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Drug interactions with thyroid hormones

Drug interactions with thyroid hormones
Author:
Martin I Surks, MD
Section Editor:
Douglas S Ross, MD
Deputy Editor:
Jean E Mulder, MD
Literature review current through: Jan 2024.
This topic last updated: Jun 13, 2023.

INTRODUCTION — Many patients whose thyroid function is evaluated also take medications for a variety of nonthyroidal illnesses. As a result, clinicians must be aware of the interactions between various drugs and thyroid function, including measurements of serum thyroid hormones and thyroid-stimulating hormone (TSH).

Issues relating to the major drug-induced or drug-related abnormalities in thyroid hormone secretion, transport, and metabolism will be reviewed here (table 1). Thyroid hormone assays and potential assay interference are reviewed separately. (See "Laboratory assessment of thyroid function", section on 'Assay interference with biotin ingestion'.)

THYROID HORMONE METABOLISM — Before discussing the different drug interactions with thyroid hormones, it is helpful to review briefly thyroid hormone metabolism and the pathways that may be affected by the administration of drugs.

Thyroidal synthesis and secretion of thyroxine (T4) and triiodothyronine (T3) are dependent on thyroid-stimulating hormone (TSH) (figure 1). Under the influence of TSH, thyroid follicular cells sequentially perform the following functions:

Transport of iodide from serum into the cells

Oxidation of iodide and iodination of tyrosine residues

Synthesis of T4 and T3

The latter two steps occur within thyroglobulin at the interface between the follicular cells and the lumen of the thyroid follicles. The thyroglobulin subsequently reenters the cell and is hydrolyzed to its constituent amino acids, including the thyroid hormones. The hormones are then secreted into the circulation, where they are tightly bound to serum binding proteins, mostly thyroxine-binding globulin (TBG) but also transthyretin and albumin. Most of the secreted hormone is T4; by comparison, serum T3 is mainly produced by deiodination of T4 in extrathyroidal tissues.

The principal pathway of thyroid hormone metabolism is progressive deiodination to inert metabolites. However, 20 percent of thyroid hormones are conjugated either with glucuronide or sulfate and excreted into the bile [1]. In the gut, some of these conjugates are hydrolyzed by bacterial enzymes and the freed hormones are then reabsorbed into the circulation.

The thyroid gland requires TSH for synthesis and secretion of thyroid hormones. In normal subjects, the serum concentrations of thyroid hormones and TSH are intimately related by a delicate negative feedback system by which serum thyroid hormones inhibit TSH secretion (figure 2). In the absence of hypothalamic or pituitary disease, the serum TSH concentration is the most valuable guide to the assessment of thyroid function and the most sensitive index of thyroid hormone action. (See "Laboratory assessment of thyroid function".)

Drugs can affect any aspect of the thyroid hormone system, including TSH secretion, thyroidal production of T4 and T3, their transport in serum, and their metabolism [2]. The result may be either overt thyroid dysfunction or biochemical abnormalities that do not result in clinically important thyroid dysfunction but may be misinterpreted as indicating its presence. (See "Laboratory assessment of thyroid function" and "Thyroid function in nonthyroidal illness".)

DRUGS THAT AFFECT TSH SECRETION — Several drugs inhibit thyroid-stimulating hormone (TSH) secretion. They include the following (table 1):

Pharmacologic doses of glucocorticoids (more than 20 mg per day of prednisone or its equivalent) [3,4]

Dobutamine in high doses [5]

Dopamine (more than 1 mcg/kg per minute) [6,7]

The somatostatin analogue octreotide (more than 100 mcg/day) [8,9]

Bexarotene, a retinoid X receptor ligand [10]

The administration of these drugs may confound the interpretation of serum TSH concentrations, depending upon the degree of sensitivity of the serum TSH assay. As examples:

If the serum TSH assay in use has a sensitivity in the range of 0.05 to 0.1 mcU/mL (mU/L), the administration of these may result in an "undetectable" serum TSH concentration, similar to that in patients with hyperthyroidism.

If a more sensitive assay that detects 0.01 mcU/mL is used, the serum TSH values in patients being given these drugs are usually in the range of 0.08 to 0.4 mcU/mL. These values can easily be distinguished from the suppressed values in patients with hyperthyroidism (<0.01 mcU/mL).

In one report, metformin caused suppression of serum TSH concentrations to subnormal levels in four hypothyroid patients receiving a stable dose of levothyroxine [11]. This was not associated with an increase in free thyroxine (T4); the mechanism is unclear.

DRUGS THAT CAUSE HYPERTHYROIDISM — Several drugs can cause hyperthyroidism, many of which can also cause hypothyroidism (table 1).

Iodine and iodide-containing drugs — High doses of iodides or drugs that contain iodide (table 2) may cause hyperthyroidism. The effect of iodide administration in patients with abnormal thyroid glands differs from that in normal subjects and depends upon the underlying disease process (see "Iodine-induced thyroid dysfunction"). As an example, iodide administration may result in hyperthyroidism in patients with endemic goiter and iodine deficiency and, in areas of iodide sufficiency, in euthyroid patients with nodular goiters containing autonomous nodules. These nodules probably function autonomously (independent of thyroid-stimulating hormone [TSH]); however, they do not secrete excessive amounts of thyroid hormones in the absence of exposure to high concentrations of iodide.

Administration of amiodarone and radiocontrast agents is a common cause of hyperthyroidism. Patients who receive radiographic contrast agents, which contain as much as 50 percent iodine by weight, may develop hyperthyroidism within several weeks after exposure [12].

Amiodarone can cause hyperthyroidism by two mechanisms (see "Amiodarone and thyroid dysfunction"):

Iodide-loading in patients with autonomous nodules [13,14]

The induction of thyroiditis [15]

Amiodarone-induced hyperthyroidism tends to increase with time. In one report, 12.1 percent of amiodarone-treated patients in an iodine-sufficient area became hyperthyroid after a mean duration of therapy of 21 months [14].

Patients with amiodarone-induced hyperthyroidism who have an underlying thyroid adenoma or toxic nodular goiter can be treated with a thionamide [16]. However, this approach is ineffective in patients with thyroiditis, who respond best to glucocorticoid therapy. In one report, as an example, 12 patients with amiodarone-induced thyroiditis (eight of whom had failed to respond to thionamides) were treated with prednisone (initial dose 40 mg/day) for three months [16]. Normal serum triiodothyronine (T3) concentrations were achieved after an average of eight days. Four patients relapsed as the prednisone dose was tapered. (See "Amiodarone and thyroid dysfunction".)

Lithium — Although better known as a cause of hypothyroidism, lithium has been associated with hyperthyroidism. This is discussed in detail elsewhere. (See "Lithium and the thyroid".)

Other — Interferon alfa and interleukin-2 have been associated with the same two types of hyperthyroidism (Graves' disease and painless thyroiditis) in a few patients, presumably by initiating or exacerbating thyroid autoimmune disease. Hyperthyroidism after ipilimumab and alemtuzumab has also been reported [17-19]. In a trial evaluating alemtuzumab versus interferon–beta-1a in patients with multiple sclerosis, thyroid dysfunction occurred more frequently in patients taking alemtuzumab (34 versus 6.5 percent) [19]. Among patients with alemtuzumab-related thyroid dysfunction, Graves' hyperthyroidism occurred most commonly (22 percent), followed by hypothyroidism and subacute thyroiditis (7 and 4 percent, respectively).

DRUGS THAT CAUSE HYPOTHYROIDISM — Several drugs can cause hypothyroidism (table 1):

Iodine — High doses of iodine can cause hypothyroidism. Normal thyroid follicular cells have several autoregulatory functions that protect against a sudden increase in iodide availability. Upon exposure to high concentrations of iodide, thyroid cells decrease the oxidation of iodide and thyroid hormone formation (the Wolff-Chaikoff effect) [9]. The efficiency of iodine transport decreases over a few weeks, thereby restoring the intrathyroidal iodide pool and thyroid hormone production toward normal. (See "Iodine-induced thyroid dysfunction".)

Thus, in normal subjects, exposure to high serum iodide concentrations causes only a small and transient decrease in serum thyroxine (T4) and triiodothyronine (T3) concentrations. However, in euthyroid patients who have Hashimoto's disease, have previously been treated with radioiodine, or have had thyroid surgery, escape from the Wolff-Chaikoff effect is impaired, and therefore, they may become hypothyroid when given high doses of iodide [20].

Similar considerations apply to amiodarone. In one report, as an example, hypothyroidism developed in 6.9 percent of patients treated with amiodarone for a mean of 21 months [14]. This complication primarily occurred in patients with preexisting thyroid disease.

Lithium — Lithium may cause hypothyroidism. A serum lithium concentration in the therapeutic range results in an increase in thyroid size in approximately 50 percent of patients and causes mild hypothyroidism in approximately 20 percent [21,22]. Some of the patients with hypothyroidism have antithyroid antibodies. If hypothyroidism develops, appropriate treatment is the administration of T4, not cessation of lithium therapy. (See "Lithium and the thyroid".)

Tyrosine kinase inhibitors — Oral tyrosine kinase inhibitors (eg, sunitinib, sorafenib, imatinib, motesanib) used for the treatment of gastrointestinal stromal tumors, renal cell carcinoma, hepatocellular cancer, chronic myeloid leukemia, and in other cancers can cause hypothyroidism [17]. Hypothyroidism may occur in patients with previously normal thyroid function and may be preceded by a destructive thyroiditis and transient suppression of thyroid-stimulating hormone (TSH) [23]. In patients with preexisting hypothyroidism, thyroid hormone requirements may increase [17,24,25]. Sorafenib treatment is associated with increased type 3 deiodination, which increases the metabolism of T4 and T3 [26]. This finding may explain, in part, the increased thyroid hormone requirements in patients taking these drugs.

Of the kinase inhibitors, sunitinib appears to cause thyroid dysfunction most frequently, with subclinical hypothyroidism reported in 30 to 80 percent of patients treated with sunitinib [27]. It is possible that kinase inhibitors like sunitinib that broadly target tyrosine kinases, specifically vascular endothelial growth factor (VEGF) receptors, are more likely to cause hypothyroidism by causing capillary regression and thyroid ischemia. Other possible mechanisms include a destructive thyroiditis [23,28], impaired iodine uptake [29], reduced thyroid peroxidase activity [30], or decreased clearance of TSH [31]. (See "Non-cardiovascular toxicities of molecularly targeted antiangiogenic agents", section on 'Thyroid dysfunction' and "Disorders that cause hypothyroidism", section on 'Drugs'.)

Checkpoint inhibitor immunotherapy — Immunologic checkpoint inhibition agents targeting cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) or programmed cell death 1 (PD-1) receptor (eg, nivolumab, pembrolizumab, ipilimumab) are used to treat patients with advanced melanoma and are rapidly being explored as therapy for other malignancies. They are associated with clinically significant endocrinopathies, the most common of which are hypophysitis and hypothyroidism (secondary to a destructive thyroiditis). (See "Overview of thyroiditis", section on 'Checkpoint inhibitor immunotherapy' and "Toxicities associated with immune checkpoint inhibitors", section on 'Endocrinopathies'.)

Interferon alfa and interleukin-2 — Interferon alfa and interleukin-2 can cause both permanent and transient hypothyroidism [17]. The thyroid injury is apparently due to the ability of these substances to induce or exacerbate thyroid autoimmune disease.

Aminoglutethimide — Aminoglutethimide, which is used to reduce adrenal secretion in patients with Cushing disease and adrenal, breast, or prostatic cancer, can cause hypothyroidism [32,33]. One report, as an example, evaluated 29 men with prostatic cancer treated with 1000 mg daily; 31 percent had clinical or biochemical evidence of hypothyroidism [33].

Other — Many other drugs, such as sulfonamides and sulfonylureas, have been implicated as causes of hypothyroidism in occasional patients (table 1). However, evidence for a cause-and-effect relationship is poor with these drugs.

Bexarotene has been reported to cause central hypothyroidism, as well as an increase in non-deiodinase metabolism of thyroid hormone [34]. Hypophysitis and panhypopituitarism, including central hypothyroidism, may also occur as a complication of ipilimumab (anti-cytotoxic T-lymphocyte-associated antigen [CTLA]-4) immunotherapy used for the treatment of metastatic melanoma. (See "Central hypothyroidism".)

Although hyperthyroidism occurs more commonly, hypothyroidism after alemtuzumab has also been reported, including spontaneous transition from Graves' hyperthyroidism to hypothyroidism due to the presence of thyrotropin receptor blocking antibodies [17,19].

Cases of hypothyroidism have also been described with thalidomide therapy, although the mechanism for this effect is unknown [35].

DRUGS THAT INTERFERE WITH THYROID HORMONE TRANSPORT AND METABOLISM — Many drugs and hormones affect thyroxine (T4) and triiodothyronine (T3) transport (binding) in serum. In addition, some drugs interfere with the absorption or metabolism of thyroid hormones (eg, T4).

Drugs that influence thyroid hormone binding in serum — Drugs may increase or decrease serum thyroxine-binding globulin (TBG) concentrations, thereby causing parallel changes in serum total, but not free, T4 and T3 concentrations (table 1). Serum thyroid-stimulating hormone (TSH) concentrations are unchanged. (See "Euthyroid hyperthyroxinemia and hypothyroxinemia".)

Among those that raise serum TBG, the most important are estrogen or selective estrogen receptor modulators (SERMs, including oral contraceptives, tamoxifen, and raloxifene), methadone, and fluorouracil. Thyroid hormone doses may need to be adjusted in hypothyroid women who initiate estrogen replacement therapy. (See "Treatment of primary hypothyroidism in adults".)

Among those that lower serum TBG, the most important are androgens, anabolic steroids, and glucocorticoids.

Several other drugs (such as salicylates, salsalate, fenclofenac and mefenamic acid, and furosemide) lower serum T4 and T3 concentrations by blocking hormone binding to TBG [36-39].

Heparin, even when administered subcutaneously, may cause an acute and transient increase in serum free T4 concentrations. This increase occurs because of generation of free fatty acids by heparin stimulation of lipoprotein lipase that displace T4 from binding proteins; this effect requires that the serum triglyceride concentration be greater than approximately 180 mg/dL (2 mmol/L). It is primarily an in vitro phenomenon [40].

Drugs that affect gastrointestinal absorption of thyroid hormone — Levothyroxine (T4) should not be taken with other medications that interfere with its absorption. It is prudent to separate the administration of these drugs and T4 by several hours. (See "Treatment of primary hypothyroidism in adults", section on 'Timing of dose' and "Treatment of primary hypothyroidism in adults", section on 'Persistent elevation in TSH'.)

The bile acid binding resins used in the treatment of hypercholesterolemia, cholestyramine and colestipol, and colesevelam bind thyroid hormones and decrease their absorption [41-43]. In euthyroid patients without thyroid disease, the administration of these resins has no adverse effects. However, hypothyroidism may occur in the following situations:

The concomitant administration of bile acid-binding resins and T4 in patients with hypothyroidism. If both are required, T4 should not be taken until several hours after administration of the bile acid-binding resin.

Although not yet reported in the literature, euthyroid patients with limited thyroid reserve due to subclinical thyroid disease or treatment with radioiodine would also seem to be at risk for the development of hypothyroidism during treatment with bile acid-binding resins.

Normal gastric acid secretion appears to be necessary for normal thyroid hormone absorption. Omeprazole [44], lansoprazole [45], and presumably other medications that reduce gastric acid secretion may interfere with thyroid hormone absorption [44].

Calcium carbonate also reduces the absorption of exogenous T4. In a prospective cohort study of 20 hypothyroid patients taking 1200 mg of elemental calcium as calcium carbonate for three months [46]:

The mean serum free and total T4 concentrations fell significantly during co-administration of calcium carbonate by 8 and 7 percent, respectively.

The mean serum TSH concentration increased by 69 percent (1.6 to 2.7 mU/L, p = 0.008), and 20 percent of patients had serum TSH concentrations above the normal range (highest 7.8 mU/L).

All changes resolved after calcium carbonate was discontinued.

Raloxifene or ciprofloxacin administered at the same time as T4 (levothyroxine) reproducibly interfered with the absorption of T4 in one patient [47] and two patients, respectively [48]. Sucralfate, ferrous sulfate, and aluminum hydroxide can also bind T4 in the gut, but their effect is smaller and also less consistent than those described above [49-51]. Sevelamer, lanthanum carbonate, and chromium have been shown to reduce T4 absorption in a formal six-hour absorption test [43,52].

Drugs that affect thyroid hormone metabolism or clearance

Antiseizure medications, rifampin – Drugs that are potent CYP3A inducers (eg, carbamazepine, phenobarbital, phenytoin, rifampin) increase the metabolism of T4 and T3 (table 1). As a result, T4-treated hypothyroid patients may need a higher dose when treated with any of these drugs. Conversely, the doses of these drugs may need adjustment because their metabolism varies according to thyroid status.

Phenobarbital and rifampin augment the rate of deiodination of T4 and T3, principally by stimulation of the hepatic drug-metabolizing enzyme system [53-55]. The hypothalamic-pituitary system in normal subjects compensates for an increase in hormone metabolism by augmenting thyroid hormone production and secretion. In the steady state, therefore, serum T4, T3, and TSH concentrations remain within the normal range. However, patients with subclinical or overt hypothyroidism who are treated with phenobarbital or rifampin cannot augment thyroid hormone production and secretion, thereby exacerbating the hypothyroidism.

By comparison, the interactions of phenytoin and carbamazepine on the thyroid system are more complex [56,57]. These drugs both augment the rate of thyroid hormone metabolism (similar to phenobarbital and rifampin) and displace thyroid hormones from the serum binding proteins, principally TBG. As a result, serum total and free T4 concentrations decrease by approximately 40 percent; the decrease in serum T3 is smaller, but TSH concentrations remain within the normal range. The decrease in free T4 is an artifact in most free T4 assays.

Oxcarbazepine, an antiseizure medication that has less of an effect on the hepatic P450 enzyme system, nonetheless is still associated with low serum T4 concentrations and normal TSH levels, suggesting a possible central effect [58].

Ritonavir-containing medicationsRitonavir is used in combination with antiviral medications to boost plasma concentrations of the antiviral medication (eg, regimens for human immunodeficiency virus [HIV] and for outpatient management of coronavirus disease 2019 [COVID-19]). Ritonavir is both an inhibitor of metabolic enzymes and transporters such as the CYP3A enzyme as well as a substrate of CYP3A. It increases the clearance of levothyroxine, in part through induction of glucuronidation, and may necessitate an increase in the dose of levothyroxine. In patients previously on a stable dose of thyroid hormone who will be receiving long-term ritonavir boosted antiretroviral therapy for HIV, TSH should be monitored, and the dose of levothyroxine increased as needed to maintain the TSH in the normal range. Some patients may require a change in their antiretroviral medication to a regimen that does not contain ritonavir [59]. (See "Thyroid gland dysfunction in the patient with HIV", section on 'Effects of medications'.)

Nirmatrelvir-ritonavir, the preferred option for COVID-19-specific therapy for symptomatic outpatients with risk for progression to severe disease, is taken for five days. Although it may increase TSH in patients previously taking a stable dose of levothyroxine, the effect is presumably reversible with discontinuation of therapy. Additional data are needed to assess the time-course of this effect. In the interim, if TSH levels obtained within a few weeks of treatment with a five-day course of nirmatrelvir-ritonavir are elevated, they should be repeated after an additional two to three weeks before altering the levothyroxine dose since it is assumed that the TSH levels will return to their pre-ritonavir treatment levels. (See "COVID-19: Management of adults with acute illness in the outpatient setting", section on 'Nirmatrelvir-ritonavir as preferred therapy'.)

Drugs that affect T3 production — Most serum triiodothyronine (T3) is produced by extrathyroidal monodeiodination of T4, a reaction catalyzed by 5'-monodeiodinase. Drugs that inhibit the action of this enzyme decrease T3 production and cause a fall in serum T3 concentrations. Drugs known to inhibit extrathyroidal T3 production include amiodarone [13], high doses of glucocorticoids (eg, more than 4 mg/day of dexamethasone) [60-64], beta-adrenergic antagonists [65-68], propylthiouracil (which is only given to treat hyperthyroidism), and the iodinated contrast agents (ipodate and iopanoic acid) used for oral cholecystography.

Amiodarone, as noted above, may cause hypothyroidism or hyperthyroidism by different mechanisms in susceptible patients. It also inhibits T4 conversion to T3 [13]. As a result, patients treated with amiodarone who do not develop hypothyroidism or hyperthyroidism often have low serum T3 concentrations, while serum total and free T4 concentrations are raised to just above the upper limit of the normal range. Serum TSH concentrations are usually normal but may be slightly high during the first few months of treatment.

High doses of propranolol or related drugs may inhibit T3 production from T4. In one study, some patients treated with more than 160 mg per day of propranolol had slightly high serum T4 and slightly low serum T3 concentrations, with normal serum TSH concentrations [65,66]. In hyperthyroid patients, atenolol, metoprolol, and alprenolol also decrease serum T3 concentrations slightly [67,68].

Serum T3 concentrations fall by approximately 30 percent for four to six days after single oral doses of sodium ipodate or iopanoic acid given for cholecystography. This effect has been used for the treatment of hyperthyroidism. These radiocontrast agents are not available in the United States. (See "Iodinated radiocontrast agents in the treatment of hyperthyroidism".)

SUMMARY

Background – Drugs can affect any aspect of thyroid hormone production, including thyroid-stimulating hormone (TSH) secretion, thyroidal production of thyroxine (T4) and triiodothyronine (T3), their transport in serum, and their metabolism. The result may be either overt thyroid dysfunction or biochemical abnormalities that do not result in clinically important thyroid dysfunction but may be misinterpreted as indicating its presence (table 1). (See 'Thyroid hormone metabolism' above.)

Drugs that inhibit TSH secretion – Drugs that in high doses may inhibit TSH secretion include glucocorticoids, dobutamine, dopamine, octreotide, and bexarotene. (See 'Drugs that affect TSH secretion' above.)

Drugs that can cause hypothyroidism or hyperthyroidism – Iodine (or iodide-containing drugs), lithium, interferon alfa, and interleukin-2 may cause hyperthyroidism or hypothyroidism. (See 'Drugs that cause hyperthyroidism' above and 'Drugs that cause hypothyroidism' above.)

Drugs that cause euthyroid hyperthyroxinemia or hypothyroxinemia – Some drugs may increase (eg, estrogen) or decrease (eg, androgens, glucocorticoids) serum thyroxine-binding globulin (TBG) concentrations, thereby causing parallel changes in serum total, but not free, T4 and T3 concentrations (table 1). Serum TSH concentrations are unchanged, and these drugs do not result in clinically important thyroid dysfunction but may be misinterpreted as indicating its presence. (See 'Drugs that influence thyroid hormone binding in serum' above and "Euthyroid hyperthyroxinemia and hypothyroxinemia".)

Drugs that interfere with T4 absorption – Several drugs can interfere with the absorption of levothyroxine (T4), including bile acid resins, proton pump inhibitors, calcium carbonate, and ferrous sulfate. It is prudent to separate the administration of these drugs and T4 by several hours. (See 'Drugs that affect gastrointestinal absorption of thyroid hormone' above and "Treatment of primary hypothyroidism in adults", section on 'Timing of dose'.)

Drugs that interfere with thyroid hormone metabolism or clearancePhenobarbital, rifampin, phenytoin, and carbamazepine increase the metabolism of T4 and T3. As a result, T4-treated hypothyroid patients may need a higher dose when treated with any of these drugs. Ritonavir (used in combination with antiviral therapy for HIV or for outpatient management of COVID-19) increases the clearance of levothyroxine and may necessitate an increase in the dose of levothyroxine, particularly for people with HIV who anticipate long-term treatment with ritonavir boosted antiretroviral therapy. For people previously taking a stable dose of levothyroxine who are treated with a five-day course of nirmatrelvir-ritonavir for COVID-19, any increase in TSH is presumably reversible with discontinuation of therapy. Additional data are needed to assess the time-course of this effect. (See 'Drugs that affect thyroid hormone metabolism or clearance' above.)

  1. Curran PG, DeGroot LJ. The effect of hepatic enzyme-inducing drugs on thyroid hormones and the thyroid gland. Endocr Rev 1991; 12:135.
  2. Burch HB. Drug Effects on the Thyroid. N Engl J Med 2019; 381:749.
  3. Brabant G, Brabant A, Ranft U, et al. Circadian and pulsatile thyrotropin secretion in euthyroid man under the influence of thyroid hormone and glucocorticoid administration. J Clin Endocrinol Metab 1987; 65:83.
  4. Brabant G, Prank K, Hoang-Vu C, et al. Hypothalamic regulation of pulsatile thyrotopin secretion. J Clin Endocrinol Metab 1991; 72:145.
  5. Lee E, Chen P, Rao H, et al. Effect of acute high dose dobutamine administration on serum thyrotrophin (TSH). Clin Endocrinol (Oxf) 1999; 50:487.
  6. Cooper DS, Klibanski A, Ridgway EC. Dopaminergic modulation of TSH and its subunits: in vivo and in vitro studies. Clin Endocrinol (Oxf) 1983; 18:265.
  7. Agner T, Hagen C, Andersen AN, Djursing H. Increased dopaminergic activity inhibits basal and metoclopramide-stimulated prolactin and thyrotropin secretion. J Clin Endocrinol Metab 1986; 62:778.
  8. Bertherat J, Brue T, Enjalbert A, et al. Somatostatin receptors on thyrotropin-secreting pituitary adenomas: comparison with the inhibitory effects of octreotide upon in vivo and in vitro hormonal secretions. J Clin Endocrinol Metab 1992; 75:540.
  9. Braverman LE. Iodine induced thyroid disease. Acta Med Austriaca 1990; 17 Suppl 1:29.
  10. Sherman SI, Gopal J, Haugen BR, et al. Central hypothyroidism associated with retinoid X receptor-selective ligands. N Engl J Med 1999; 340:1075.
  11. Vigersky RA, Filmore-Nassar A, Glass AR. Thyrotropin suppression by metformin. J Clin Endocrinol Metab 2006; 91:225.
  12. Martin FI, Tress BW, Colman PG, Deam DR. Iodine-induced hyperthyroidism due to nonionic contrast radiography in the elderly. Am J Med 1993; 95:78.
  13. Figge HL, Figge J. The effects of amiodarone on thyroid hormone function: a review of the physiology and clinical manifestations. J Clin Pharmacol 1990; 30:588.
  14. Trip MD, Wiersinga W, Plomp TA. Incidence, predictability, and pathogenesis of amiodarone-induced thyrotoxicosis and hypothyroidism. Am J Med 1991; 91:507.
  15. Bartalena L, Grasso L, Brogioni S, et al. Serum interleukin-6 in amiodarone-induced thyrotoxicosis. J Clin Endocrinol Metab 1994; 78:423.
  16. Bartalena L, Brogioni S, Grasso L, et al. Treatment of amiodarone-induced thyrotoxicosis, a difficult challenge: results of a prospective study. J Clin Endocrinol Metab 1996; 81:2930.
  17. Hamnvik OP, Larsen PR, Marqusee E. Thyroid dysfunction from antineoplastic agents. J Natl Cancer Inst 2011; 103:1572.
  18. Aranha AA, Amer S, Reda ES, et al. Autoimmune thyroid disease in the use of alemtuzumab for multiple sclerosis: a review. Endocr Pract 2013; 19:821.
  19. Daniels GH, Vladic A, Brinar V, et al. Alemtuzumab-related thyroid dysfunction in a phase 2 trial of patients with relapsing-remitting multiple sclerosis. J Clin Endocrinol Metab 2014; 99:80.
  20. Philippou G, Koutras DA, Piperingos G, et al. The effect of iodide on serum thyroid hormone levels in normal persons, in hyperthyroid patients, and in hypothyroid patients on thyroxine replacement. Clin Endocrinol (Oxf) 1992; 36:573.
  21. Spaulding SW, Burrow GN, Bermudez F, Himmelhoch JM. The inhibitory effect of lithium on thyroid hormone release in both euthyroid and thyrotoxic patients. J Clin Endocrinol Metab 1972; 35:905.
  22. Perrild H, Hegedüs L, Baastrup PC, et al. Thyroid function and ultrasonically determined thyroid size in patients receiving long-term lithium treatment. Am J Psychiatry 1990; 147:1518.
  23. Shinohara N, Takahashi M, Kamishima T, et al. The incidence and mechanism of sunitinib-induced thyroid atrophy in patients with metastatic renal cell carcinoma. Br J Cancer 2011; 104:241.
  24. de Groot JW, Zonnenberg BA, Plukker JT, et al. Imatinib induces hypothyroidism in patients receiving levothyroxine. Clin Pharmacol Ther 2005; 78:433.
  25. Brassard M, Neraud B, Trabado S, et al. Endocrine effects of the tyrosine kinase inhibitor vandetanib in patients treated for thyroid cancer. J Clin Endocrinol Metab 2011; 96:2741.
  26. Abdulrahman RM, Verloop H, Hoftijzer H, et al. Sorafenib-induced hypothyroidism is associated with increased type 3 deiodination. J Clin Endocrinol Metab 2010; 95:3758.
  27. Makita N, Iiri T. Tyrosine kinase inhibitor-induced thyroid disorders: a review and hypothesis. Thyroid 2013; 23:151.
  28. Desai J, Yassa L, Marqusee E, et al. Hypothyroidism after sunitinib treatment for patients with gastrointestinal stromal tumors. Ann Intern Med 2006; 145:660.
  29. Mannavola D, Coco P, Vannucchi G, et al. A novel tyrosine-kinase selective inhibitor, sunitinib, induces transient hypothyroidism by blocking iodine uptake. J Clin Endocrinol Metab 2007; 92:3531.
  30. Wong E, Rosen LS, Mulay M, et al. Sunitinib induces hypothyroidism in advanced cancer patients and may inhibit thyroid peroxidase activity. Thyroid 2007; 17:351.
  31. Verloop H, Smit JW, Dekkers OM. Sorafenib therapy decreases the clearance of thyrotropin. Eur J Endocrinol 2013; 168:163.
  32. Dowsett M, Mehta A, Cantwell BM, Harris AL. Low-dose aminoglutethimide in postmenopausal breast cancer: effects on adrenal and thyroid hormone secretion. Eur J Cancer 1991; 27:846.
  33. Figg WD, Thibault A, Sartor AO, et al. Hypothyroidism associated with aminoglutethimide in patients with prostate cancer. Arch Intern Med 1994; 154:1023.
  34. Smit JW, Stokkel MP, Pereira AM, et al. Bexarotene-induced hypothyroidism: bexarotene stimulates the peripheral metabolism of thyroid hormones. J Clin Endocrinol Metab 2007; 92:2496.
  35. Badros AZ, Siegel E, Bodenner D, et al. Hypothyroidism in patients with multiple myeloma following treatment with thalidomide. Am J Med 2002; 112:412.
  36. Stockigt JR, Lim CF, Barlow JW, et al. Interaction of furosemide with serum thyroxine-binding sites: in vivo and in vitro studies and comparison with other inhibitors. J Clin Endocrinol Metab 1985; 60:1025.
  37. Faber J, Waetjen I, Siersbaek-Nielsen K. Free thyroxine measured in undiluted serum by dialysis and ultrafiltration: effects of non-thyroidal illness, and an acute load of salicylate or heparin. Clin Chim Acta 1993; 223:159.
  38. McConnell RJ. Abnormal thyroid function test results in patients taking salsalate. JAMA 1992; 267:1242.
  39. Samuels MH, Pillote K, Asher D, Nelson JC. Variable effects of nonsteroidal antiinflammatory agents on thyroid test results. J Clin Endocrinol Metab 2003; 88:5710.
  40. Jaume JC, Mendel CM, Frost PH, et al. Extremely low doses of heparin release lipase activity into the plasma and can thereby cause artifactual elevations in the serum-free thyroxine concentration as measured by equilibrium dialysis. Thyroid 1996; 6:79.
  41. Harmon SM, Seifert CF. Levothyroxine-cholestyramine interaction reemphasized. Ann Intern Med 1991; 115:658.
  42. Witztum JL, Jacobs LS, Schonfeld G. Thyroid hormone and thyrotropin levels in patients placed on colestipol hydrochloride. J Clin Endocrinol Metab 1978; 46:838.
  43. Weitzman SP, Ginsburg KC, Carlson HE. Colesevelam hydrochloride and lanthanum carbonate interfere with the absorption of levothyroxine. Thyroid 2009; 19:77.
  44. Centanni M, Gargano L, Canettieri G, et al. Thyroxine in goiter, Helicobacter pylori infection, and chronic gastritis. N Engl J Med 2006; 354:1787.
  45. Sachmechi I, Reich DM, Aninyei M, et al. Effect of proton pump inhibitors on serum thyroid-stimulating hormone level in euthyroid patients treated with levothyroxine for hypothyroidism. Endocr Pract 2007; 13:345.
  46. Singh N, Singh PN, Hershman JM. Effect of calcium carbonate on the absorption of levothyroxine. JAMA 2000; 283:2822.
  47. Siraj ES, Gupta MK, Reddy SS. Raloxifene causing malabsorption of levothyroxine. Arch Intern Med 2003; 163:1367.
  48. Cooper JG, Harboe K, Frost SK, Skadberg Ø. Ciprofloxacin interacts with thyroid replacement therapy. BMJ 2005; 330:1002.
  49. Liel Y, Sperber AD, Shany S. Nonspecific intestinal adsorption of levothyroxine by aluminum hydroxide. Am J Med 1994; 97:363.
  50. Campbell NR, Hasinoff BB, Stalts H, et al. Ferrous sulfate reduces thyroxine efficacy in patients with hypothyroidism. Ann Intern Med 1992; 117:1010.
  51. Campbell JA, Schmidt BA, Bantle JP. Sucralfate and the absorption of L-thyroxine. Ann Intern Med 1994; 121:152.
  52. John-Kalarickal J, Pearlman G, Carlson HE. New medications which decrease levothyroxine absorption. Thyroid 2007; 17:763.
  53. Oppenheimer JH, Bernstein G, Surks MI. Increased thyroxine turnover and thyroidal function after stimulation of hepatocellular binding of thyroxine by phenobarbital. J Clin Invest 1968; 47:1399.
  54. Cavlieri RR, Sung LC, Becker CE. Effects of phenobarbital on thyroxine and triiodothyronine kinetics in Graves' disease. J Clin Endocrinol Metab 1973; 37:308.
  55. Isley WL. Effect of rifampin therapy on thyroid function tests in a hypothyroid patient on replacement L-thyroxine. Ann Intern Med 1987; 107:517.
  56. Smith PJ, Surks MI. Multiple effects of 5,5'-diphenylhydantoin on the thyroid hormone system. Endocr Rev 1984; 5:514.
  57. Surks MI, DeFesi CR. Normal serum free thyroid hormone concentrations in patients treated with phenytoin or carbamazepine. A paradox resolved. JAMA 1996; 275:1495.
  58. Miller J, Carney P. Central hypothyroidism with oxcarbazepine therapy. Pediatr Neurol 2006; 34:242.
  59. Sahajpal R, Ahmed RA, Hughes CA, Foisy MM. Probable interaction between levothyroxine and ritonavir: Case report and literature review. Am J Health Syst Pharm 2017; 74:587.
  60. LoPresti JS, Eigen A, Kaptein E, et al. Alterations in 3,3'5'-triiodothyronine metabolism in response to propylthiouracil, dexamethasone, and thyroxine administration in man. J Clin Invest 1989; 84:1650.
  61. Degroot LJ, Hoye K. Dexamethasone suppression of serum T3 and T4. J Clin Endocrinol Metab 1976; 42:976.
  62. Gamstedt A, Järnerot G, Kågedal B. Dose related effects of betamethasone on iodothyronines and thyroid hormone-binding proteins in serum. Acta Endocrinol (Copenh) 1981; 96:484.
  63. Duick DS, Warren DW, Nicoloff JT, et al. Effect of single dose dexamethasone on the concentration of serum triiodothyronine in man. J Clin Endocrinol Metab 1974; 39:1151.
  64. Chopra IJ, Williams DE, Orgiazzi J, Solomon DH. Opposite effects of dexamethasone on serum concentrations of 3,3',5'-triiodothyronine (reverse T3) and 3,3'5-triiodothyronine (T3). J Clin Endocrinol Metab 1975; 41:911.
  65. Kristensen BO, Weeke J. Propranolol-induced increments in total and free serum thyroxine in patients with essential hypertension. Clin Pharmacol Ther 1977; 22:864.
  66. Cooper DS, Daniels GH, Ladenson PW, Ridgway EC. Hyperthyroxinemia in patients treated with high-dose propranolol. Am J Med 1982; 73:867.
  67. Perrild H, Hansen JM, Skovsted L, Christensen LK. Different effects of propranolol, alprenolol, sotalol, atenolol and metoprolol on serum T3 and serum rT3 in hyperthyroidism. Clin Endocrinol (Oxf) 1983; 18:139.
  68. Reeves RA, From GL, Paul W, Leenen FH. Nadolol, propranolol, and thyroid hormones: evidence for a membrane-stabilizing action of propranolol. Clin Pharmacol Ther 1985; 37:157.
Topic 7845 Version 22.0

References

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