acid has been used as adjunct treatment of severe hyperthyroidism. However, because these compounds can provide iodide, they could exacerbate hyperthyroidism, unless the patient has been pretreated with a thioureylene drug to inhibit organification. Further, the effects of the thioureylenes can be decreased by concurrent use of iopanate.


The pharmacokinetic parameters for thyroid hormones and representative antithyroid drugs are listed in Table 42-2.

TABLE 42–2 Pharmacokinetic Parameters of Thyroid Hormones and Antithyroid Drugs


Thyroid Hormones

The absorption of orally administered T3 is virtually complete with a t1/2 of 24 hours in euthyroid subjects. Thus blood levels rise and fall appreciably after each dose. In contrast, oral absorption of T4 is incomplete and variable. Because T4 has a t1/2 of approximately 7 days in euthyroid subjects, its blood levels do not display substantial variations after a daily dose. Oral absorption of T4 can be impeded by several compounds, including dietary constituents such as ferrous sulfate, Ca++, and soy flour. Conjugated thyroid hormone metabolites are secreted in the bile, and there is substantial enterohepatic recirculation, which can be blocked by ingestion of drugs like cholestyramine (Chapter 25).

T4 and T3 are almost completely protein-bound in the blood, with the highest affinity for thyroxine binding globulin (TBG) plasma proteins, binding approximately 70% of circulating hormones. Transthyretin (thyroxine-binding prealbumin, or TBPA) binds 15% of circulating hormones, whereas albumin, which has a lower affinity but massive binding capacity, accounts for 10% to 15%. Several drugs inhibit binding of thyroid hormones to plasma proteins, including salsalate, salicylate, and phenytoin. Acute illness can decrease the levels of TBG and TBPA, thus reducing total blood levels of thyroid hormone. Sex hormone levels also influence expression of TBG; a rise in estrogen increases hepatic production of TBG, whereas a rise in androgen decreases TBG production. When levels of binding proteins change, the total level of thyroid hormones measured in the blood also change. Thus it is important to measure serum TSH levels when assessing a patient’s thyroid status. The effective level of binding proteins can be assessed by measuring the amount of tracer-labeled T3 that binds to a resin or by measuring free hormone level by dialysis.

T4 is metabolized peripherally primarily by deiodination. Removal of an iodide from the outer ring of T4 produces T3, which is more biologically active than T4. However, removing an iodide from the inner ring of T4 (see Fig. 42-1) produces reverse T3 (rT3), which is biologically inactive. Similarly, removing an iodide from either ring inactivates T3.

The metabolism and excretion of the iodothyronines are increased by sulfation or glucuronidation. Because rT3 is more susceptible to sulfate conjugation than either T3 or T4, it is metabolized faster. The alanine side chain of the amino acids on T3 and T4 can also be metabolized to form the thyroacetic acids, TRIAC and TETRAC, which have very short half-lives.

Three iodothyronine deiodinases, which are intrinsic membrane selenoproteins, remove iodide from thyroid hormones. Deiodinase type 1 (D1) removes iodide from both rings, type 2 (D2) selectively deiodinates the outer ring, whereas type 3 (D3) selectively deiodinates the inner ring. D1 is most active in removing iodide from the inner ring of T3 sulfate and less active on T4; it is even less active in removing iodide from the outer ring of T3. D1 is the major deiodinase present in liver, kidney, and thyroid and is regulated by thyroid hormone levels in some tissues. D2 is the “activating” enzyme, selectively deiodinating the outer ring of T4, converting it to T3. D2 is the major enzyme in brown fat, heart, skeletal muscle, pituitary, and pineal, and thyroid hormone levels and adrenergic agents regulate D2 in some tissues. D3 deiodinates the inner ring of iodothyronines selectively, inactivating both T4 and T3. It is the major isoform in brain, fetal liver, and placenta.

In hyperthyroidism, transcription of D1 and D3 increases in some tissues, whereas transcription of D2 is reduced and its degradation is increased. In contrast, in hypothyroidism, D2 activity increases in some tissues, increasing conversion of T4 to T3.

Many factors influence the metabolism of thyroid hormones. Prolonged fasting reduces peripheral conversion of T4 to T3 by half while doubling the amount of T4 converted to rT3. The composition of a patient’s diet or nonthyroidal illness can also influence metabolism of thyroid hormones. Turnover of thyroid hormones is increased in hyperthyroidism and is slowed in hypothyroidism. Of the drugs that affect thyroid hormone metabolism, the iodine-rich antiarrhythmic agent amiodarone is the most egregious (Chapter 22). Amiodarone inhibits 5′-deiodinase activity, thus increasing serum T4 and rT3 levels while decreasing the level of T3. However, amiodarone has direct effects on the thyroid, promoting thyroiditis, and can cause hyperthyroidism or hypothyroidism as it releases iodide. One tablet of amiodarone contains 75 mg iodine.


Daily intake of approximately 150 µg iodide is considered normal, and doses up to 500 µg do not affect thyroid function appreciably. Depending upon underlying pathophysiology, large doses of iodine can exacerbate hyperthyroidism, induce hypothyroidism, or cause goiter formation. Two solutions of iodine are used therapeutically: Lugol’s solution (which contains 5% KI and 5% elemental iodine, or approximately 6 mg per drop) and saturated solution of potassium iodide (SSKI), which contains 1gm/mL KI or approximately 40 mg per drop. Surgeons often administer 30 mg iodine twice a day for a few days or weeks before surgery to inhibit hormone release and reduce thyroid vascularity in patients with Graves’ disease who are undergoing a partial thyroidectomy. In general, iodine preparations should be administered only after blocking organification, to prevent iodide from being incorporated into thyroid hormones.


Gastrointestinal absorption of thioureylenes is nearly complete. Because PTU has a relatively short serum t1/2, it must be administered every 8 hours to maintain effective circulating levels. In contrast, methimazole is not bound appreciably to plasma proteins, has a longer serum t1/2, and is concentrated substantially by the thyroid, with a slow turnover; thus it is effective administered once a day. Because the thioureylenes act primarily by inhibiting thyroid hormone synthesis, long periods of administration are required before euthyroidism is achieved. Both agents are metabolized by oxidation and conjugation.

Relationship of Mechanisms of Action to Clinical Response


Initial treatment of most patients with hyperthyroidism involves a thioureylene drug. Once the levels of thyroid hormone and TSH begin to normalize, the dose is usually reduced, reflecting the slower metabolism of thyroid hormone in euthyroid subjects. To avoid the risk of hypothyroidism once hormone levels return to normal, a smaller dose of T4 can be initiated and increased as individually required.

Long-term therapy for hyperthyroidism includes radioiodine, surgery or continued treatment with thioureylene drugs. In the United States, the therapy used most commonly for the definitive treatment of hyperthyroidism is radioactive iodine. Most patients treated with [131I] will become hypothyroid eventually, so it is common to administer a dose that will ablate thyroid function, rather than try to tailor the dose to the percent of radioiodine taken up and the size of the gland.

In selected patients a partial thyroidectomy can offer definitive therapy, and thyroid hormone supplementation may not be required. If hyperthyroidism is due to Graves’ disease, which has an immune etiology, remission may occur. After maintaining euthyroidism with a thioureylene for 1 to 2 years, the drug can be discontinued and the patient monitored for recurrence. Patients who have had the disease for a short time, or who have relatively small goiters, are more likely to experience remission. The percentage of patients likely to exhibit permanent remission varies but is less common (~20%) in areas where iodine intake is relatively high, such as in North America. If hyperthyroidism is due to autonomous thyroid nodules, spontaneous remission is unlikely.


Maintenance of a hypothyroid patient is most commonly accomplished with T4, which is the primary circulating form of thyroid hormone and has a duration of action that allows daily administration. Other commercially available forms include T3, T4 plus T3, desiccated thyroglobulin, and thyroid extract. To treat most hypothyroid patients, the thyroid hormone dose is increased gradually while the patient’s symptoms and serum levels of TSH are monitored. Because T4 has a long t1/2 in euthyroid individuals, which is even longer in hypothyroidism, it can take several months to establish the appropriate replacement dose for an individual patient. If a patient has a functioning remnant of thyroid tissue initially, that remnant can either hypertrophy or atrophy, affecting the replacement dose. In addition, the dose will change if drugs that alter thyroid hormone absorption or metabolism are prescribed or discontinued. Thus symptoms and TSH levels should be periodically monitored in hypothyroid patients.

To reduce the risk of precipitating or worsening angina, particularly in older hyperthyroid patients, the dose of thyroid hormone should be increased gradually. However, more aggressive replacement is required occasionally in myxedema stupor/coma, despite the increased risk of precipitating acute cardiac disease.

Pharmacovigilance: Clinical Problems, Side Effects, and Toxicity

Potential problems associated with some of the important drugs for thyroid disorders are summarized in the Clinical Problems Box.

Numerous drugs have been reported to decrease the action of T4 including central nervous system depressants, antihypertensive agents, antacids, and antibiotics. When prescribing thyroxine, it is critical to be aware of these important drug-drug interactions.

Common side effects of thioureylene drugs include pruritus, rash, and fever. Some patients taking PTU complain of a bitter or metallic taste. Worrisome but rare side effects include agranulocytosis (0.2% to 0.5%) and hepatic dysfunction (1%). Side effects can occur at any time during therapy, so it is important to warn the patient that if a persistent fever or other symptoms of infection develop, the drug must be stopped until it has been established that the white blood count is normal. PTU and methimazole both cross the placenta, so the doses used in pregnant women should be minimized. Both agents are also secreted in breast milk.

Acute side effects of a large oral dose of iodine include gastrointestinal upset and rash, whereas longer exposure can cause swelling of the lachrymal or salivary glands with persistent tearing and salivation and sore gums and teeth (iodism). The use of T4 to promote weight loss has decreased dramatically in the United States as a result of


Thyroid Hormones

Acute overdose: Angina, arrhythmias, or myocardial infarction

Chronic overdose: Accelerate osteoporosis or alter metabolism of other drugs

Chronic low dose: Bradycardia, sleepiness, hypercholesterolemia and coronary artery disease


Goiter, hyperthyroidism, hypothyroidism, iodism (swollen salivary and lachrymal glands)

Thioureylene drugs

Skin rash, granulocytopenia, serum sickness, hepatic toxicity


(In addition to generic and fixed-combination preparations, the following trade-named materials are some of the important compounds available in the United States.)


L-thyroxine, T4 (Levothroid, Levoxyl, Synthroid, Unithroid)

Liothyronine, T3 (Cytomel, Triostat)

Liotrix, T4:T3 [4:1] (Euthyroid, Thyrolar)

Recombinant human TSH (Thyrogen)

Thyroglobulin (Proloid)

Antithyroid Drugs

Methimazole (Tapazole, Thiamazole)

Propylthiouracil (generic)

side effects, although it can be very effective leading to loss of adipose and muscle tissue.

New Horizons

Recent data indicate that different TR isoforms can mediate different functional responses. Synthetic thyroid analogs with receptor specificity are currently being developed, such as GC-24, which binds relatively selectively to the β isoform. Such agents could be used potentially to selectively modulate certain thyroid hormone responsive genes in certain tissues.

If the level of serum Tg becomes undetectable after a thyroid cancer has been resected, Tg levels can be monitored for development of recurrent disease. Although it is very expensive, recombinant human TSH is available and can stimulate a poorly functioning metastasis to produce enough Tg to be detectable. Recombinant human TSH can also increase the amount of radioiodine taken up by a poorly functioning thyroid cancer, enhancing its therapeutic effect. Intensive research is being conducted for the early detection of thyroid cancer using biomarkers for simple laboratory detection.


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Anonymous. Potassium iodide for thyroid protection in a nuclear accident or attack. Med Lett. 2002;44:97-98.

Cooper D. Antithyroid drugs. N Engl J Med. 2005;352:905-917.

Duncan Bassett JH, Harvey CB, Williams GR. Mechanisms of thyroid hormone receptor-specific nuclear and extra nuclear actions. Mol Cell Endocrinol. 2003;213:1-11.

Shi etal 2002 Shi YB, Ritchie JWA, Taylor PM. Complex regulation of thyroid hormone action: Multiple opportunities for pharmacological intervention. Pharmacol Ther. 2002;94:235-251.


1. A 40-year-old woman presents for an annual physical. She is concerned that she is entering menopause. A physical examination revealed a slightly elevated heart rate and blood pressure. Palpation of her neck elicited a complaint of tenderness, and an enlarged thyroid was felt. Laboratory testing revealed elevated TSH, decreased thyroid hormone levels, and elevated thyroglobulin antibodies. Which of the following is the most likely diagnosis?

A. Graves’ disease

B. Hashimoto’s disease

C. Nontoxic goiter

D. Pituitary adenoma

E. Thyroid cancer

2. Which of the following would be the most likely diagnosis if the patient that is described in Question 1 had laboratory results of low TSH, elevated thyroid hormones, and elevated thyroglobulin antibodies?

A. Graves’ disease

B. Hashamoto’s disease

C. Pituitary adenoma

D. Thyroid cancer

E. Toxic goiter

3. A middle-aged woman has been newly diagnosed with hyperthyroidism. Her pharmacological management was initiated by oral administration of propranolol. Which of the following is the most likely reason for this decision?

A. Age and gender of patient

B. Medical history of agranulocytosis

C. Medical history of transient hyperthyroidism

D. Positive pregnancy test

E. Family history of toxic multinodular goiters

4. A patient with a history of hypertension is diagnosed with thyroid cancer requiring thyroid ablation. Because the patient rapidly developed hypothyroidism, she was evaluated for thyroid hormone replacement. Which of the following is the primary concern for thyroid hormone replacement for this patient?

A. It is necessary to rapidly restore the circulating levels of thyroxine, because this patient’s physiology has adapted to hypertension.

B. Patient’s hypertension will require a slower than normal rate of restoration of thyroid hormone levels.

C. There are gender differences in the levels of thyroid hormone that must be considered.

D. This patient is an ideal candidate for combination therapy with triidothyronine and tetraiodothyronine.

E. To prevent the growth-promoting properties of TSH, thyroid hormones levels must be adequate to suppress its formation by the anterior pituitary.

5. Which of the following potential problems that can affect the pharmacological management of hypothyroidism is most likely to have the greatest influence on long-term management of thyroiditis?

A. Effective immunosupression by oral prednisone

B. Extent of thyroid gland function

C. Recovery of TSH levels

D. Regeneration of the thyroid gland

E. Responsiveness to levothyroxine replacement therapy